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| Main Authors: | , |
|---|---|
| Format: | Artículo científico |
| Language: | en |
| Published: |
Physiological reports
2026
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| Subjects: | |
| Online Access: | https://pubmed.ncbi.nlm.nih.gov/41986283/ |
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Table of Contents:
- A carbon monoxide cycle drives carbon monoxide uptake and poisoning. Coburn, Ronald F Tift, Michael S Carbon Monoxide Poisoning Carbon Monoxide Humans Carboxyhemoglobin Oxyhemoglobins Lung Animals Pulmonary Alveoli Oxygen An understanding of the physiology of acute carbon monoxide (CO) poisoning remains incomplete. This study describes a novel approach-considering a CO cycle driven by CO inhalation which includes: alveolar CO uptake → the transport to peripheral tissues → an increase in the P and [COHb] in peripheral capillary blood → and a return of COHb to the lungs. Unlike earlier models, this model allows evaluation of how [COHb] changes will affect physiological events at different sites in this cycle. We calculated increases in the P and the [COHb] at these sites during constant breathing of different CO concentrations, using an approach that emphasizes the importance of the rate of the replacement reaction (CO + oxyhemoglobin (OHb) ↔ COHb + oxygen (O)) in the physiology of CO poisoning. Key findings include: (i) how interactions between inhaled CO, COHb recirculating back to alveolar capillaries, and alveolar capillary P back-pressure regulate pulmonary CO uptake; (ii) how a decrease in the arterial [OHb] evokes an amplification of the P in blood entering peripheral tissues; (iii) that hemoglobin's R-to-T allosteric shifts influence CO delivery to peripheral tissues; and (iv) a clearer characterization of how tissue P is increased during CO exposures.