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. 1986;27(4):548-59.
doi: 10.1186/BF03548134.

The use of atropine to control heart rate responses during detomidine sedation in horses

C E Short, J L Stauffer, G Goldberg, O Vainio

The use of atropine to control heart rate responses during detomidine sedation in horses

C E Short et al. Acta Vet Scand. 1986.

Abstract
in English, German

Detomidine is a sedative-analgesic which has a pharmacological profile similar to xylazine. There is evidence that the sedative effects are mediated through alpha-2 adrenoceptors.

Cardiopulmonary responses were determined using detomidine as the principal agent and as a preanesthetic prior to the induction of general anesthesia. Compatibility with guaifenesin, sodium thia-mylal and halothane were determined.

As in the case of xylazine, detomidine produces a slowing of heart rates. This was found to be either sinus bradycardia or heart block. There may be a corresponding increase in systolic blood pressures. The respiratory pattern is altered through the arterial blood gases and pH data supported evidence of adequate ventilation. The heart rate response to detomidine without anticholinergic treatment was transient and related to he duration of drug action.

Atropine sulfate, 0.02 mg/kg i.v. was effective in preventing or treating bradycardia or heart block from detomidine. Heart rates also increased during the administration of guaifenesin and sodium thia-mylal when given 50 min poisit-detomidine.

Detomidin är ett sedativt analgetikum med en farmakologisk profil lik xylazinets. De sedativa effekterna medieras uppenbarligen genom alfa-2 adrenoreceptorer.

De kardiopulmonära effekterna av detomidin studerades med detomidin som den principiella faktorn och som ett preanestetikum före induktion av allmän anestesi med guaifenesin, natrium thiamylal och halotan.

I likhet med xylazin förorsakar detomidin bradykardi, vilken befanns vare antingen sinus-bradykardi eller hjärtblock. En motsvarande ökning i systoliskt blodtryck kan inträffa. Respirationen kan vara förändrad även om arteriella blodgaser och pH tyder på adekvat ventilation. Effekten på hjärtfrekvensen av detomidin utan antikolinergisk behandling var tillfällig och berodde på längden av detomidinets verkan.

Intravenös applicering av atropinsulfat, 0,02 mg/kg, förhindrade effektivt den av detomidin förorsakade bradykardin eller hjärtblocket. Hjärtfrekvensen ökade också efter administrering av guaifenesin och natrium thiamylal 30 min efter detomidin.

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