Coronary and cerebral metabolism-blood flow coupling and pulmonary alveolar ventilation-blood flow coupling may be disabled during acute carbon monoxide poisoning.

Abstract

Current evidence indicates that the toxicity of carbon monoxide (CO) poisoning results from increases in reactive oxygen species (ROS) generation plus tissue hypoxia resulting from decreases in capillary Po2 evoked by effects of increases in blood [carboxyhemoglobin] on the oxyhemoglobin dissociation curve. There has not been consideration of how increases in Pco could influence metabolism-blood flow coupling, a physiological mechanism that regulates the uniformity of tissue Po2, and alveolar ventilation-blood flow coupling, a mechanism that increases the efficiency of pulmonary O2 uptake. Using published data, I consider hypotheses that these coupling mechanisms, triggered by O2 and CO sensors located in arterial and arteriolar vessels in the coronary and cerebral circulations and in lung intralobar arteries, are disrupted during acute CO poisoning. These hypotheses are supported by calculations that show that the Pco in these vessels can reach levels during CO poisoning that would exert effects on signal transduction molecules involved in these coupling mechanisms.NEW & NOTEWORTHY This article introduces and supports a postulate that the tissue hypoxia component of carbon monoxide poisoning results in part from impairment of physiological adaptation mechanisms whereby tissues can match regional blood flow to O2 uptake, and the lung can match regional blood flow to alveolar ventilation.