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Chemotherapy‐induced nausea and vomiting (CINV) is a common side‐effect of cisplatin therapy. Maropitant (Cerenia?), a novel neurokinin‐1 receptor antagonist, was evaluated for prevention and treatment of cisplatin‐induced emesis in tumour‐bearing dogs. Dogs (n= 122) were randomly allocated to three treatment groups: T01, placebo before and after cisplatin; T02, placebo before and maropitant after cisplatin; or T03, maropitant before and placebo after cisplatin. Maropitant treatment (T02) following a cisplatin‐induced‐emetic event resulted in significantly fewer subsequent emetic events (P= 0.0005) than in placebo‐treated dogs (T01). In placebo‐treated (T01) dogs, 56.4% were withdrawn from the study because of treatment failure compared with 5.3% in group T02. When maropitant was administered prior to cisplatin treatment (T03) in a prevention regime, 94.9% did not vomit compared with only 4.9% of placebo‐treated dogs, and significantly fewer emetic events (P < 0.0001) were observed in those dogs that did vomit. In summary, maropitant was safe and highly effective in reducing or completely preventing cisplatin‐induced emesis.  相似文献   
3.
ObjectiveTo evaluate the efficacy of maropitant for prevention of vomiting and gastroesophageal reflux (GER) in dogs following acepromazine-hydromorphone premedication and inhalation anesthesia.Study designRandomized, blinded, prospective clinical study.AnimalsTwenty-six dogs admitted for elective soft tissue or orthopedic procedures that were 3.1 ±3.1 years of age and weighed 20.5 ± 11.4 kg.MethodsDogs were randomly assigned to one of two groups: Group M received maropitant (1.0 mg kg?1) and Group S received 0.9% saline (0.1 mL kg?1) intravenously 45–60 minutes before premedication with hydromorphone (0.1 mg kg?1) and acepromazine (0.03 mg kg?1) intramuscularly. An observer blinded to treatment documented any retching or vomiting for 20 minutes before induction with propofol (2–6 mg kg?1) and inhalation anesthesia. A pH probe inserted into the distal esophagus was used to detect GER.ResultsNone of the dogs in Group M retched or vomited (0/13), 6/13 (46%) in Group S were observed to retch or vomit, and the difference between groups was significant (p = 0.015). There were no differences between groups in the number of dogs with GER (Group M: 4/13, Group S: 6/13 dogs) or the number of reflux events. Esophageal pH at the end of anesthesia was significantly lower in both M and S groups in dogs with GER versus dogs without GER (p = 0.004 and 0.011, respectively). Only dogs with GER in Group S had significantly lower pH at the end compared to the beginning of anesthesia (p = 0.004).Conclusions and clinical relevanceIntravenous maropitant prevented retching and vomiting associated with acepromazine-hydromorphone premedication. Maropitant did not prevent the occurrence of GER. Fewer dogs in Group M developed GER but further study with a larger number of dogs is necessary to determine if there is a significant difference.  相似文献   
4.
This study was conducted to compare the efficacy of combinations of morphine, dexmedetomidine and maropitant in preventing the changes in electroencephalographic (EEG) indices of nociception in anaesthetized dogs subjected to a noxious electrical stimulus. In a crossover study, eight healthy adult dogs were randomly allocated to four groups: Mor: morphine 0.6 mg/kg; Dex + Mor: morphine 0.3 mg/kg + dexmedetomidine 5 μg/kg; Maro + Mor: morphine 0.3 mg/kg + maropitant 1 mg/kg; and Dex + Maro + Mor: morphine 0.2 mg/kg + dexmedetomidine 3 μg/kg + maropitant 0.7 mg/kg. Following intramuscular administration of test drugs in a minimal anaesthesia model, a supramaximal electrical stimulus (50 V at 50 Hz for 2 s) was applied and the EEG data were recorded. There were significant increases (p < .05) in the poststimulus median frequency (F50) only in groups Mor and Maro + Mor. Dex + Mor group had a significantly lower change in F50 and F95 compared to all other treatment groups. There was no correlation of the changes in EEG frequencies with blood plasma concentration of the drugs during and after noxious stimulation. Combination of dexmedetomidine and morphine was most effective in abolishing the changes in EEG indices in response to a noxious stimulus indicating a supra-additive interaction between these two drugs.  相似文献   
5.
ObjectiveThe goal of this study was to evaluate the effectiveness of maropitant (Cerenia®) in preventing vomiting after premedication with hydromorphone.Study designRandomized, blinded, prospective clinical study.AnimalsEighteen dogs ASA I/II admitted for elective orthopedic surgical procedures. The dogs were a mixed population of males and females, purebreds and mixed breeds, 1.0–10.2 years of age, weighing 3–49.5 kg.MethodsDogs were admitted to the study if they were greater than 1 year of age, healthy and scheduled to undergo elective orthopedic surgery. Dogs were randomly selected to receive one of two treatments administered by subcutaneous injection. Group M received 1.0 mg kg?1 of maropitant, Group S received 0.1 mL kg?1 of saline 1 hour prior to anesthesia premedication. Dogs were premedicated with 0.1 mg kg?1 of hydromorphone intramuscularly. A blinded observer documented the presence of vomiting, retching and/or signs of nausea for 30 minutes after premedication.ResultsAll dogs in S vomited (6/9), retched (1/9) or displayed signs of nausea (2/9). None (0/9) of the dogs in M vomited, retched or displayed signs of nausea. Dogs in M had significantly fewer incidences of vomiting (p = 0.0090), vomiting and retching (p = 0.0023) and vomiting, retching and nausea (p < 0.0001) when compared to S.Conclusion and clinical relevanceMaropitant prevents vomiting, retching and nausea associated with intramuscular hydromorphone administration in dogs.  相似文献   
6.
