Cardiac function in goats exposed to carbon monoxide.
To investigate the possibility that prolonged carbon monoxide (CO) exposure would depress myocardial function, six chronically instrumented, unsedated goats were exposed to 160--200 ppm CO for 2 wk, resulting in a mean carboxyhemoglobin saturation of 20%. Cardiac index and stroke volume remained unchanged during and after exposure. Hematocrit and hemoglobin concentration started increasing on the 10th day of exposure, this increase reached statistical significance (P less than 0.05) on the 6th postexposure day. Contractility (Vmax) of the left ventricular myocardium and heart rate were unchanged during exposure to CO, but both were significantly (P less than 0.05) decreased at some time during the 1st wk after removal from CO. If there was a decrease in intrinsic myocardial function during CO exposure, it may have been masked by increased sympathetic activity. The mechanism(s) that might produce the decrease in heart rate and contractility after removal from CO are not obvious. Possible explanations are discussed.
D000818:Animals; D002248:Carbon Monoxide / Q000494:pharmacology*; D005260:Female; D006041:Goats / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D006339:Heart Rate; D009200:Myocardial Contraction / Q000187:drug effects*; D012119:Respiration; D013318:Stroke Volume; D013997:Time Factors
D002248:Carbon Monoxide