Coronary and cerebral metabolism-blood flow coupling and pulmonary alveolar ventilation-blood flow coupling may be disabled during acute carbon monoxide poisoning
Autor: | Ronald F. Coburn |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Physiology 030204 cardiovascular system & hematology 03 medical and health sciences chemistry.chemical_compound Carbon Monoxide Poisoning 0302 clinical medicine Physiology (medical) Internal medicine medicine Humans Hypoxia chemistry.chemical_classification Reactive oxygen species Carbon Monoxide Lung Carbon monoxide poisoning Oxygen–haemoglobin dissociation curve Blood flow medicine.disease Coupling (electronics) Oxygen 030104 developmental biology medicine.anatomical_structure chemistry Carboxyhemoglobin Cerebrovascular Circulation Oxyhemoglobins Cardiology Carbon monoxide |
Zdroj: | Journal of applied physiology (Bethesda, Md. : 1985). 129(5) |
ISSN: | 1522-1601 |
Popis: | 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. |
Databáze: | OpenAIRE |
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