We interrogated the neurokinin‐1 receptor (NK‐1R)/substance P (SP) pathway in canine melanoma tumour tissues and cell lines. NK‐1R messenger RNA (mRNA) and protein expression were observed in the majority of tumour tissues. Immunohistochemical assessment of archived tissue sections revealed NK‐1R immunoreactivity in 11 of 15 tumours, which may have diagnostic, prognostic and therapeutic utility. However, we were unable to identify a preclinical in vitro cell line or in vivo xenograft model that recapitulates NK‐1R mRNA and protein expression documented in primary tumours. While maropitant inhibited proliferation and enhanced apoptosis in cell lines, in the absence of documented NK‐1R expression, this may represent off‐target effects. Furthermore, maropitant failed to suppress tumour growth in a canine mouse xenograft model derived from a cell line expressing mRNA but not protein. While NK‐1R represents a novel target, in the absence of preclinical models, in‐species clinical trials will be necessary to investigate the therapeutic potential for antagonists such as maropitant.  相似文献   
7.
ObjectiveDetermine if maropitant decreases the minimum alveolar concentration (MAC) of sevoflurane during stimulation of the ovarian ligament in cats.Study designProspective study.AnimalsFifteen, female cats weighing 2.5 ± 0.6kg (mean ± SD).MethodsAnesthesia was induced and maintained with sevoflurane. The right ovary was accessed via laparoscopy. A suture around the ovary and ovarian ligament was exteriorized through the abdominal wall for stimulation. A stimulus–response curve was created to identify the optimal force for MAC comparisons. In 10 cats, MAC was determined with only sevoflurane (baseline) then after 1 and 5 mg kg?1 intravenous maropitant administration. The stimulation tension force used was 4.9 N. Repeated measures anova was used to compare the groups. MAC was defined as the average of the cross‐over concentrations and reported MAC is adjusted to sea‐level and depicted as mean ± SD.ResultsThe stimulus‐response curve was hyperbolic and plateaued at 4.3 ± 3 N. The optimal tension force chosen to compare MAC was 4.9 N. The baseline sevoflurane MAC was 2.96 ± 0.3%. Maropitant, 1 mg kg?1, decreased the MAC to 2.51 ± 0.3% (15%, p < 0.01). The higher maropitant dose of 5 mg kg?1 did not change MAC further when compared to the low dose (2.46 ± 0.4%, p = 0.33).Conclusion and clinical relevanceThe ovarian ligament stimulation model is suitable to determine MAC during visceral stimulation in cats. Maropitant decreased the anesthetic requirements during visceral ovarian and ovarian ligament stimulation in cats. Maropitant (1 mg kg?1) decreases MAC by 15%; a higher dose had no additional effect.  相似文献   
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9.
ObjectiveTo determine the effect of maropitant, an NK-1 receptor antagonist on the minimum alveolar concentration (MAC) of sevoflurane after intravenous and epidural administration to dogs.Study designProspective experimental study.AnimalsSeven, adult, spayed-female dogs (24.8 ± 1.9 kg).MethodsEach dog was anesthetized twice with sevoflurane in oxygen, with at least 10 days separating the anesthetic events. The minimum alveolar concentration (MAC) of sevoflurane was determined using the tail-clamp technique. During the first anesthetic event, the MAC of sevoflurane was determined initially and again after intravenous administration of maropitant (5 mg kg?1) and an infusion (150 μg kg?1 hour?1). During the second anesthetic event, an epidural catheter was advanced to the 4th lumbar vertebra and MAC was determined after administration of saline and maropitant (1 mg kg?1) epidurally. All MAC determinations were done in duplicate. The MAC values were adjusted to sea level and compared using student's t-test.ResultsThe baseline MAC for sevoflurane was 2.08 ± 0.25%. Intravenous maropitant decreased (p < 0.05) MAC by 16% (1.74 ± 0.17%). In contrast, epidural administration of either saline or maropitant did not change (p > 0.05) the MAC (2.17 ± 0.34% and 1.92 ± 0.12%, respectively).Conclusion and clinical relevanceMaropitant decreased the MAC of sevoflurane when administered intravenously to dogs but not after epidural administration.  相似文献   
10.
The neurokinin‐1 (NK) receptor antagonist, maropitant citrate, mitigates nausea and vomiting in dogs and cats. Nausea is poorly understood and likely under‐recognized in horses. Use of NK‐1 receptor antagonists in horses has not been reported. The purpose of this study was to determine the pharmacokinetic profile of maropitant in seven adult horses after single intravenous (IV; 1 mg/kg) and intragastric (IG; 2 mg/kg) doses. A randomized, crossover design was performed. Serial blood samples were collected after dosing; maropitant concentrations were measured using LC‐MS/MS. Pharmacokinetic parameters were determined using noncompartmental analysis. The mean plasma maropitant concentration 3 min after IV administration was 800 ± 140 ng/ml, elimination half‐life was 10.37 ± 2.07 h, and volume of distribution was 6.54 ± 1.84 L/kg. The maximum concentration following IG administration was 80 ± 40 ng/ml, and elimination half‐life was 9.64 ± 1.27 hr. Oral bioavailability was variable at 13.3 ± 5.3%. Maropitant concentrations achieved after IG administration were comparable to those in small animals. Concentrations after IV administration were lower than in dogs and cats. Elimination half‐life was longer than in dogs and shorter than in cats. This study is the basis for further investigations into using maropitant in horses.  相似文献   
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