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1.
Objective To determine the electrocardiographic and cardiopulmonary effects of romifidine with and without prior or concurrent administration of glycopyrrolate. Study design Randomized crossover experimental study. Animals Six (three male, three female) cross‐bred dogs weighing 23 ± 2.4 kg. Methods Baseline cardiopulmonary measurements were obtained in conscious dogs and one of five treatments was administered. Glycopyrrolate (G) 0.01 mg kg?1, or saline (S) 0.5 mL, were administered IM as premedication (Gp or Sp), or G was administered concurrently (Gc) with romifidine (RO). Treatments were as follows T1, Sp + RO 40 µg kg?1; T2, Gp + RO (40 µg kg?1); T3, Sp + RO 120 µg kg?1; T4, Gp + RO (120 µg kg?1); T5, Sp + Gc + RO (120 µg kg?1). Romifidine or RO + Gc was administered subcutaneously 20 minutes after premedication (time 0), and further measurements were taken 10, 20, 30, 60 and 90 minutes after RO. The main treatment effect was evaluated using two‐way anova for repeated measures, followed by one‐way anova and a post‐hoc least squares difference test with a modified Bonferroni correction (p < 0.02). A Student's t‐test was used to compare the effect of romifidine at 20 and 60 minutes versus baseline values (p < 0.05). Results Both low‐ and high‐dose RO (T1, T3) significantly decreased heart rate (HR), respiratory rate (RR), cardiac index (CI) and stroke volume index, and increased arterial blood pressure (SAP), systemic vascular resistance (SVR), pulmonary arterial occlusion pressure (PAOP) and central venous pressure. High‐dose RO produced greater increases in SVR and SAP measurements. Neither dose of RO produced an alteration in blood gas values or the alveolar to arterial oxygen gradient. Glycopyrrolate significantly increased HR and CI from 10 to 90 minutes between T1/T2 and T3/T4. Increases in SAP were dose related with significant differences between T1/T3 and T2/T4 at 90 and 10 minutes, respectively, and were highest in animals receiving Gp or Gc. High‐dose RO groups (T3, T4) had higher values for SVR than low‐dose RO groups (T1, T2), unrelated to G administration. There was an increase in PAOP in all treatments. The oxygen extraction ratio was increased with all treatments: larger increases were observed in T1, T3 and T4 compared with only minimal changes in T2. Concurrent G administration was associated with an increased frequency of high‐grade second‐degree atrioventricular heart block with variable conduction at 10 and 20 minutes. Conclusions Romifidine produced effects consistent with other selective α2‐adrenoreceptor agonists. Glycopyrrolate offset the decrease in HR and partially offset the decrease in CI associated with RO administration. Glycopyrrolate premedication produced an initial tachycardia and added to the increase in SAP associated with RO. Concurrent G administration was associated with a higher frequency of dysrhythmias and is not recommended. Despite the decrease in RR, RO sedation did not alter blood gas values. Clinical relevance It appears likely that G administration prior to or concurrent with RO produces an increase in myocardial workload and oxygen demand suggesting that this combination should not be used in dogs with cardiomyopathy or heart failure. The improvement in oxygen extraction ratio with T2 suggests that G may be beneficial with lower doses of RO, nevertheless, the use of G and RO in cardiovascularly compromised patients is not advised.  相似文献   

2.
Objective To determine the cardiopulmonary response to romifidine (RO) in the dog with or without prior or concurrent administration of glycopyrrolate. Study Design Randomized, cross‐over experimental study. Animals Six (three male, three female) cross‐bred dogs weighing 23 ± 2.4 kg. Methods Two‐dimensional guided M‐mode echocardiography was performed in conscious dogs simultaneously with measurement of systolic arterial blood pressure (SBP) and heart rate (HR). Dimensions of the left ventricle (LVID), interventricular septum (IVS), and left ventricular free wall (LVFW) were obtained in systole (S) and diastole (D). Amplitude of motion (Amp) of the IVS and LVFW were also measured. From these, measures of wall stress (WS) and fractional shortening (FS) of the left ventricle were derived. Baseline echocardiographic measurements were recorded, following which one of the five treatments was administered. Glycopyrrolate (G) 0.01 mg kg?1, or saline (S) 0.5 mL, was administered IM as pre‐medication (Gp or Sp), or G was administered concurrently (Gc) with romifidine (RO). Treatments were: T1, Sp + RO (40 μg kg?1); T2, Gp + RO (40 μg kg?1); T3, Sp + RO (120 μg kg?1); T4, Gp + RO (120 μg kg?1); and T5, Sp + Gc +RO (120 μg kg?1). Romifidine or RO + Gc was administered SC 20 minutes after pre‐medication (time 0), and further measurements were taken 10, 20, 30, 60, and 90 minutes after RO. Results Echocardiographic indices of cardiac systolic function (LVID‐S, FS, Amp‐LVFW) and HR were decreased in RO‐sedated dogs (p < 0.0001) . The magnitude of change in cardiac indices was least with low‐dose RO. At most sampling times, high‐dose RO produced significantly more alteration in cardiac indices. Systolic blood pressure increased in all treatment groups, with the greatest increases in those groups receiving G. Glycopyrrolate significantly increased HR; however, cardiac indices were further reduced. Wall stress significantly increased, with a more dramatic increase in groups receiving G. Conclusions Indices of LV systolic function were reduced in RO‐sedated dogs in a dose‐related manner. Glycopyrrolate further reduced these indices and dramatically increased measurements of wall stress in dogs sedated with RO. Clinical relevance Use of low‐dose RO minimizes cardiac dysfunction; however, it should still be used cautiously in dogs with cardiomyopathy or heart failure. The routine use of G is not recommended to alleviate the bradycardia associated with RO in conscious dogs.  相似文献   

