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1.
Objective To quantitate the dose‐ and time‐related magnitude of the anesthetic sparing effect of, and selected physiological responses to detomidine during isoflurane anesthesia in horses. Study design Randomized cross‐over study. Animals Three, healthy, young adult horses weighing 485 ± 14 kg. Methods Horses were anesthetized on two occasions to determine the minimum alveolar concentration (MAC) of isoflurane in O2 and then to measure the anesthetic sparing effect (time‐related MAC reduction) following IV detomidine (0.03 and 0.06 mg kg?1). Selected common measures of cardiopulmonary function, blood glucose and urinary output were also recorded. Results Isoflurane MAC was 1.44 ± 0.07% (mean ± SEM). This was reduced by 42.8 ± 5.4% and 44.8 ± 3.0% at 83 ± 23 and 125 ± 36 minutes, respectively, following 0.03 and 0.06 mg kg?1, detomidine. The MAC reduction was detomidine dose‐ and time‐dependent. There was a tendency for mild cardiovascular and respiratory depression, especially following the higher detomidine dose. Detomidine increased both blood glucose and urine flow; the magnitude of these changes was time‐ and dose‐dependent Conclusions Detomidine reduces anesthetic requirement for isoflurane and increases blood glucose concentration and urine flow in horses. These changes were dose‐ and time‐related. Clinical relevance The results imply potent anesthetic sparing actions by detomidine. The detomidine‐related increased urine flow should be considered in designing anesthetic protocols for individual horses.  相似文献   

2.
ObjectiveTo study the effects of oromucosal detomidine gel administered sublingually to calves prior to disbudding, and to compare its efficacy with intravenously (IV) administered detomidine.Study designRandomised, prospective clinical study.AnimalsTwenty dairy calves aged 12.4 ± 4.4days (mean ± SD), weight 50.5 ± 9.0 kg.MethodsDetomidine at 80 μg kg?1 was administered to ten calves sublingually (GEL) and at 30 μg kg?1 to ten control calves IV (V. jugularis). Meloxicam (0.5 mg kg?1) and local anaesthetic (lidocaine 3 mg kg?1) were administered before heat cauterization of horn buds. Heart rate (HR), body temperature and clinical sedation were monitored over 240 minutes. Blood was collected from the V. cephalica during the same period for drug concentration analysis. Pharmacokinetic variables were calculated from the plasma detomidine concentration-time data using non-compartmental methods. Statistical analyses compared routes of administration by Student’s t-test and linear mixed models as relevant.ResultsThe maximum plasma detomidine concentration after GEL was 2.1 ± 1.2 ng mL?1 (mean ±SD) and the time of maximum concentration was 66.0 ± 36.9 minutes. The bioavailability of detomidine was approximately 34% with GEL. Similar sedation scores were reached in both groups after administration of detomidine, but maximal sedation was reached earlier in the IV group (10 minutes) than in the GEL group (40 minutes). HR was lower after IV than GEL from 5 to 10 minutes after administration. All animals were adequately sedated, and we were able to administer local anaesthetic without resistance to all of the calves before disbudding.Conclusions and clinical relevanceOromucosally administered detomidine is an effective sedative agent for calves prior to disbudding.  相似文献   

3.

Objective

To evaluate intravenous (IV) detomidine with methadone in horses to identify a combination which provides sedation and antinociception without adverse effects.

Study design

Randomized, placebo-controlled, blinded, crossover.

Animals

A group of eight adult healthy horses aged (mean ± standard deviation) 7 ± 2 years and 372 ± 27 kg.

Methods

A total of six treatments were administered IV: saline (SAL); detomidine (5 μg kg?1; DET); methadone (0.2 mg kg?1; MET) alone or combined with detomidine [2.5 (MLD), 5 (MMD) or 10 (MHD) μg kg?1]. Thermal, mechanical and electrical nociceptive thresholds were measured, and sedation, head height above ground (HHAG), cardiopulmonary variables and intestinal motility were evaluated at 5, 15, 30, 45, 60, 75, 90, 120 and 180 minutes. Normal data were analyzed by mixed-model analysis of variance and non-normal by Kruskal–Wallis (p < 0.05).

