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  • Author or Editor: Sirirat Niyom x
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Objective—To evaluate the analgesic efficacy of ABT-116, a transient receptor potential cation channel vanilloid subfamily V member 1 antagonist, and compare it with that of buprenorphine by measurement of mechanical and thermal nociceptive thresholds in dogs.

Animals—Six 7- to 8-month-old dogs (3 males and 3 females).

Procedures—In a crossover study design, all dogs received ABT-116 (30 mg/kg, PO) and buprenorphine (0.03 mg/kg, orotransmucosally), with each treatment separated by 1 week. Physiologic variables were recorded prior to and 1, 6, and 24 hours after drug administration. Thermal (thoracic) and mechanical (dorsolateral aspect of the radius [proximal] and dorsopalmar aspect of the forefoot [distal]) nociceptive thresholds were assessed prior to (baseline) and 15 minutes and 1, 2, 4, 6, 12, 18, and 24 hours after treatment.

Results—Buprenorphine administration resulted in higher overall thermal and proximal mechanical nociceptive thresholds, compared with ABT-116. Distal mechanical nociceptive thresholds after treatment were higher than baseline values for both treatments, but the magnitude of change was greater for buprenorphine at 1 hour after administration. Whereas HR and RR sporadically differed from baseline values after ABT-116 administration, rectal temperature increased from a baseline value of 39 ± 0.2°C (mean ± SD) to a peak of 40.6 ± 0.2°C at 6 hours.

Conclusions and Clinical Relevance—In dogs without inflammation or nerve injury, PO administration of ABT-116 did not consistently result in an increase in nociceptive thresholds. However, clinically relevant increases in rectal temperature were identified after ABT-116 administration.

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in American Journal of Veterinary Research


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