3.
ObjectiveTo investigate the cardiovascular effects of epidural romifidine in isoflurane-anaesthetized dogs.Study designProspective, randomized, blinded experiment.AnimalsA total of six healthy adult female Beagles aged 1.25 ± 0.08 years and weighing 12.46 ± 1.48 (10.25–14.50) kg.MethodsAnaesthesia was induced with propofol (6–9 mg kg?1) and maintained with 1.8–1.9% end-tidal isoflurane in oxygen. End-tidal CO2 was kept between 35 and 45 mmHg (4.7–6.0 kPa) using intermittent positive pressure ventilation. Heart rate (HR), arterial blood pressure and cardiac output (CO) were monitored. Cardiac output was determined using a LiDCO monitor and the derived parameters were calculated. After baseline measurements, either 10 μg kg?1 romifidine or saline (total volume 1 mL 4.5 kg?1) was injected into the lumbosacral epidural space. Data were recorded for 1 hour after epidural injection. A minimum of 1 week elapsed between treatments.ResultsAfter epidural injection, the overall means (± standard deviation, SD) of HR (95 ± 20 bpm), mean arterial blood pressure (MAP) (81 ± 19 mmHg), CO (1.63 ± 0.66 L minute?1), cardiac index (CI) (2.97 ± 1.1 L minute?1 m?2) and stroke volume index (SI) (1.38 ± 0.21 mL beat?1 kg?1) were significantly lower in the romifidine treatment compared with the overall means in the saline treatment [HR (129 ± 24 bpm), MAP (89 ± 17 mmHg), CO (3.35 ± 0.86 L minute?1), CI (6.17 ± 1.4 L minute?1 m?2) and SI (2.21 ± 0.21 mL beat?1 kg?1)]. The overall mean of systemic vascular resistance index (SVRI) (7202 ± 2656 dynes seconds cm?5 m?2) after epidural romifidine injection was significantly higher than the overall mean of SVRI (3315 ± 1167 dynes seconds cm?5 m?2) after epidural saline injection.ConclusionEpidural romifidine in isoflurane-anaesthetized dogs caused significant cardiovascular effects similar to those reportedly produced by systemic romifidine administration.Clinical relevanceSimilar cardiovascular monitoring is required after epidural and systemically administered romifidine. Further studies are required to evaluate the analgesic effects of epidural romifidine.  相似文献   

4.
ObjectiveTo compare the cardiopulmonary effects of intravenous (IV) and intramuscular (IM) medetomidine and butorphanol with or without MK-467.Study designProspective, randomized experimental cross-over.AnimalsEight purpose–bred beagles (two females, six males), 3–4 years old and weighing 14.5 ±1.6 kg (mean ± SD).MethodsAll dogs received four different treatments as follows: medetomidine 20 μg kg?1 and butorphanol tartrate 0.1 mg kg?1 IV and IM (MB), and MB combined with MK-467,500 μg kg?1 (MBMK) IV and IM. Heart rate (HR), arterial blood pressures (SAP, MAP, DAP), central venous pressure (CVP), cardiac output, respiratory rate (fR), rectal temperature (RT) were measured and arterial blood samples were obtained for gas analysis at baseline and at 3, 10, 20, 30, 45 and 60 minutes after drug administration. The cardiac index (CI), systemic vascular resistance index (SVRI) and oxygen delivery index (DO2I) were calculated. After the follow-up period atipamezole 50 μg kg?1 IM was given to reverse sedation.ResultsHR, CI and DO2I were significantly higher with MBMK after both IV and IM administration. Similarly, SAP, MAP, DAP, CVP, SVRI and RT were significantly lower after MBMK than with MB. There were no differences in fR between treatments, but arterial partial pressure of oxygen decreased transiently after all treatments. Recoveries were uneventful following atipamezole administration after all treatments.Conclusions and clinical relevanceMK-467 attenuated the cardiovascular effects of a medetomidine-butorphanol combination after IV and IM administration.  相似文献   