Results

Nociceptive thresholds in horses administered methadone with the higher doses of detomidine (MMD, MHD) were increased above baseline to a greater degree and for longer duration (MMD: 15–30 minutes, MHD: 30–60 minutes) than in horses administered low dose with methadone or detomidine alone (MLD, DET: 5–15 minutes). No increases in nociceptive thresholds were recorded in SAL or MET. Compared with baseline, HHAG was lower for 30 minutes in MMD and DET, and for 45 minutes in MHD. No significant sedation was observed in SAL, MET or MLD. Intestinal motility was reduced for 75 minutes in MHD and for 30 minutes in all other treatments.

Conclusions

Methadone (0.2 mg kg?1) potentiated the antinociception produced by detomidine (5 μg kg?1), with minimal sedative effects.

Clinical relevance

Detomidine (5 μg kg?1) with methadone (0.2 mg kg?1) produced antinociception without the adverse effects of higher doses of detomidine.  相似文献   

4.
ObjectivesTo evaluate the sedative effects and pharmacokinetics of detomidine gel administered intravaginally to alpacas in comparison with intravenously (IV) administered detomidine.Study designRandomized, crossover, blinded experiment.AnimalsA group of six healthy adult female Huacaya alpacas (70.3 ± 7.9 kg).MethodsAlpacas were studied on two occasions separated by ≥5 days. Treatments were IV detomidine hydrochloride (70 μg kg−1; treatment DET–IV) or detomidine gel (200 μg kg−1; treatment DET–VAG) administered intravaginally. Sedation and heart rate (HR) were evaluated at intervals for 240 minutes. Venous blood was collected at intervals for 360 minutes after treatment for analysis of detomidine, carboxydetomidine and hydroxydetomidine using liquid chromatography–tandem mass spectrometry. Measured variables were compared between treatments and over time using mixed model analysis. Data are presented as the mean ± standard error of the mean, and a p value of <0.05 was considered significant.ResultsOnset of sedation was faster in treatment DET–IV (1.6 ± 0.2 minutes) than in treatment DET–VAG (13.0 ± 2.5 minutes). Time to maximum sedation was shorter in treatment DET–IV (8.3 ± 1.3 minutes) than in treatment DET–VAG (25 ± 4 minutes). Duration of sedation was not different between treatments. There was a significant linear relationship between sedation score and plasma detomidine concentration. HR was less than baseline for 60 and 125 minutes for treatments DET–IV and DET–VAG, respectively. The maximal decrease in HR occurred at 15 minutes for both treatments. The mean maximum plasma concentration of detomidine, time to maximum concentration and bioavailability for treatment DET–VAG were 39.6 ng mL−1, 19.9 minutes and 20%, respectively.Conclusions and clinical relevanceDetomidine administration at the doses studied resulted in moderate sedation when administered IV or intravaginally to alpacas.  相似文献   

5.
Detomidine (10 micrograms/kg and 20 micrograms/kg) was administered to seven horses with and without epinephrine infusion (0.1 microgram/kg/min) from 5 minutes before to 5 minutes after detomidine injection. One or more single supraventricular premature heartbeats were observed in three horses after detomidine administration. Epinephrine infusion did not modify the incidence of cardiac arrhythmias in detomidine-treated horses at the doses tested. Relatively high momentary peak systolic pressures were registered in some horses after detomidine administration during epinephrine infusion. The highest systolic arterial blood pressure was 290 mm Hg, but this value was not higher than that reported in horses during maximum physical exercise. Epinephrine infusion did not alter blood gases, arterial pH, or base excess.  相似文献   

