Pathogenesis of Cor Pulmonale, February 6, 2001

Pathogenesis of Cor Pulmonale, February 6, 2001

Hypoxia is the primary cause of pulmonary hypertension, leading to pulmonary vasoconstriction. In the mechanism of increased pulmonary vascular tension, the role of the autonomic nervous system is evident. For example, its effects on smooth muscles, as well as on mediators such as histamine, angiotensin, and prostaglandins. It should also be noted that leukotrienes (LT3) and prostaglandins (PG) are produced by various cells in the lungs, being metabolites of arachidonic acid via lipoxygenase. Among them, LTC4, LTD4, and LTE4 can all cause pulmonary vasoconstriction. When animals experience hypoxia, the concentration of LT substances in alveolar lavage fluid increases significantly, leading to a corresponding rise in pulmonary arterial pressure. In addition, platelet-activating factor, endothelial-derived vasodilator and vasoconstrictor, reactive oxygen species, and atrial natriuretic peptide all participate in certain reactions. In summary, hypoxia causes pulmonary vasoconstriction; moreover, the reactivity of pulmonary vessels is also a contributing factor, along with the intrinsic contractility of the vessels themselves, which varies greatly among individuals. Even under the same partial pressure of oxygen, some people develop the disease while others do not. Some believe that carbon dioxide partial pressure influences pulmonary vasoconstriction, but recent experimental studies indicate that this relationship is relatively weak, whereas blood pH is more relevant, suggesting that metabolic acidosis has a slightly greater impact on vascular reactivity than respiratory acidosis.