5.
The purpose of this study was to determine the cardiovascular, analgesic, and sedative effects of IV medetomidine (M, 20 µg kg?1), medetomidine–hydromorphone (MH, 20 µg kg?1 ? 0.1 mg kg?1), and medetomidine–butorphanol (MB, 20 µg kg?1 ? 0.2 mg kg?1) in dogs. Using a randomized cross‐over design and allowing 1 week between treatments, six healthy, mixed‐breed dogs (five males and one female) weighing 20 ± 3 kg, were induced to anesthesia by face‐mask administration of 2.9% ET sevoflurane to facilitate instrumentation prior to administration of the treatment combinations. Dogs were intubated and instrumented to enable measurement of heart rate (HR), systolic arterial pressure (SAP), mean arterial pressure (MAP), diastolic arterial pressure (DAP), mean pulmonary arterial pressure (PAP), pulmonary arterial occlusion pressure (PAOP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), and cardiac output via thermodilution using 5 mL of 5% dextrose, and recording the average of the three replicate measurements. Cardiac index (CI) and systemic (SVR) and pulmonary vascular resistances were calculated. After instrumentation was completed, administration of sevoflurane was discontinued, and the dogs were allowed to recover for 30 minutes prior to administration of the treatment drugs. After collection of the baseline samples for blood gas analysis and recording the baseline cardiovascular variables, the test agents were administered IV over 10 seconds and the CV variables recorded at 5, 10, 15, 30, 45, and 60 minutes post‐injection. In addition, arterial blood was sampled for blood gas analysis at 15 and 45 minutes following injection. Intensity and duration of analgesia (assessed by toe‐pinch response using a hemostat) and level of sedation were evaluated at the above time points and at 75 and 90 minutes post‐injection. Data were analyzed using anova for repeated measures with posthoc differences between means identified using Bonferroni's method (p < 0.05). Administration of M, MH, or MB was associated with increases in SAP, MAP, DAP, PAP, PAOP, CVP, SVR, and TEMP and with decreases in HR and CI. No differences in CV variables between treatment groups were identified at any time. PaO2 increased over time in all groups and was significantly higher when MH was compared with M. At 45 minutes, PaO2 tended to decrease over time and was significantly lower when MH and MB were compared with M at 15 minutes. Analgesia scores for MH and MB were significantly higher compared with M through 45 minutes, while analgesia scores for MH were significantly higher compared with M through 90 minutes. Sedation scores were higher for MH and MB compared with M throughout 90 minutes. Durations of lateral recumbency were 108 ± 10.8, 172 ± 15.5, and 145 ± 9.9 minutes for M, MH, and MB, respectively. We conclude that MH and MB are associated with improved analgesia and sedation and have similar CV effects when compared with M.  相似文献   

6.
ObjectiveTo evaluate the cardiovascular, respiratory, electrolyte and acid–base effects of a continuous infusion of dexmedetomidine during propofol–isoflurane anesthesia following premedication with dexmedetomidine.Study designProspective experimental study.AnimalsFive adult male Walker Hound dogs 1–2 years of age averaging 25.4 ± 3.6 kg.MethodsDogs were sedated with dexmedetomidine 10 μg kg?1 IM, 78 ± 2.3 minutes (mean ± SD) before general anesthesia. Anesthesia was induced with propofol (2.5 ± 0.5 mg kg?1) IV and maintained with 1.5% isoflurane. Thirty minutes later dexmedetomidine 0.5 μg kg?1 IV was administered over 5 minutes followed by an infusion of 0.5 μg kg?1 hour?1. Cardiac output (CO), heart rate (HR), ECG, direct blood pressure, body temperature, respiratory parameters, acid–base and arterial blood gases and electrolytes were measured 30 and 60 minutes after the infusion started. Data were analyzed via multiple linear regression modeling of individual variables over time, compared to anesthetized baseline values. Data are presented as mean ± SD.ResultsNo statistical difference from baseline for any parameter was measured at any time point. Baseline CO, HR and mean arterial blood pressure (MAP) before infusion were 3.11 ± 0.9 L minute?1, 78 ± 18 beats minute?1 and 96 ± 10 mmHg, respectively. During infusion CO, HR and MAP were 3.20 ± 0.83 L minute?1, 78 ± 14 beats minute?1 and 89 ± 16 mmHg, respectively. No differences were found in respiratory rates, PaO2, PaCO2, pH, base excess, bicarbonate, sodium, potassium, chloride, calcium or lactate measurements before or during infusion.Conclusions and clinical relevanceDexmedetomidine infusion using a loading dose of 0.5 μg kg?1 IV followed by a constant rate infusion of 0.5 μg kg?1 hour?1 does not cause any significant changes beyond those associated with an IM premedication dose of 10 μg kg?1, in propofol–isoflurane anesthetized dogs. IM dexmedetomidine given 108 ± 2 minutes before onset of infusion showed typical significant effects on cardiovascular parameters.  相似文献   

7.
ObjectiveTo evaluate the anti-nociceptive and sedative effects of slow intravenous (IV) injection of tramadol, romifidine, or a combination of both drugs in ponies.Study designWithin-subject blinded.AnimalsTwenty ponies (seven male, 13 female, weighing mean ± SD 268.0 ± 128 kg).MethodsOn separate occasions, each pony received one of the following three treatments IV; romifidine 50 μg kg− (R) tramadol 3 mg kg−1 given over 15 minutes (T) or tramadol 3 mg kg−1followed by romifidine 50 μg kg−1 (RT). Physiologic parameters and caecal borborygmi (CB) were measured and sedation and response to electrical stimulation of the coronary band assessed before and up to 120 minutes following drugs administration. Results were analyzed using the Friedman’s test and 2 way anova as relevant.ResultsWhen compared to baseline, heart (HR, beats minute−1) and respiratory rates (fR, breaths minute−1) increased with treatment T (highest mean ± SD, HR 43 ± 1; fR 33 ± 2) and decreased with R (lowest HR 29 ± 1 and fR 10 ± 4) and RT (lowest HR 32 ± 1 and fR 9 ± 3). There were no changes in other measured physiological variables. The height of head from the ground was lower following treatments R and TR than T. There was slight ataxia with all three treatments. No excitatory behavioural effects were observed. The response to electrical stimulation was reduced for a prolonged period relative to baseline following all three treatments, the effect being significantly greatest with treatment RT.ConclusionTramadol combined with romifidine at the stated doses proved an effective sedative and anti-nociceptive combination in ponies, with no unacceptable behavioural or physiologic side effects.Clinical relevanceSlow controlled administration of tramadol should reduce the occurrence of adverse behavioural side effects.  相似文献   