6.
ObjectiveTo assess anesthetic induction, recovery quality and cardiopulmonary variables after intramuscular (IM) injection of three drug combinations for immobilization of horses.Study designRandomized, blinded, three-way crossover prospective design.AnimalsA total of eight healthy adult horses weighing 470–575 kg.MethodsHorses were administered three treatments IM separated by ≥1 week. Combinations were tiletamine–zolazepam (1.2 mg kg−1), ketamine (1 mg kg−1) and detomidine (0.04 mg kg−1) (treatment TKD); ketamine (3 mg kg−1) and detomidine (0.04 mg kg−1) (treatment KD); and tiletamine–zolazepam (2.4 mg kg−1) and detomidine (0.04 mg kg−1) (treatment TD). Parametric data were analyzed using mixed model linear regression. Nonparametric data were compared using Skillings–Mack test. A p value <0.05 was considered statistically significant.ResultsAll horses in treatment TD became recumbent. In treatments KD and TKD, one horse remained standing. PaO2 15 minutes after recumbency was significantly lower in treatments TD (p < 0.0005) and TKD (p = 0.001) than in treatment KD. Times to first movement (25 ± 15 minutes) and sternal recumbency (55 ± 11 minutes) in treatment KD were faster than in treatments TD (57 ± 17 and 76 ± 19 minutes; p < 0.0005, p = 0.001) and TKD (45 ± 18 and 73 ± 31 minutes; p = 0.005, p = 0.021). There were no differences in induction quality, muscle relaxation score, number of attempts to stand or recovery quality.Conclusions and clinical relevanceIn domestic horses, IM injections of tiletamine–zolazepam–detomidine resulted in more reliable recumbency with a longer duration when compared with ketamine–detomidine and tiletamine–zolazepam–ketamine–detomidine. Recoveries were comparable among protocols.  相似文献   

7.

Objective

Influence of detomidine or romifidine constant rate infusion (CRI) on plasma lactate concentration and isoflurane requirements in horses undergoing elective surgery.

Study design

Prospective, randomised, blinded, clinical trial.

Animals

A total of 24 adult healthy horses.

Methods

All horses were administered intramuscular acepromazine (0.02 mg kg?1) and either intravenous detomidine (0.02 mg kg?1) (group D), romifidine (0.08 mg kg?1) (group R) or xylazine (1.0 mg kg?1) (group C) prior to anaesthesia. Group D was administered detomidine CRI (10 μg kg?1 hour?1) in lactated Ringer's solution (LRS), group R romifidine CRI (40 μg kg?1 hour?1) in LRS and group C an equivalent amount of LRS intraoperatively. Anaesthesia was induced with ketamine and diazepam and maintained with isoflurane in oxygen. Plasma lactate samples were taken prior to anaesthesia (baseline), intraoperatively (three samples at 30 minute intervals) and in recovery (at 10 minutes, once standing and 3 hours after end of anaesthesia). End-tidal isoflurane percentage (Fe′Iso) was analysed by allocating values into three periods: Prep (15 minutes after the start anaesthesia–start surgery); Surgery 1 (start surgery–30 minutes later); and Surgery 2 (end Surgery 1–end anaesthesia). A linear mixed model was used to analyse the data. A value of p < 0.05 was considered significant.

Results

There was a difference in plasma lactate between ‘baseline’ and ‘once standing’ in all three groups (p < 0.01); values did not differ significantly between groups. In groups D and R, Fe′Iso decreased significantly by 18% (to 1.03%) and by 15% (to 1.07%), respectively, during Surgery 2 compared with group C (1.26%); p < 0.006, p < 0.02, respectively.

Conclusions and clinical relevance

Intraoperative detomidine or romifidine CRI in horses did not result in a clinically significant increase in plasma lactate compared with control group. Detomidine and romifidine infusions decreased isoflurane requirements during surgery.  相似文献   

