Ischemic brain damage after ketamine and xylazine treatment in a young laboratory monkey (Macaca fascicularis).

Katsuhiko Yoshizawa, Yuji Oishi, Masahiro Matsumoto, Abraham Nyska
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Abstract

After a 4-year-old female laboratory cynomolgus monkey manifested neurological abnormalities, including tetanic spasm, after intramuscular injection of 20 mg/kg ketamine, we administered 2 mg/kg xylazine in an attempt to control the seizure. However, the animal continued to display opisthotonus, nystagmus, and symptomatic epilepsia. Analysis of blood chemistry revealed a dramatically increased creatine phosphokinase level. Abnormal histopathological findings included acute neuronal necrosis or glial reaction or both in the cerebral cortex, nucleus lentiformis, hippocampus, cerebellar cortex and nucleus, and medulla oblongata; severe myocardial hemorrhagic necrosis; and hepatic subcapsular hematoma. Although the mechanism of this neuronal damage has not been clarified, it may be attributable to an ischemic condition in the brain, probably due to temporal cardiac arrest or hemorrhagic change in the liver and heart, with subsequent decreased blood pressure, after ketamine and/or xylazine treatment. Because both drugs often are used as general anesthetics in veterinary medicine, attention should be paid to this rare case with neural damage.

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氯胺酮和噻嗪治疗对幼龄实验室猴(Macaca fascularis)的缺血性脑损伤。
一只4岁雌性实验室食蟹猴在肌肉注射20 mg/kg氯胺酮后出现神经异常,包括强直性痉挛,我们给药2 mg/kg噻嗪试图控制癫痫发作。然而,动物继续表现出斜视、眼球震颤和癫痫症状。血液化学分析显示肌酸磷酸激酶水平显著升高。异常组织病理表现为:大脑皮层、状核、海马、小脑皮质和核、延髓出现急性神经元坏死或胶质反应或两者兼有;心肌出血性坏死严重;肝包膜下血肿。虽然这种神经元损伤的机制尚不清楚,但它可能是由于脑缺血,可能是由于暂时性心脏骤停或肝脏和心脏出血性改变,随后在氯胺酮和/或噻嗪治疗后血压下降。由于这两种药物在兽医学中经常用作全身麻醉剂,因此应注意这种罕见的神经损伤病例。
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