8.
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9.
Same‐day mass sterilization of feral cats requires rapid onset, short‐duration anesthesia. The purpose of this study was to compare our current anesthetic protocol, Telazol–ketamine–xylazine (TKX) with medetomidine–ketamine–buprenorphine (MKB). Feral female cats received either IM TKX (n = 68; 0.25 mL cat?1; tiletamine 12.5 mg, zolazepam 12.5 mg, K 20 mg, and X 5 mg per 0.25 mL) or MKB (n = 17; M 40 µg kg?1, K 15 mg kg?1, and B 10 µg kg?1). Intervals measured included time from injection to recumbency, time to surgery, duration of surgery, and time from reversal of anesthesia (TKX: yohimbine 0.50 mg cat?1 IV; MKB: atipamezole 0.50 mg cat?1 IM) to sternal recumbency. Following instrumentation (Vet/Ox 4403 and Vet/BP Plus 6500), physiological measurements were recorded at 5‐minute intervals, and included rectal temperature, heart rate (HR), respiratory rate (RR), SpO2 (lingual or rectal probes), and indirect mean arterial blood pressure (MAP) (oscillometric method). Nonparametric means were compared using Mann–Whitney U‐tests. Parametric means were compared using a two‐factorial anova with Bonferroni's t‐tests. The alpha‐priori significance level was p < 0.05. Values were mean ± SD. Body weight (TKX: 2.9 ± 0.5 kg, MKB: 2.7 ± 0.7 kg), time to recumbency (TKX: 4 ± 1 minutes, MKB: 3 ± 1 minutes), time to surgery (TKX: 28 ± 7 minutes, MKB: 28 ± 5 minutes), and duration of surgery (TKX: 11 ± 7 minutes, MKB: 8 ± 5 minutes) did not differ between groups. In contrast, MKB cats required less time from reversal to sternal recumbency (TKX: 68 ± 41 minutes, MKB: 7 ± 2 minutes) and were recumbent for shorter duration (TKX: 114 ± 39 minutes, MKB: 53 ± 6 minutes). Temperature decreased during the study in both groups, but overall temperature was higher in MKB cats (38.0 ± 0.95 °C) than in TKX cats (37.5 ± 0.95 °C). RR, HR, and SpO2 did not change during the study in either group. However, overall HR and RR were higher in TKX cats (RR: 18 ± 8 breaths minute?1, HR: 153 ± 30 beats minute?1) compared to MKB cats (RR: 15 ± 7 breaths minute?1, HR: 128 ± 19 beats minute?1). In contrast, overall SpO2 was lower in the TKX group (90 ± 6%) compared to the MKB group (94 ± 4%). MAP was also lower in the TKX group (112 ± 29 mm Hg) compared to that in the MKB group (122 ± 20 mm Hg). However, MAP increased in the TKX group during surgery compared to pre‐surgical values, but did not change in the MKB group. The results of this study suggested that MKB might be more suitable as an anesthetic for the purpose of mass sterilization of feral female cats.  相似文献   

10.
ObjectiveTo investigate the impact of intramuscular (IM) co-administration of the peripheral α2-adrenoceptor agonist vatinoxan (MK-467) with medetomidine and butorphanol prior to intravenous (IV) ketamine on the cardiopulmonary and anaesthetic effects in dogs, followed by atipamezole reversal.Study designRandomized, masked crossover study.AnimalsA total of eight purpose-bred Beagle dogs aged 3 years.MethodsEach dog was instrumented and administered two treatments 2 weeks apart: medetomidine (20 μg kg–1) and butorphanol (100 μg kg–1) premedication with vatinoxan (500 μg kg–1; treatment MVB) or without vatinoxan (treatment MB) IM 20 minutes before IV ketamine (4 mg kg–1). Atipamezole (100 μg kg–1) was administered IM 60 minutes after ketamine. Heart rate (HR), mean arterial (MAP) and central venous (CVP) pressures and cardiac output (CO) were measured; cardiac (CI) and systemic vascular resistance (SVRI) indices were calculated before and 10 minutes after MVB or MB, and 10, 25, 40, 55, 70 and 100 minutes after ketamine. Data were analysed with repeated measures analysis of covariance models. A p-value <0.05 was considered statistically significant. Sedation, induction, intubation and recovery scores were assessed.ResultsAt most time points, HR and CI were significantly higher, and SVRI and CVP significantly lower with MVB than with MB. With both treatments, SVRI and MAP decreased after ketamine, whereas HR and CI increased. MAP was significantly lower with MVB than with MB; mild hypotension (57–59 mmHg) was recorded in two dogs with MVB prior to atipamezole administration. Sedation, induction, intubation and recovery scores were not different between treatments, but intolerance to the endotracheal tube was observed earlier with MVB.Conclusions and clinical relevanceHaemodynamic performance was improved by vatinoxan co-administration with medetomidine–butorphanol, before and after ketamine administration. However, vatinoxan was associated with mild hypotension after ketamine with the dose used in this study. Vatinoxan shortened the duration of anaesthesia.  相似文献   

