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心脏毒性动物模型:一氧化碳诱导的心电图缺氧在轻度麻醉中被掩盖。

Animal model of cardiotoxicity: carbon monoxide induced ECG hypoxia masked in light narcosis.

作者信息

Mikisková H, Frantík E

机构信息

Institute of Hygiene and Epidemiology, Centre of Industrial Medicine and Occupational Diseases, Praha.

出版信息

Act Nerv Super (Praha). 1987 Dec;29(4):274-8.

PMID:3439427
Abstract

Inhalation exposure of restrained conscious rats to carbon monoxide (1000 ppm, 120 min.) led to a peak carboxyhaemoglobine concentration of 40-45%. At this concentrations spontaneous motor activity was not affected significantly but the physical capacity at endurance run was depressed by 70%. From the 30th min. of exposure a typical two-phasic change in heart rate with initial tachycardia and obvious but unstable hypoxic changes in ECG were observed. Quieting of animals (light anesthesia with phenobarbitone; 100 mg/kg ip) removed almost completely all pathological changes. The level and fluctuations of functional requirements to the circulation seem thus substantial for the development of the cardiotoxic effects.

摘要

将清醒的束缚大鼠吸入一氧化碳(1000 ppm,120分钟)会导致羧基血红蛋白浓度峰值达到40 - 45%。在此浓度下,自发运动活性未受到显著影响,但耐力跑的体能下降了70%。从暴露第30分钟起,观察到心率出现典型的双相变化,起初是心动过速,心电图出现明显但不稳定的缺氧变化。使动物安静(用苯巴比妥轻度麻醉;腹腔注射100 mg/kg)几乎完全消除了所有病理变化。因此,对循环系统功能需求的水平和波动似乎对心脏毒性作用的发展至关重要。

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