Cardiodynamic changes during prolonged carbon monoxide exposure in the rat
Penney, D.G.; Sodt, P.C.; Cutilletta, A.
Toxicology and Applied Pharmacology 50(2): 213-218
1979
ISSN/ISBN: 0041-008X PMID: 505453 Document Number: 140573
Adult male rats were exposed to 500 ppm CO (38-42% COHb) for 1-42 days. Hematocrit rose gradually from 49.8-69.7%. Caridomegaly developed as reported earlier. Using an open chest anesthetized preparation, stroke index, mean stroke power and mean cardiac output were seen to increase sharply upon initial CO exposure and to remain elevated for the duration of exposure. Both total systemic resistance and total pulmonary resistance fell sharply and remained depressed. Left ventricle (LV) and right ventricle (RV) systolic pressures and mean aortic pressure rose modestly, but nonsignificantly over the first 14 days of exposure, declining somewhat thereafter. The maximum rate of change of LV pressure (dP/dt) tended to rise above control values during the first 2 wk of exposure. There was no consistent change in heart rate. Enhanced cardiac output via increased stroke volume is seen as a compensatory mechanism to provide adequate tissue O2 delivery during CO intoxication. The greater continuous heart work involved may be the major factor responsible for development of CO-induced cardiomegaly.