11.
ObjectiveTo assess cardiopulmonary function in sedated and anesthetized dogs administered intravenous (IV) dexmedetomidine and subsequently administered IV lidocaine to treat dexmedetomidine-induced bradycardia.Study designProspective, randomized, crossover experimental trial.AnimalsA total of six purpose-bred female Beagle dogs, weighing 9.1 ± 0.6 kg (mean ± standard deviation).MethodsDogs were randomly assigned to one of three treatments: dexmedetomidine (10 μg kg–1 IV) administered to conscious (treatments SED1 and SED2) or isoflurane-anesthetized dogs (end-tidal isoflurane concentration 1.19 ± 0.04%; treatment ISO). After 30 minutes, a lidocaine bolus (2 mg kg–1) IV was administered in treatments SED1 and ISO, followed 20 minutes later by a second bolus (2 mg kg–1) and a 30 minute lidocaine constant rate infusion (L-CRI) at 50 (SED1) or 100 μg kg–1 minute–1 (ISO). In SED2, lidocaine bolus and L-CRI (50 μg kg–1 minute–1) were administered 5 minutes after dexmedetomidine. Cardiopulmonary measurements were obtained after dexmedetomidine, after lidocaine bolus, during L-CRI and 30 minutes after discontinuing L-CRI. A mixed linear model was used for comparisons within treatments (p < 0.05).ResultsWhen administered after a bolus of dexmedetomidine, lidocaine bolus and L-CRI significantly increased heart rate and cardiac index, decreased mean blood pressure, systemic vascular resistance index and oxygen extraction ratio, and did not affect stroke volume index in all treatments.Conclusion and clinical relevanceLidocaine was an effective treatment for dexmedetomidine-induced bradycardia in healthy research dogs.  相似文献   

12.
ObjectiveTo study the anaesthetic and cardiorespiratory effects of intramuscular (IM) administration of different combinations of romifidine and ketamine in cats.Study designProspective, randomized, cross-over experiment.AnimalsSeven healthy adult cats weighing (mean ± SD) 3.4 ± 0.7 kg and aged 4.6 ± 3.2 years.MethodsAnimals received romifidine 100 μg kg?1 with ketamine 7.5 (R100/K7.5) and 10 mg kg?1 (R100/K10), romifidine 200 μg kg?1 with ketamine 5 (R200/K5), 7.5 (R200/K7.5) and 10 mg kg?1 (R200/K10) by IM injection. The time required to perform orotracheal intubation (IT) was measured and the ease of intubation assessed. The onset of anaesthesia (OA), duration of anaesthesia (DA) and anaesthesia recovery times (AR) were measured. Analgesia and muscle relaxation scores were recorded every 5 minutes for 60 minutes after OA. Heart rate, systolic arterial pressure, arterial haemoglobin saturation, respiratory rate, end-tidal carbon dioxide and oesophageal temperature were also measured.ResultsThe IT, OA and DA were not significantly different between the treatments. The analgesia and muscle relaxation scores were similar between all treatments at most time points. The cardiorespiratory variables were not significantly different between the treatments in most cases. The adverse effects were dose dependent and similar to those previously described for other combinations of α2-agonists and ketamine.Conclusions and clinical relevanceAnaesthesia produced by the studied combinations of romifidine and ketamine may only be reliable when conducting brief and noninvasive procedures in cats. The OA times were slower and the DA shorter than those reported for other alpha-2 agonists combined with ketamine. A dose-related increase in the intensity of the anaesthetic effects could not be demonstrated in this study.  相似文献   

13.
Alpha2 agonists have a significant role in epidural anaesthetic techniques. However, there are few reports regarding epidural administration of these drugs especially in small animals ( Greene et al. 1995; Keegan et al. 1995; Vesal et al. 1996 ). This study compared the haemodynamic effects of xylazine and medetomidine after epidural injection in dogs. Six dogs (four females and two males) weighing 27.5 ± 3.39 kg, aged 5.6 ± 1.42 years were studied on two separate occasions one month apart. Dogs were sedated with 0.5 mg kg?1 diazepam IM and 0.1 mg kg?1 acepromazine IM. After 20 minutes, a lumbosacral epidural injection of 0.25 mg kg?1 xylazine was administered (group X). One month later, following the same sedation, 15 µg kg?1 medetomidine was administered epidurally (group M). Haemodynamic variables (ECG and indirect blood pressure (Doppler)), respiratory rate and rectal temperature were recorded before (baseline) and then every 5 minutes after the epidural injection, up to 60 minutes. Differences between groups were compared by a paired t‐test. Within group changes were compared to basal values by anova . A p‐value of < 0.05 was considered statistically significant. Both groups showed significant reductions in heart rate (106.3 ± 7.7 beats minute?1 baseline versus 67.7 ± 7.6 (group M); 91 ± 3.8 baseline versus 52.3 ± 9 (group X)) and mean arterial blood pressure (113.1 ± 12.3 mm Hg baseline versus 87 ± 11 (group M); 118 ± 7 baseline versus 91 ± 14 (group X)). There were no differences between groups in these variables. After epidural injection, first degree atrioventricular block was recorded significantly more often in group X (50% against 33%) but second degree block was significantly more frequent in group M (66% against 33%). Also 50% of dogs in group X and 66% in group M showed sinus arrest. Respiratory rate decreased significantly in both groups following the epidural injection (20.66 ± 0.66 minute?1 baseline versus 16.33 ± 4.77 (group M); 37.66 ± 0.56 baseline versus 16.33 ± 1.81 group X), but no differences between groups were observed. Rectal temperature decreased significantly in group X (38.16 ± 0.21) with respect to the basal measurement (39.30 ± 0.14 °C). In group M, there was no significant reduction in temperature, however, no statistical difference in rectal temperature was found between groups. This study shows that 0.25 mg kg?1 xylazine and 15 µg kg?1 medetomidine produce similar, significant cardiovascular and respiratory changes following lumbosacral epidural administration in dogs.  相似文献   

