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decrease in the diameter of blood vessels

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/05/25 11:39:20」(JST)

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Hypoxic pulmonary vasoconstriction is a 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

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

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

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

External links

American Thoracic Society
American Journal of Physiology, Lung Cellular and Molecular Physiology
Overview at ccmtutorials.com

UpToDate Contents

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1. 肺高血圧症の病因 pathogenesis of pulmonary hypertension
2. 高二酸化炭素血症の発症機序、原因、および影響 mechanisms causes and effects of hypercapnia
3. 一側肺換気の一般的原則 general principles of one lung ventilation
4. Inhalation injury from heat, smoke, or chemical irritants
5. 高地肺水腫 high altitude pulmonary edema

English Journal

sGC stimulation totally reverses hypoxia-induced pulmonary vasoconstriction alone and combined with dual endothelin-receptor blockade in a porcine model.

Lundgren J, Kylhammar D, Hedelin P, Rådegran G.SourceThe Öresund Cardiovascular Research Collaboration, The Clinic for Heart Failure and Valvular Disease, Skåne University Hospital, Lund, Sweden; The Department of Cardiology, Clinical Sciences, Lund University, Lund, Sweden.
Acta physiologica (Oxford, England).Acta Physiol (Oxf).2012 Nov;206(3):178-94. doi: 10.1111/j.1748-1716.2012.02445.x. Epub 2012 Jun 9.
AIM: Stimulation of soluble guanylate cyclase (sGC) with BAY 41-8543 was hypothesized to attenuate acute hypoxic pulmonary vasoconstriction alone and combined with dual endothelin (ET)-receptor antagonist tezosentan.METHODS: Measurements were taken in 18 anaesthetized pigs with a mean ± SEM weigh
PMID 22682645

Platelet-derived growth factor (PDGF) induces pulmonary vascular remodeling through 15-LO/15-HETE pathway under hypoxic condition.

Zhang L, Ma J, Shen T, Wang S, Ma C, Liu Y, Ran Y, Wang L, Liu L, Zhu D.SourceDepartment of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University, Daqing, China.
Cellular signalling.Cell Signal.2012 Oct;24(10):1931-9. Epub 2012 Jun 23.
15-lipoxygenase (15-LO) is known to play an important role in chronic pulmonary hypertension. Accumulating evidence for its down-stream participants in the vasoconstriction and remodeling processes of pulmonary arteries, while how hypoxia regulates 15-LO/15-hydroxyeicosatetraenoic acid (15-HETE) to
PMID 22735810