8.
Objective To characterize intravenous anaesthesia with detomidine, ketamine and guaiphenesin in pregnant ponies. Animals Twelve pony mares, at 260–320 days gestation undergoing abdominal surgery to implant fetal and maternal vascular catheters. Materials and methods Pre‐anaesthetic medication with intravenous (IV) acepromazine (30 µg kg?1), butorphanol (20 µg kg?1) and detomidine (10 µg kg?1) preceded induction of anaesthesia with detomidine (10 µg kg?1) and ketamine (2 mg kg?1) IV Maternal arterial blood pressure was measured directly throughout anaesthesia and arterial blood samples were taken at 20‐minute intervals for measurement of blood gases and plasma concentrations of cortisol, glucose and lactate. Anaesthesia was maintained with an IV infusion of detomidine (0.04 mg mL?1), ketamine (4 mg mL?1) and guaiphenesin (100 mg mL?1) (DKG) for 140 minutes. Oxygen was supplied by intermittent positive pressure ventilation (IPPV) adjusted to maintain PaCO2 between 5.0 and 6.0 kPa (38 and 45 mm Hg), while PaO2 was kept close to 20.0 kPa (150 mm Hg) by adding nitrous oxide. Simultaneous fetal and maternal blood samples were withdrawn at 90 minutes. Recovery quality was assessed. Results DKG was infused at 0.67 ± 0.17 mL kg?1 hour?1 for 1 hour then reduced, reaching 0.28 ± 0.14 mL kg?1 hour?1 at 140 minutes. Arterial blood gas values and pH remained within intended limits. During anaesthesia there was no change in heart rate, but arterial blood pressure decreased by 10%. Plasma glucose and lactate increased (10‐fold and 2‐fold, respectively) and cortisol decreased by 50% during anaesthesia. Fetal umbilical venous pH, PO2 and PCO2 were 7.34 ± 0.06, 5.8 ± 0.9 kPa (44 ± 7 mm Hg) and 6.7 ± 0.8 kPa (50 ± 6 mm Hg); and fetal arterial pH, PO2 and PCO2 were 7.29 ± 0.06, 4.0 ± 0.7 kPa (30 ± 5 mm Hg) and 7.8 ± 1.7 kPa (59 ± 13 mm Hg), respectively. Surgical conditions were good but four ponies required a single additional dose of ketamine. Ponies took 60 ± 28 minutes to stand and recovery was good. Conclusions and clinical relevance Anaesthesia produced with DKG was smooth while cardiovascular function in mare and fetus was well preserved. This indicates that DKG infusion is suitable for maintenance of anaesthesia in pregnant equidae.  相似文献   

9.
ObjectiveTo evaluate the effects of detomidine on visceral and somatic nociception, heart and respiratory rates, sedation, and duodenal motility and to correlate these effects with serum detomidine concentrations.Study designNonrandomized, experimental trial.AnimalsFive adult horses, each with a permanent gastric cannula weighing 534 ± 46 kg.MethodsVisceral nociception was evaluated by colorectal (CRD) and duodenal distension (DD). The duodenal balloon was used to assess motility. Somatic nociception was assessed via thermal threshold (TT). Nose–to–ground (NTG) height was used as a measure of sedation. Serum was collected for pharmacokinetic analysis. Detomidine (10 or 20 μg kg?1) was administered intravenously. Data were analyzed by means of a three–factor anova with fixed factors of treatment and time and random factor of horse. When a significant time × treatment interaction was detected, differences were compared with a simple t–test or Bonferroni t–test. Significance was set at p < 0.05.ResultsDetomidine produced a significant, dose–dependent decrease in NTG height, heart rate, and skin temperature and a significant, nondose–dependent decrease in respiratory rate. Colorectal distension threshold was significantly increased with 10 μg kg?1 for 15 minutes and for at least 165 minutes with 20 μg kg?1. Duodenal distension threshold was significantly increased at 15 minutes for the 20 μg kg?1 dose. A significant change in TT was not observed at either dose. A marked, immediate decrease in amplitude of duodenal contractions followed detomidine administration at both doses for 50 minutes.Conclusions and clinical relevanceDetomidine caused a longer period of visceral anti–nociception as determined by CRD but a shorter period of anti–nociception as determined by DD than has been previously reported. The lack of somatic anti–nociception as determined by TT testing may be related to the marked decrease in skin temperature, likely caused by peripheral vasoconstriction and the low temperature cut–off of the testing device.  相似文献   

