Cardiovascular effects of xylazine and detomidine in horses

Ann E. Wagner From, the Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, OH 43210.

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 DVM, MS
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William W. Muir III From, the Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, OH 43210.

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 DVM, PhD
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Kenneth W. Hinchcliff From, the Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, OH 43210.

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 BVSc, MS

SUMMARY

The cardiovascular effects of xylazine and detomidine in horses were studied. Six horses were given each of the following 5 treatments, at 1-week intervals: xylazine, 1.1 mg/kg, iv; xylazine, 2.2 mg/kg, im; detomidine, 0.01 mg/ kg, iv; detomidine, 0.02 mg/kg, iv; and detomidine, 0,04 mg/kg, im. All treatments resulted in significantly decreased heart rate, increased incidence of atrioventricular block, and decreased cardiac output and cardiac index; cardiac output and cardiac index were lowest following iv administration of 0.02 mg of detomidine/kg. Mean arterial pressure was significantly reduced for various periods with all treatments; however, iv administration of 0.02 nig of detomidine/kg caused hypertension initially. Systemic vascular resistance was increased by all treatments. Indices of ventricular contractility and relaxation, + dP/dt and − dP/dt, were significantly depressed by all treatments. Significant changes were not detected in stroke volume or ejection fraction. The pcv was significantly reduced by all treatments. Respiratoiy rate was significantly decreased with all treatments, but arterial carbon dioxide tension did not change. Arterial oxygen tension was significantly decreased briefly with the 3 iv treatments only.

SUMMARY

The cardiovascular effects of xylazine and detomidine in horses were studied. Six horses were given each of the following 5 treatments, at 1-week intervals: xylazine, 1.1 mg/kg, iv; xylazine, 2.2 mg/kg, im; detomidine, 0.01 mg/ kg, iv; detomidine, 0.02 mg/kg, iv; and detomidine, 0,04 mg/kg, im. All treatments resulted in significantly decreased heart rate, increased incidence of atrioventricular block, and decreased cardiac output and cardiac index; cardiac output and cardiac index were lowest following iv administration of 0.02 mg of detomidine/kg. Mean arterial pressure was significantly reduced for various periods with all treatments; however, iv administration of 0.02 nig of detomidine/kg caused hypertension initially. Systemic vascular resistance was increased by all treatments. Indices of ventricular contractility and relaxation, + dP/dt and − dP/dt, were significantly depressed by all treatments. Significant changes were not detected in stroke volume or ejection fraction. The pcv was significantly reduced by all treatments. Respiratoiy rate was significantly decreased with all treatments, but arterial carbon dioxide tension did not change. Arterial oxygen tension was significantly decreased briefly with the 3 iv treatments only.

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