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

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.