10.
ObjectiveTo describe selected pharmacodynamic effects of detomidine and yohimbine when administered alone and in sequence.Study designRandomized crossover design.AnimalsNine healthy adult horses aged 9 ± 4 years and weighing 561 ± 56 kg.MethodsThree dose regimens were employed in the current study. 1) 0.03 mg kg?1 detomidine IV, 2) 0.2 mg kg?1 yohimbine IV and 3) 0.03 mg kg?1 detomidine IV followed 15 minutes later by 0.2 mg kg?1 yohimbine IV. Each horse received all three treatments with a minimum of 1 week between treatments. Blood samples were obtained and plasma analyzed for detomidine and yohimbine concentrations by liquid chromatography-mass spectrometry. Behavioral effects, heart rate and rhythm, glucose, packed cell volume and plasma proteins were monitored.ResultsYohimbine rapidly reversed the sedative effects of detomidine in the horse. Additionally, yohimbine effectively returned heart rate and the percent of atrio-ventricular conduction disturbances to pre-detomidine values when administered 15 minutes post-detomidine administration. Plasma glucose was significantly increased following detomidine administration. The detomidine induced hyperglycemia was effectively reduced by yohimbine administration. Effects on packed cell volume and plasma proteins were variable.Conclusions and clinical relevanceIntravenous administration of yohimbine effectively reversed detomidine induced sedation, bradycardia, atrio-ventricular heart block and hyperglycemia.  相似文献   

11.
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   

12.
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13.
ObjectiveTo evaluate and compare the antinociceptive effects of the three alpha-2 agonists, detomidine, romifidine and xylazine at doses considered equipotent for sedation, using the nociceptive withdrawal reflex (NWR) and temporal summation model in standing horses.Study designProspective, blinded, randomized cross-over study.AnimalsTen healthy adult horses weighing 527–645 kg and aged 11–21 years old.MethodsElectrical stimulation was applied to the digital nerves to evoke NWR and temporal summation in the left thoracic limb and pelvic limb of each horse. Electromyographic reflex activity was recorded from the common digital extensor and the cranial tibial muscles. After baseline measurements a single bolus dose of detomidine, 0.02 mg kg?1, romifidine 0.08 mg kg?1, or xylazine, 1 mg kg?1, was administered intravenously (IV). Determinations of NWR and temporal summation thresholds were repeated at 10, 20, 30, 40, 60, 70, 90, 100, 120 and 130 minutes after test-drug administration alternating the thoracic limb and the pelvic limb. Depth of sedation was assessed before measurements at each time point. Behavioural reaction was observed and recorded following each stimulation.ResultsThe administration of detomidine, romifidine and xylazine significantly increased the current intensities necessary to evoke NWR and temporal summation in thoracic limbs and pelvic limbs of all horses compared with baseline. Xylazine increased NWR thresholds over baseline values for 60 minutes, while detomidine and romifidine increased NWR thresholds over baseline for 100 and 120 minutes, respectively. Temporal summation thresholds were significantly increased for 40, 70 and 130 minutes after xylazine, detomidine and romifidine, respectively.Conclusions and clinical relevanceDetomidine, romifidine and xylazine, administered IV at doses considered equipotent for sedation, significantly increased NWR and temporal summation thresholds, used as a measure of antinociceptive activity. The extent of maximal increase of NWR and temporal summation thresholds was comparable, while the duration of action was drug-specific.  相似文献   

14.
ObjectiveTo describe the effects of alpha2-adrenergic receptor antagonists on the pharmacodynamics of sublingual (SL) detomidine in the horse.Study designRandomized crossover design.AnimalsNine healthy adult horses with an average age of 7.6 ± 6.5 years.MethodsFour treatment groups were studied: 1) 0.04 mg kg?1 detomidine SL; 2) 0.04 mg kg?1 detomidine SL followed 1 hour later by 0.075 mg kg?1 yohimbine intravenously (IV); 3) 0.04 mg kg?1 detomidine SL followed 1 hour later by 4 mg kg?1 tolazoline IV; and 4) 0.04 mg kg?1 detomidine SL followed 1 hour later by 0.12 mg kg?1 atipamezole IV. Each horse received all treatments with a minimum of 1 week between treatments. Blood samples were obtained and plasma analyzed for yohimbine, atipamezole and tolazoline concentrations by liquid chromatography-mass spectrometry. Behavioral effects, heart rate and rhythm, glucose, packed cell volume (PCV) and plasma proteins were monitored.ResultsChin-to-ground distance increased following administration of the antagonists, however, this effect was transient, with a return to pre-reversal values as early as 1 hour. Detomidine induced bradycardia and increased incidence of atrioventricular blocks were either transiently or incompletely antagonized by all antagonists. PCV and glucose concentrations increased with tolazoline administration, and atipamezole subjectively increased urination frequency but not volume.Conclusions and clinical relevanceAt the doses administered in this study, the alpha2-adrenergic antagonistic effects of tolazoline, yohimbine and atipamezole on cardiac and behavioral effects elicited by SL administration of detomidine are transient and incomplete.  相似文献   

