Effects of the Prophylactic Administration of Atropine on the Ephedrine‐Induced Cardiac Baroreceptor Reflex in Anesthetized Dogs

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Auteurs principaux: Daichi Seki, Seijirow Goya, Kenji Teshima, Yoshiki Yamaya
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Publié: Wiley 2025
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author Daichi Seki
Seijirow Goya
Kenji Teshima
Yoshiki Yamaya
author_facet Daichi Seki
Seijirow Goya
Kenji Teshima
Yoshiki Yamaya
Daichi Seki
Seijirow Goya
Kenji Teshima
Yoshiki Yamaya
collection Wiley Open Access
contents Effects of the Prophylactic Administration of Atropine on the Ephedrine‐Induced Cardiac Baroreceptor Reflex in Anesthetized Dogs Daichi Seki Seijirow Goya Kenji Teshima Yoshiki Yamaya Journal of Veterinary Emergency and Critical Care ABSTRACT Objective To confirm the reproducibility of the cardiac baroreceptor reflex (CBR) and bradycardia induced by ephedrine administration and to evaluate the safety of administering prophylactic atropine to prevent the CBR in anesthetized dogs. Design Experimental, single‐blind, crossover study. Setting Veterinary university research facility. Animals Six healthy Beagle dogs. Interventions Dogs were anesthetized with propofol and maintained with isoflurane. After various biological monitors were attached, dogs received IV premedication with saline (saline–ephedrine [SE] group) or atropine (0.04 mg/kg; atropine–ephedrine [AE] group). Subsequently, ephedrine (0.1 mg/kg) was administered intravenously. Measurements and Main Results Cardiovascular parameters (invasive arterial blood pressure, heart rate [HR], stroke volume index, and cardiac index) and immediate parasympathetic tone activity (PTAi) were recorded 15 min after premedication (baseline [BL]) and for 30 min after ephedrine administration. All data were recorded by the same blinded recorder. Consequently, the MAP in the SE and AE groups significantly increased after ephedrine administration. The HR in the SE group significantly decreased from BL; two dogs exhibited bradycardia (<50/min), and atrioventricular block was seen in one dog. In the AE group, the HR significantly increased from BL; no tachycardia was observed. The cardiac index in the SE group was maintained at BL, but the cardiac index in the AE group was significantly higher than that at BL during the experimental period. In both groups, PTAi rapidly decreased after ephedrine administration at 1 min. In the SE group, PTAi recovered to BL after 2 min. However, PTAi in the AE group remained significantly lower at 1–3 min than at BL and was significantly lower than that at 1–4 min in the SE group. Conclusions We confirmed the CBR‐induced bradycardia after ephedrine administration in anesthetized dogs, showing that atropine administration for prevention of ephedrine‐induced bradycardia is safe with no adverse events. 10.1111/vec.70055 http://onlinelibrary.wiley.com/termsAndConditions#vor
doi_str_mv 10.1111/vec.70055
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spellingShingle Effects of the Prophylactic Administration of Atropine on the Ephedrine‐Induced Cardiac Baroreceptor Reflex in Anesthetized Dogs
Daichi Seki
Seijirow Goya
Kenji Teshima
Yoshiki Yamaya
Journal of Veterinary Emergency and Critical Care
Effects of the Prophylactic Administration of Atropine on the Ephedrine‐Induced Cardiac Baroreceptor Reflex in Anesthetized Dogs Daichi Seki Seijirow Goya Kenji Teshima Yoshiki Yamaya Journal of Veterinary Emergency and Critical Care ABSTRACT Objective To confirm the reproducibility of the cardiac baroreceptor reflex (CBR) and bradycardia induced by ephedrine administration and to evaluate the safety of administering prophylactic atropine to prevent the CBR in anesthetized dogs. Design Experimental, single‐blind, crossover study. Setting Veterinary university research facility. Animals Six healthy Beagle dogs. Interventions Dogs were anesthetized with propofol and maintained with isoflurane. After various biological monitors were attached, dogs received IV premedication with saline (saline–ephedrine [SE] group) or atropine (0.04 mg/kg; atropine–ephedrine [AE] group). Subsequently, ephedrine (0.1 mg/kg) was administered intravenously. Measurements and Main Results Cardiovascular parameters (invasive arterial blood pressure, heart rate [HR], stroke volume index, and cardiac index) and immediate parasympathetic tone activity (PTAi) were recorded 15 min after premedication (baseline [BL]) and for 30 min after ephedrine administration. All data were recorded by the same blinded recorder. Consequently, the MAP in the SE and AE groups significantly increased after ephedrine administration. The HR in the SE group significantly decreased from BL; two dogs exhibited bradycardia (<50/min), and atrioventricular block was seen in one dog. In the AE group, the HR significantly increased from BL; no tachycardia was observed. The cardiac index in the SE group was maintained at BL, but the cardiac index in the AE group was significantly higher than that at BL during the experimental period. In both groups, PTAi rapidly decreased after ephedrine administration at 1 min. In the SE group, PTAi recovered to BL after 2 min. However, PTAi in the AE group remained significantly lower at 1–3 min than at BL and was significantly lower than that at 1–4 min in the SE group. Conclusions We confirmed the CBR‐induced bradycardia after ephedrine administration in anesthetized dogs, showing that atropine administration for prevention of ephedrine‐induced bradycardia is safe with no adverse events. 10.1111/vec.70055 http://onlinelibrary.wiley.com/termsAndConditions#vor
title Effects of the Prophylactic Administration of Atropine on the Ephedrine‐Induced Cardiac Baroreceptor Reflex in Anesthetized Dogs
topic Journal of Veterinary Emergency and Critical Care
url https://onlinelibrary.wiley.com/doi/10.1111/vec.70055