Hypoxic pulmonary vasoconstriction

Source: Wikipedia, the free encyclopedia.

Hypoxic pulmonary vasoconstriction (HPV), also known as the Euler-Liljestrand mechanism, is a

hypoxia (low oxygen levels). By redirecting blood flow from poorly-ventilated lung regions to well-ventilated lung regions, HPV is thought to be the primary mechanism underlying ventilation/perfusion matching.[1][2]

The process might initially seem counterintuitive, as low oxygen levels might theoretically stimulate increased blood flow to the lungs to increase gas exchange. However, the purpose of HPV is to distribute bloodflow regionally to increase the overall efficiency of gas exchange between air and blood. While the maintenance of

pulmonary vascular resistance, and pulmonary arterial pressure, potentially leading to pulmonary hypertension and pulmonary edema
.

Several factors inhibit HPV including increased

vasodilators
.

Molecular mechanism

The classical explanation of HPV involves inhibition of hypoxia-sensitive

epithelial cells (neuroepithelial bodies) that release serotonin have been suggested to contribute to hypoxic pulmonary venoconstriction.[8]

High altitude pulmonary edema

High-altitude mountaineering can induce pulmonary hypoxia due to decreased atmospheric pressure. This hypoxia causes vasoconstriction that ultimately leads to

high altitude pulmonary edema (HAPE). For this reason, some 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. Additionally, several studies on native populations remaining at high altitudes have demonstrated to varying degrees the blunting of the HPV response.[9]

References

  1. ^ Silverthorn, D.U. (2016). "Chapter 14-15". Human physiology (7th ed.). New York: Pearson Education. p. 544.
  2. S2CID 78887723
    .
  3. .
  4. .
  5. .
  6. .
  7. .
  8. .
  9. .

External links