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A 4-year-old 31.0-kg (68.2-lb) castrated male mixed-breed dog was examined by the cardiology service at the Colorado State University Veterinary Teaching Hospital for a scheduled recheck examination and pacemaker interrogation. Previous diagnoses include bartonellosis; severe, chronic hepatitis; and third-degree (ie, complete) atrioventricular (AV) block. Intermittent atrial standstill attributable to some degree of sinoatrial dysfunction was also present. Two weeks prior to the recheck examination, a pacemaker with transdiaphragmatic epicardial leads had been placed in response to a 3-month history of labored breathing, lethargy, and syncope. Epicardial leads had been selected, rather than transvenous, endocardial leads, because the previously diagnosed

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in Journal of the American Veterinary Medical Association

Abstract

Objective—To evaluate degree of sedation and cardiovascular, respiratory, acid-base excess, and electrolyte variables in response to IM administration of dexmedetomidine or dexmedetomidine with atropine.

Design—Randomized crossover study.

Animals—5 healthy 1- to 2-year-old sexually intact male Treeing Walker Coonhounds.

Procedures—Dogs were instrumented with catheters placed in the dorsal pedal artery and lateral saphenous vein. All dogs received dexmedetomidine (10 μg/kg [4.5 μg/lb], IM) or dexmedetomidine with atropine (0.02 mg/kg [0.009 mg/lb], IM). Variables were measured at baseline (time 0) and 5, 15, 30, and 60 minutes after drug administration.

Results—In all dogs, lithium dilution cardiac output decreased from a mean ± SD baseline value of 5.07 ± 1.0 L/min to 2.1 ± 0.9 L/min. Cardiac output was not different between dexmedetomidine group dogs and dexmedetomidine-atropine group dogs. Mean arterial pressure increased from baseline in both groups but was significantly higher in dexmedetomidine-atropine group dogs, compared with dexmedetomidine group dogs. Heart rate in dexmedetomidine group dogs decreased from 110 ± 14.2 beats/min to 49.4 ± 10.4 beats/min by 15 minutes. No differences were seen in blood gas values, electrolyte concentration, or hemoglobin values over time or between groups. Arrhythmias were detected in dexmedetomidine-atropine group dogs and included atrioventricular block, ventricular premature contractions, and ventricular bigeminy.

Conclusions and Clinical Relevance—Administration of atropine at 0.02 mg/kg, IM, with dexmedetomidine at 10 μg/kg, IM, resulted in an increase in mean arterial blood pressure and heart rate; deleterious cardiac arrhythmias were also observed. Use of atropine with dexmedetomidine is not recommended in dogs.

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in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine the anesthetic-sparing effect of maropitant, a neurokinin 1 receptor antagonist, during noxious visceral stimulation of the ovary and ovarian ligament in dogs.

Animals—Eight 1-year-old female dogs.

Procedures—Dogs were anesthetized with sevoflurane. Following instrumentation and stabilization, the right ovary and ovarian ligament were accessed by use of laparoscopy. The ovary was stimulated with a traction force of 6.61 N. The minimum alveolar concentration (MAC) was determined before and after 2 doses of maropitant.

Results—The sevoflurane MAC value was 2.12 ± 0.4% during stimulation without treatment (control). Administration of maropitant (1 mg/kg, IV, followed by 30 μg/kg/h, IV) decreased the sevoflurane MAC to 1.61 ± 0.4% (24% decrease). A higher maropitant dose (5 mg/kg, IV, followed by 150 μg/kg/h, IV) decreased the MAC to 1.48 ± 0.4% (30% decrease).

Conclusions and Clinical Relevance—Maropitant decreased the anesthetic requirements during visceral stimulation of the ovary and ovarian ligament in dogs. Results suggest the potential role for neurokinin 1 receptor antagonists to manage ovarian and visceral pain.

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in American Journal of Veterinary Research