Myocardial perfusion abnormalities in carbon monoxide poisoned dogs.

Abstract

The effect of carbon monoxide 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 oxygen (21-40%) and carbon monoxide (1.5-2.0%) for 10 min. Myocardial blood flow was measured (15 micron radionuclide-labeled spheres) during control conditions, and 10 and 60 min following discontinuation of carbon monoxide corresponding to carboxyhemoglobin levels (COHb) of 41.6 +/- 2.8 and 26.5 +/- 1.6% (mean +/- SE), respectively. At COHb 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 gram and 1.72 +/- 0.12 vs. 0.91 +/- 0.07 mL/min per gram, respectively, P less than 0.002). At a COHb 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 fivefold. The right and left ventricular subendocardial-subepicardial flow ratios were reduced at both COHb levels (P less than 0.05). Thus, in addition to the global myocardial hypoxia that occurs following elevation of the COHb level, relative subendocardial underperfusion is a component of carbon monoxide poisoning in the intact dog.