15.
ObjectiveTo evaluate the effects of detomidine or romifidine on cardiovascular function, isoflurane requirements and recovery quality in horses undergoing isoflurane anaesthesia.Study designProspective, randomized, blinded, clinical study.AnimalsA total of 63 healthy horses undergoing elective surgery during general anaesthesia.MethodsHorses were randomly allocated to three groups of 21 animals each. In group R, horses were given romifidine intravenously (IV) for premedication (80 μg kg–1), maintenance (40 μg kg–1 hour–1) and before recovery (20 μg kg–1). In group D2.5, horses were given detomidine IV for premedication (15 μg kg–1), maintenance (5 μg kg–1 hour–1) and before recovery (2.5 μg kg–1). In group D5, horses were given the same doses of detomidine IV for premedication and maintenance but 5 μg kg–1 prior to recovery. Premedication was combined with morphine IV (0.1 mg kg–1) in all groups. Cardiovascular and blood gas variables, expired fraction of isoflurane (Fe′Iso), dobutamine or ketamine requirements, recovery times, recovery events scores (from sternal to standing position) and visual analogue scale (VAS) were compared between groups using either anova followed by Tukey, Kruskal-Wallis followed by Bonferroni or chi-square tests, as appropriate (p < 0.05).ResultsNo significant differences were observed between groups for Fe′Iso, dobutamine or ketamine requirements and recovery times. Cardiovascular and blood gas measurements remained within physiological ranges for all groups. Group D5 horses had significantly worse scores for balance and coordination (p = 0.002), overall impression (p = 0.021) and final score (p = 0.008) than group R horses and significantly worse mean scores for VAS than the other groups (p = 0.002).Conclusions and clinical relevanceDetomidine or romifidine constant rate infusion provided similar conditions for maintenance of anaesthesia. Higher doses of detomidine at the end of anaesthesia might decrease the recovery quality.  相似文献   

16.
ObjectiveVarious drugs administered to horses undergoing surgical procedures can release histamine. Histamine concentrations were evaluated in horses prepared for surgery and administered butorphanol or morphine intraoperative infusions.Study designProspective studies with one randomized.AnimalsA total of 44 client-owned horses.MethodsIn one study, anesthesia was induced with xylazine followed by ketamine–diazepam. Anesthesia was maintained with guaifenesin–xylazine–ketamine (GXK) during surgical preparation. For surgery, isoflurane was administered with intravenous (IV) morphine (group M: 0.15 mg kg–1 and 0.1 mg kg–1 hour–1; 15 horses) or butorphanol (group B: 0.05 mg kg–1 and 0.01 mg kg–1 hour–1; 15 horses). Histamine and morphine concentrations were measured using enzyme-linked immunoassay before opioid injection (time 0), and after 1, 2, 5, 30, 60 and 90 minutes. In a subsequent study, plasma histamine concentrations were measured in 14 horses before drug administration (baseline), 15 minutes after IV sodium penicillin and 15 minutes after starting GXK IV infusion. Statistical comparison was performed using anova for repeated measures. Pearson correlation compared morphine and histamine concentrations. Data are presented as mean ± standard deviation. Significance was assumed when p ≤ 0.05.ResultsWith histamine, differences occurred between baseline (3.2 ± 2.4 ng mL–1) and GXK (5.2 ± 7.1 ng mL–1) and between baseline and time 0 in group B (11.9 ± 13.4 ng mL–1) and group M (11.1 ± 12.4 ng mL–1). No differences occurred between baseline and after penicillin or between groups M and B. Morphine concentrations were higher at 1 minute following injection (8.1 ± 5.1 ng mL–1) than at 30 minutes (4.9 ± 3.1 ng mL–1) and 60 minutes (4.0 ± 2.5 ng mL–1). Histamine correlated with morphine at 2, 30 and 60 minutes.Conclusions and clinical relevanceGXK increased histamine concentration, but concentrations were similar with morphine and butorphanol.  相似文献   

