Hypoxic pulmonary vasoconstriction

Hypoxic pulmonary vasoconstriction is a physiological phenomenon in which pulmonary arterioles 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.^[1]

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, nitric oxide, and vasodilators.

High altitude pulmonary edema

Main article: 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.

Euler–Liljestrand mechanism

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

↑ Silverthorn, D.U. (2016). Human physiology, 7nd Ed, Chapter 14-15, 544. New York: Pearson Education.

Silverthorn, D.U. (2016). Human physiology, 7nd Ed, Chapter 14-15, 544. New York: Pearson Education.⁽¹⁾
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.
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.

External links

Respiratory physiology

Respiration	breath inhalation exhalation respiratory rate respirometer pulmonary surfactant compliance elastic recoil hysteresivity airway resistance bronchial hyperresponsiveness constriction dilatation mechanical ventilation

Control	pons pneumotaxic center apneustic center medulla dorsal respiratory group ventral respiratory group chemoreceptors central peripheral pulmonary stretch receptors Hering–Breuer reflex

Lung volumes	VC FRC Vt dead space CC PEF calculations respiratory minute volume FEV1/FVC ratio Lung function tests spirometry body plethysmography peak flow meter nitrogen washout

Circulation	pulmonary circulation hypoxic pulmonary vasoconstriction pulmonary shunt

Interactions	Perfusion (V) ventilation (Q) ventilation/perfusion scan zones of the lung gas exchange pulmonary gas pressures alveolar gas equation alveolar–arterial gradient hemoglobin oxygen–haemoglobin dissociation curve (Oxygen saturation 2,3-BPG Bohr effect Haldane effect) carbonic anhydrase (chloride shift) oxyhemoglobin respiratory quotient arterial blood gas diffusion capacity (DLCO)

Insufficiency	high altitude oxygen toxicity hypoxia

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