Mechanism of Hypoxic Pulmonary Vasoconstriction
HPV is a locally mediated phenomenon. HPV may be observed in
isolated perfused lungs and experimental animals after autonomic nervous system blockade
or catecholamine depletion in vivo. The sympathetic nervous system may play a role
in augmenting the HPV response under some conditions, especially during hypoxemia.
HPV occurs when alveolar oxygen tension falls to less than 100 mm Hg in the normal
lung and is maximal when oxygen tension is approximately 30 mm Hg.[140]
[141]
HPV has been studied in humans with healthy
lungs.[142]
Unilateral graded or single-step hypoxia
(FIO2
= 0.05) produced similar reductions
in the perfusion of the hypoxic lung to approximately 30% of control. Mixed venous
oxygen tension may also influence HPV in the atelectatic lung because alveolar oxygen
tension approaches venous oxygen tension in the collapsed lung.[143]
[144]
Hypercapnia-induced acidosis increases PVR
in intact animals and isolated, perfused lungs. Acidosis-induced increases in PVR
are relatively small at normal alveolar oxygen tensions but are dramatically enhanced
during alveolar hypoxia. Local acidosis and increases in alveolar carbon dioxide
tension may augment HPV and may further improve arterial oxygenation in healthy lungs.
High carbon dioxide concentrations reduce NO levels,[145]
but whether this action is responsible for hypercarbia-induced improvements in ventilation
and perfusion remains unclear.[146]
[147]
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