17.
Reasons for performing study: Detomidine is commonly used i.v. for sedation and analgesia in horses, but the pharmacokinetics and metabolism of this drug have not been well described. Objectives: To describe the pharmacokinetics of detomidine and its metabolites, 3‐hydroxy‐detomidine (OH‐detomidine) and detomidine 3‐carboxylic acid (COOH‐detomidine), after i.v. and i.m. administration of a single dose to horses. Methods: Eight horses were used in a balanced crossover design study. In Phase 1, 4 horses received a single dose of i.v. detomidine, administered 30 μg/kg bwt and 4 a single dose i.m. 30 üg/kg bwt. In Phase 2, treatments were reversed. Plasma detomidine, OH‐detomidine and COOH‐detomidine were measured at predetermined time points using liquid chromatography‐mass spectrometry. Results: Following i.v. administration, detomidine was distributed rapidly and eliminated with a half‐life (t1/2(el)) of approximately 30 min. Following i.m. administration, detomidine was distributed and eliminated with t1/2(el) of approximately one hour. Following, i.v. administration, detomidine clearance had a mean, median and range of 12.41, 11.66 and 10.10–18.37 ml/min/kg bwt, respectively. Detomidine had a volume of distribution with the mean, median and range for i.v. administration of 470, 478 and 215–687 ml/kg bwt, respectively. OH‐detomidine was detected sooner than COOH‐detomidine; however, COOH‐detomidine had a much greater area under the curve. Conclusions and potential relevance: These pharmacokinetic parameters provide information necessary for determination of peak plasma concentrations and clearance of detomidine in mature horses. The results suggest that, when a longer duration of plasma concentration is warranted, the i.m. route should be considered.  相似文献   

18.
ObjectiveTo compare the efficacy of a medetomidine constant rate infusion (CRI) with a detomidine CRI for standing sedation in horses undergoing high dose rate brachytherapy.Study designRandomized, controlled, crossover, blinded clinical trial.AnimalsA total of 50 horses with owner consent, excluding stallions.MethodsEach horse was sedated with intravenous acepromazine (0.02 mg kg–1), followed by an α2-adrenoceptor agonist 30 minutes later and then by butorphanol (0.1 mg kg–1) 5 minutes later. A CRI of the same α2-adrenoceptor agonist was started 10 minutes after butorphanol administration and maintained for the treatment duration. Treatments were given 1 week apart. Each horse was sedated with detomidine (bolus dose, 10 μg kg–1; CRI, 6 μg kg–1 hour–1) or medetomidine (bolus dose, 5 μg kg–1; CRI, 3.5 μg kg–1 hour–1). If sedation was inadequate, a quarter of the initial bolus of the α2-adrenoceptor agonist was administered. Heart rate (HR) was measured via electrocardiography, and sedation and behaviour evaluated using a previously published scale. Between treatments, behaviour scores were compared using a Wilcoxon signed-rank test, frequencies of arrhythmias with chi-square tests, and HR with two-tailed paired t tests. A p value <0.05 indicated statistical significance.ResultsTotal treatment time for medetomidine was longer than that for detomidine (p = 0.04), and ear movements during medetomidine sedation were more numerous than those during detomidine sedation (p = 0.03), suggesting there may be a subtle difference in the depth of sedation. No significant differences in HR were found between treatments (p ≥ 0.09). Several horses had arrhythmias, with no difference in their frequency between the two infusions.Conclusions and clinical relevanceMedetomidine at this dose rate may produce less sedation than detomidine. Further studies are required to evaluate any clinical advantages to either drug, or whether a different CRI may be more appropriate.  相似文献   

