PubMed · 584341
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D S Ross. 1977. Case history: postscript: low Hb/high altitude.. https://pubmed.ncbi.nlm.nih.gov/584341/
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The author discusses factors promoting the occurrence of acute mountain sickness and high altitude pulmonary edema. The level of altitude as well as the speed of ascent are important determinants and can be influenced by behaviour. A low hypoxic ventilatory drive presents a constitutional factor predisposing to acute mountain sickness and high altitude pulmonary edema. Individuals susceptible to high altitude pulmonary edema also show increased hypoxia vasoconstriction of pulmonary arterioles. The importance of an exaggerated hypoxic pulmonary vascular response for the pathogenesis of high altitude pulmonary edema is demonstrated by the observation that this illness can be treated or prevented by lowering pulmonary artery pressure with nifedipine. In most cases, however, acute mountain sickness and high altitude pulmonary edema can be prevented without the help of drugs, by adjusting the speed of ascent to the degree of susceptibility to these illnesses.
Altitude hypoxia induces an increase in adrenergic activity in humans. However, a decrease in maximal heart rate is observed after a few days of exposure to altitudes above 3500 m, as well as a decrease in chronotropic response to isoproterenol infusion. This phenomenon has been linked to a desensitization of beta-adrenoceptors (beta AR), and/or an increase in parasympathetic activity. A decrease in the density of beta AR in chronic hypoxia has been found in rat left ventricle and in human lymphocytes, without modification of the affinity of beta AR for an agonist or antagonist, and a decreased adenylate cyclase activity in the right ventricle. In the same conditions, the density of adenosine A1 receptors is decreased by 46% in rat myocardium, without alteration in the coupling between hormone, receptor and Gi protein. The density of muscarinic receptors is increased by 40%, with an increase in the affinity for an agonist, suggesting an augmented parasympathetic effect. Hypoxia probably acts on all the receptors involved in the modulation of cardiac chronotropic activity; the combined effects of chronic hypoxia on these receptors tend to a beneficial limitation of myocardial oxygen consumption, especially during heavy exercise.