Myocardial perfusion abnormalities in carbon monoxide poisoned dogs

Abstract

The effect of CO inhalation on the regional distribution of right and left ventricular myocardial blood flow was studied in 12 closed-chest anesthetized dogs. Dogs were exposed to a nonhypoxic mixture of O2 (21-40%) and CO (1.5-2.0%) for 10 min. Myocardial blood flow was measured (15 .mu.m radionuclide-labeled spheres) during control conditions, and 10 and 60 min following discontinuation of CO corresponding to HbCO levels of 41.6 .+-. 2.8 and 26.5 .+-. 1.6% (mean .+-. SE), respectively. At a HbCO level of 26.5%, right and left ventricular blood flows were increased to approximately 1.8-1.9 times the control values (1.06 .+-. 0.10 vs. 0.64 .+-. 0.08 ml/min per g and 1.72 .+-. 0.12 vs. 0.91 .+-. 0.07 ml/min per g, respectively, P < 0.002). At a HbCO level of 41.6%, both right and left ventricular vascular beds were maximally or near maximally dilated as right ventricular and left ventricular myocardial blood flow values were increased approximately five-fold. The right and left ventricular subendocardial-subepicardial flow ratios were reduced at both HbCO levels (P < 0.05). In addition to the global myocardial hypoxia that occurs following elevation of the HbCO level, relative subendocardial underperfusion is a component of CO poisoning in the intact dog.