19.
The effectiveness of detomidine with or without atropine sulfate premedication in producing sedation and analgesia for arthrocentesis was studied in 12 horses. The effects were evaluated by monitoring heart and respiratory rates, borborygmi, distance from the lower lip to the floor, systolic blood pressure, and response to needle insertion. Either atropine or saline (as a placebo) was administered immediately prior to detomidine. All drugs were administered intravenously. Measurements were taken prior to drug injection and at 1, 5, 10, 15, 20, 25, 30, 40, 50, 60, 120, 180 and 240 minutes postinjection. Detomidine with atropine resulted in significantly higher heart rates than detomidine without atropine for the three hours of observation. Borborygmi were significantly decreased for four hours following detomidine with atropine and for three hours following detomidine without atropine, when compared to preinjection levels. Systolic blood pressure was significantly increased for 15 minutes following detomidine and atropine compared to the preinjection level. The head was markedly lowered for 60 minutes with either treatment. Atropine prevented the bradyarrhythmia and bradycardia induced by detomidine, but it induced a tachycardia. A satisfactory response for needle insertion and adequate synovial fluid aspiration was achieved in 95% of the trials with detomidine, with or without atropine sulfate premedication. The results suggest that, although atropine prevents bradyarrhythmia and bradycardia following detomidine, administering detomidine without atropine is satisfactory for arthrocentesis in untrained horses.  相似文献   

20.
Propofol is a potentially useful intravenous anesthetic agent for total intravenous anesthesia (TIVA) in horses. The purpose of this study was to compare the anesthetic and cardiorespiratory effects of TIVA following the administration of propofol alone(P–TIVA) and ketamine–medetomidine–propofol (KM–P–TIVA) in adult horses. The carotid artery was translocated to a subcutaneous position during TIVA with P–TIVA (n = 6) or KM–P–TIVA (n = 6). All horses were premedicated with medetomidine [0.005 mg kg–1, intravenously (IV)]. Anesthesia was induced with midazolam (0.04 mg kg–1 IV) and ketamine (2.5 mg kg IV). All horses were orotracheally intubated and breathed 100% oxygen. The KM drug combination (ketamine 40 mg mL–1 and medetomidine 0.05 mg mL–1) was infused at a rate of 0.025 mL kg–1 hour–1. Subsequently, a loading dose of propofol (0.5 mg kg–1, bolus IV) was administered to all horses; surgical anesthesia (determined by horse response to incision and surgical manipulation, positive response being purposeful or spontaneous movement of limbs or head) was maintained by varying the propofol infusion rate as needed. Arterial blood pressure and HR were also monitored. Both methods of producing TIVA provided excellent general anesthesia for the surgical procedure. Anesthesia time was 115 ± 17 (mean ± SD) and 112 ± 11 minutes in horses anesthetized with KM–P–TIVA and P–TIVA, respectively. The infusion rate of propofol required to maintain surgical anesthesia with KM–P–TIVA was significantly less than for P–TIVA (mean infusion rate of propofol during anesthesia; KM–P–TIVA 0.15 0.02 P–TIVA 0.23 ± 0.03 mg kg–1 minute–1, p = 0.004). Apnea occurred in all horses lasting 1–2 minutes and intermittent positive pressure ventilation was started. Cardiovascular function was maintained during both methods of producing TIVA. There were no differences in the time to standing after the cessation of anesthesia (KM–P–TIVA 62 ± 10 minutes versus P–TIVA 87 ± 36 minutes, p = 0.150). The quality of recovery was good in KM–P–TIVA and satisfactory in P–TIVA. KM–P–TIVA and P–TIVA produced clinically useful general anesthesia with minimum cardiovascular depression. Positive pressure ventilation was required to treat respiratory depression. Respiratory depression and apnea must be considered prior to the use of propofol in the horse.  相似文献   

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