14.
S(+) ketamine, one of the two enantiomers of racemic ketamine, is a phencyclidine derivative that induces amnesia and analgesia. Its activity is related to blockade of NMDA receptors and some opioid action. We compared anesthetic induction and recovery quality with S(+) ketamine in combination with diazepam or midazolam in 10 dogs (ASA 1) admitted for elective surgery. After all clinical examinations, the dogs were separated into two groups (G I and G II). All animals received acepromazine (0.1 mg kg?1) and fentanyl (5 µg kg?1) IM, 20 minutes before induction with S(+) ketamine (6 mg kg?1) and diazepam (0.5 mg kg?1) IV (G I) or midazolam 0.2 mg kg?1 (G II) IV. The doses of diazepam and midazolam were chosen according to the literature. All dogs were intubated and then maintained with halothane in oxygen at a vaporizer setting sufficient to maintain surgical anesthesia. Quality of induction, time needed for intubation, heart rate, respiratory rate, SpO2, time to extubation, and quality of recovery were evaluated. The results were analyzed by Student's t‐test. Smooth induction and recovery were observed in all animals. The time to intubation was 45 ± 20 (GI) and 25 ± 6 seconds (GII), HR was 122 ± 12 (GI) and 125 ± 7 beats minute?1 (GII), RR was 17 ± 2 (GI) and 21 ± 3 breaths minute?1 (GII), SpO2 was 96 ± 2 (GI) and 94 ± 1% (GII), time to extubation was 7 ± 3 (GI) and 4 ± 1 minutes (GII). No statistical differences were found in analyses, although time to intubation was less in GII. The results suggested that both combinations could be used safely for anesthetic induction in healthy dogs.  相似文献   

15.
ObjectiveTo evaluate the effects of intravenous (IV) or intramuscular (IM) hyoscine premedication on physiologic variables following IV administration of medetomidine in horses.Study designRandomized, crossover experimental study.AnimalsEight healthy crossbred horses weighing 330 ± 39 kg and aged 7 ± 4 years.MethodsBaseline measurements of heart rate (HR), cardiac index (CI), respiratory rate, systemic vascular resistance (SVR), percentage of patients with second degree atrioventricular (2oAV) block, mean arterial pressure (MAP), pH, and arterial partial pressures of carbon dioxide (PaCO2) and oxygen (PaO2) were obtained 5 minutes before administration of IV hyoscine (0.14 mg kg?1; group HIV), IM hyoscine (0.3 mg kg?1; group HIM), or an equal volume of physiologic saline IV (group C). Five minutes later, medetomidine (7.5 μg kg?1) was administered IV and measurements were recorded at various time points for 130 minutes.ResultsMedetomidine induced bradycardia, 2oAV blocks and increased SVR immediately after administration, without significant changes in CI or MAP in C. Hyoscine administration induced tachycardia and hypertension, and decreased the percentage of 2oAV blocks induced by medetomidine. Peak HR and MAP were higher in HIV than HIM at 88 ± 18 beats minute?1 and 241 ± 37 mmHg versus 65 ± 16 beats minute?1 and 192 ± 38 mmHg, respectively. CI was increased significantly in HIV (p ≤ 0.05). Respiratory rate decreased significantly in all groups during the recording period. pH, PaCO2 and PaO2 were not significantly changed by administration of medetomidine with or without hyoscine.Conclusion and clinical relevanceHyoscine administered IV or IM before medetomidine in horses resulted in tachycardia and hypertension under the conditions of this study. The significance of these changes, and responses to other dose rates, requires further investigation.  相似文献   

16.

Objective

To compare the cardiopulmonary effects of low and high doses of fentanyl before and after the correction of bradycardia in isoflurane-anesthetized dogs.

Study design

Prospective, randomized crossover trial.

Animals

Eight healthy male Beagle dogs weighing 11.1 ± 1.3 kg [mean ± standard deviation (SD)] and aged approximately 1 year.

Methods

The dogs were anesthetized with isoflurane [1.3 × minimum alveolar concentration (MAC)] on two occasions and fentanyl was administered intravenously; either low-dose fentanyl, loading dose (33 μg kg–1) and infusion (0.2 μg kg–1 minute–1) or a high-dose, loading dose (102 μg kg–1) and infusion (0.8 μg kg–1 minute–1). Cardiopulmonary variables were measured at three time points in equipotent isoflurane concentrations (1.3 MAC): before fentanyl administration (ISO), during fentanyl-induced bradycardia (ISO–F) and after administration of glycopyrrolate normalized heart rate (ISO–FNHR). Data are mean ± SD.

