Hypoxic pulmonary vasoconstriction

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Hypoxic pulmonary vasoconstriction is a paradoxical, physiological phenomenon in which pulmonary arteries constrict in the presence of hypoxia (low oxygen levels) without hypercapnia (high carbon dioxide levels), redirecting blood flow to alveoli with a higher oxygen content.

The process might at first seem illogical, as low oxygen levels should theoretically lead to increased blood flow to the lungs to receive increased gaseous exchange. However, it is explained by the fact that constriction leads to redistribution of bloodflow to better-ventilated areas of the lung, which increases the total area involved in gaseous exchange.

This improves ventilation/perfusion ratio and arterial oxygenation, but is less helpful in the case of long-term whole-body hypoxia. This is seen in COPD, at altitude and in heart failure.

Several factors inhibit this process including increased cardiac output, hypocapnia, hypothermia, acidosis/alkalosis, increased pulmonary vascular resistance, inhaled anesthetics, calcium channel blockers, positive end-expiratory pressure (PEEP), high-frequency ventilation (HFV), isoproterenol, nitrous oxide, and vasodilators.

High altitude pulmonary edema[edit]

Climbing tall mountains can induce full lung hypoxia due to decreased atmospheric pressure. This hypoxia causes hypoxic vasoconstriction that ultimately leads to high altitude pulmonary edema (HAPE). For this reason, most climbers carry supplemental oxygen to prevent hypoxia, edema, and HAPE. The standard drug treatment of dexamethasone does not alter the hypoxia or the consequent vasoconstriction, but stimulates fluid reabsorption in the lungs to reverse the edema.

Euler–Liljestrand mechanism[edit]

This describes the connection between ventilation and blood circulation (perfusion) of the lung. If the ventilation in a part of the lung decreases it leads to local hypoxia. The local hypoxia leads to pulmonary vasoconstriction. This adaptive mechanism is beneficial, because it diminishes the amount of blood that passes the lung without being oxygenated. The mechanism was discovered by two Swedish pharmacologists, Ulf von Euler and Göran Liljestrand at the Department of Pharmacology of Karolinska Institute in Stockholm.

The molecular mechanism seems to be mediated by oxygen-sensitive potassium ion channels in the cell membrane of pulmonary smooth muscle. With a low partial pressure of oxygen, these channels are blocked, leading to the depolarization of the cell membrane. Calcium channels are activated and cause the influx of Ca2+ ions over the membrane and to the release of calcium from the endoplasmic reticulum. The rise of calcium concentration causes contraction of the blood vessels smooth muscle fibers and the resulting vasoconstriction. Histamine has also been implicated in this mechanism.

References[edit]

  • Von Euler, US; Liljestrand, G (1946). "Observations on the pulmonary arterial blood pressure in the cat". Acta Physiol. Scand. 12 (301–320)
  • Völkel, N; Duschek, W; Kaukel, E; Beier, W; Siemssen, S; Sill, V (1975). "Histamine-an important mediator for the Euler-Liljestrand mechanism?". Pneumonologie. Pneumonology 152 (1-3): 113–21. doi:10.1007/BF02101579. PMID 171630.  edit
  • Porcelli, R. J.; Viau, A.; Demeny, M.; Naftchi, N. E.; Bergofsky, E. H. (1977). "Relation between hypoxic pulmonary vasoconstriction, its humoral mediators and alpha-beta adrenergic receptors". Chest 71 (2 suppl): 249–251. doi:10.1378/chest.71.2_Supplement.249. PMID 12924.  edit

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