Results

Heart rate and cardiac index (CI) decreased and systemic vascular resistance index (SVRI) increased at ISO–F in both treatments. Bradycardia and vasoconstriction at ISO–F were greater in high than in low-dose fentanyl (42 ± 7 versus 57 ± 15 beats minute–1 and 3457 ± 1108 versus 2528 ± 968 dyne second cm–5 m–2), respectively. Oxygen delivery index (DO2I) decreased only during high-dose fentanyl. CI and DO2I were higher in both treatments at ISO–FNHR than at ISO–F; however, they were higher only during the high-dose fentanyl than at ISO. SVRI was higher at ISO–F than at ISO and ISO–FNHR in both treatments, and was higher at ISO–F in the high than in the low-dose treatment.

Conclusions and clinical relevance

An overall improvement in cardiovascular function of dogs anesthetized with equipotent isoflurane doses (1.3 MAC) was observed after the treatment of bradycardia only with the high-dose fentanyl.  相似文献   

17.
Beat‐to‐beat variation of heart rate is reflective of autonomic balance and has been used to assess pain and stress in human beings. The purpose of this investigation was to pharmacologically manipulate the autonomic nervous system and to determine the effect of these manipulations on heart rate variability (HRV) in dogs. Four adult male hound dogs (27 ± 1 kg) were used in the investigation. Each dog was given five treatments: Parasympathetic blockade (glycopyrrolate; 0.01 mg kg–1 IV and 0.01 mg kg–1 IM), parasympathetic stimulation (phenylephrine; 0.005 mg kg–1 IV + 0.05 mg kg–1hour–1), sympathetic blockade (propranolol; 0.11 mg kg–1 IV), sympathetic stimulation propranolol; 0.01 μg kg–1 minute–1), and saline control. At least 48 hours were allowed between treatments. ECG recordings were obtained using an ambulatory ECG monitor. A 5‐minutes period of continuous recording obtained ~30 minutes after initiation of drug administration was used for data analysis. Changes in HRV were evaluated by time and frequency‐domain analysis. The standard deviation of normal R‐R intervals (SDNN), as well as the standard deviation of successive differences in RR intervals (SDSD) were assessed for each treatment. Low frequency (LFP; 0.05–0.15 Hz), high frequency (HFP; 0.15–0.35 Hz), and total (TP; 0.017–0.5 Hz) spectral power were also determined. The LFP:HFP ratio was also evaluated. A two‐way anova with a Tukey's test was used to detect differences (p < 0.05). Administration of glycopyrrolate or isoproterenol increased HR and decreased SDNN and SDSD below control levels. Phenylephrine or propranolol administration were without effect. LFP was diminished by glycopyrrolate and isoproterenol, but was unaffected by phenylephrine and propranolol. HFP, TP, and LFP:HFP were unaffected by treatment. Both branches of the autonomic nervous system influence SDNN and LFP. SDSD, in contrast, is altered primarily by parasympathetic activity. Thus, it appears that parasympathetic activity modulates HRV in the resting dog, as either withdrawal of parasympathetic influence or accentuated sympathetic activity led to significant changes in these measures of HRV. Conversely, augmentation of parasympathetic activity or withdrawal of sympathetic tone minimally affected HRV.  相似文献   

18.
Propofol anaesthesia for surgery in late gestation pony mares   总被引：2，自引：0，他引：2  
Objective To characterize propofol anaesthesia in pregnant ponies. Animals Fourteen pony mares, at 256 ± 49 days gestation, undergoing abdominal surgery to implant fetal and maternal vascular catheters. Materials and methods Pre‐anaesthetic medication with intravenous (IV) acepromazine (20 µg kg?1), butorphanol (20 µg kg?1) and detomidine (10 µg kg?1) was given 30 minutes before induction of anaesthesia with detomidine (10 µg kg?1) and ketamine (2 mg kg?1) IV Maternal arterial blood pressure was recorded (facial artery) throughout anaesthesia. Arterial blood gas values and plasma concentrations of glucose, lactate, cortisol and propofol were measured at 20‐minute intervals. Anaesthesia was maintained with propofol infused initially at 200 µg kg?1 minute?1, and at 130–180 µg kg?1 minute?1 after 60 minutes, ventilation was controlled with oxygen and nitrous oxide to maintain PaCO2 between 5.0 and 6.0 kPa (37.6 and 45.1 mm Hg) and PaO2 between 13.3 and 20.0 kPa (100 and 150.4 mm Hg). During anaesthesia flunixin (1 mg kg?1), procaine penicillin (6 IU) and butorphanol 80 µg kg?1 were given. Lactated Ringer's solution was infused at 10 mL kg?1 hour?1. Simultaneous fetal and maternal blood samples were withdrawn at 85–95 minutes. Recovery from anaesthesia was assisted. Results Arterial blood gas values remained within intended limits. Plasma propofol levels stabilized after 20 minutes (range 3.5–9.1 µg kg?1); disposition estimates were clearance 6.13 ± 1.51 L minute?1 (mean ± SD) and volume of distribution 117.1 ± 38.9 L (mean ± SD). Plasma cortisol increased from 193 ± 43 nmol L?1 before anaesthesia to 421 ± 96 nmol L?1 60 minutes after anaesthesia. Surgical conditions were excellent. Fetal umbilical venous pH, PO2 and PCO2 were 7.35 ± 0.04, 6.5 ± 0.5 kPa (49 ± 4 mm Hg) and 6.9 ± 0.5 kPa (52 ± 4 mm Hg); fetal arterial pH, PO2 and PCO2 were 7.29 ± 0.06, 3.3 ± 0.8 kPa (25 ± 6 mm Hg) and 8.7 ± 0.9 kPa (65 ± 7 mm Hg), respectively. Recovery to standing occurred at 46 ± 17 minutes, and was generally smooth. Ponies regained normal behaviour patterns immediately. Conclusions and clinical relevance Propofol anaesthesia was smooth with satisfactory cardiovascular function in both mare and fetus; we believe this to be a suitable anaesthetic technique for pregnant ponies.  相似文献   

19.
ObjectiveTo determine the effect of intravenous vatinoxan administration on bradycardia, hypertension and level of anaesthesia induced by medetomidine–tiletamine–zolazepam in red deer (Cervus elaphus).Study design and animalsA total of 10 healthy red deer were included in a randomised, controlled, experimental, crossover study.MethodsDeer were administered a combination of 0.1 mg kg–1 medetomidine hydrochloride and 2.5 mg kg–1 tiletamine–zolazepam intramuscularly, followed by 0.1 mg kg–1 vatinoxan hydrochloride or equivalent volume of saline intravenously (IV) 35 minutes after anaesthetic induction. Heart rate (HR), mean arterial blood pressure (MAP), respiration rate (fR), end-tidal CO2 (Pe′CO2), arterial oxygen saturation (SpO2), rectal temperature (RT) and level of anaesthesia were assessed before saline/vatinoxan administration (baseline) and at intervals for 25 minutes thereafter. Differences within treatments (change from baseline) and between treatments were analysed with linear mixed effect models (p < 0.05).ResultsMaximal (81 ± 10 beats minute–1) HR occurred 90 seconds after vatinoxan injection and remained significantly above baseline (42 ± 4 beats minute–1) for 15 minutes. MAP significantly decreased from baseline (122 ± 10 mmHg) to a minimum MAP of 83 ± 6 mmHg 60 seconds after vatinoxan and remained below baseline until end of anaesthesia. HR remained unchanged from baseline (43 ± 5 beats minute–1) with the saline treatment, whereas MAP decreased significantly (112 ± 16 mmHg) from baseline after 20 minutes. Pe′CO2, fR and SpO2 showed no significant differences between treatments, whereas RT decreased significantly 25 minutes after vatinoxan. Level of anaesthesia was not significantly influenced by vatinoxan.Conclusions and clinical relevanceVatinoxan reversed hypertension and bradycardia induced by medetomidine without causing hypotension or affecting the level of anaesthesia in red deer. However, the effect on HR subsided 15 minutes after vatinoxan IV administration. Vatinoxan has the potential to reduce anaesthetic side effects in non-domestic ruminants immobilised with medetomidine–tiletamine–zolazepam.  相似文献   

20.
Treatment of bradycardia in horses has been historically ignored because of the motility depressant effects of nonselective antimuscarinics. This study evaluated the cardiopulmonary effects of a cardioselective (M2) muscarinic antagonist, methoctramine (MET), in anesthetized horses. In a previous in vitro study, we determined that supraphysiological doses of MET were necessary to inhibit acetylcholine‐induced longitudinal jejunal smooth muscle contractions in this species. Six adult horses were allocated to two treatments in a randomized complete block design. Anesthesia was induced with xylazine/ketamine, and maintained with halothane (1% end‐tidal) and a constant infusion of xylazine (1 mg kg?1 hour?1) under mechanical ventilation. Invasive hemodynamic variables were monitored at baseline (approximately 45 minutes after induction) and for 120 minutes after MET or saline (control) had been injected. MET was titrated at 10‐minute intervals (10 µg kg?1 IV) until the heart rate (HR) increased at least 30% above the baseline, or a maximum cumulative dose of 30 µg kg?1 had been injected. A person blinded to the treatment evaluated recovery scores and monitored intestinal auscultation until 24 hours after the end of anesthesia using previously published methods. Cardiovascular parameters were analyzed by anova followed by a Dunnet's test, and nonparametrical data were analyzed by a Mann–Whitney U‐test (p < 0.05). Values were mean ± SEM unless otherwise stated. MET significantly increased HR from baseline to 120 minutes post‐injection (from 29 ± 1 to 36 ± 2 beats minute?1 at 20 minutes). Thermodilution cardiac output (CO) and mean arterial pressure (MAP) were increased from baseline to 75 minutes post‐MET injection (from 13.9 ± 0.8 to 19.4 ± 2.0 L minute?1 for CO at 20 minutes, and from 82 ± 3 to 103 ± 5 mm Hg for MAP at 20 minutes). Recovery characteristics and bowel auscultation scores did not differ among the groups. The return to at least 75% of the maximum auscultation score occurred at 10 (8–18) hours [median (range)] for controls and at 9 (8–12) hours for MET. It was concluded that MET increased HR and improved hemodynamic function during halothane/xylazine anesthesia with no apparent effect on return to full‐bowel motility, as assessed by auscultation. Accordingly, M2 muscarinic antagonists might be represented as a safer alternative to treat intraoperative bradycardia in horse.  相似文献   

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