Ventilation Perfusion Matching

Hypoxic pulmonary vasoconstriction

• Contraction of smooth muscles in small arterioles in hypoxic regions of lungs
• Important in directing blood flow away from poorly ventilated ares of the diseased lung in adults
• Mechanism of is this is unknown - but it occurs in isolated excised lung, and doesn't depend on nervous input
• Even excised pulmonary artery segments constrict when their environment is made hypoxic (even if there are good oxygen levels in the blood)
• Very non-linear stimulus-response curve for this constriction:

• If alveolar PO₂ is above 100mmHg, very little change in vascular resistance
• If alveolar PO₂ is below 70mmHg, marked vasoconstriction occurs
• At very low PO₂, local blood flow may be almost zero
• Similar chart to an oxygen dissociation curve

• Mechanism seems to be inhibition of voltage gated K⁺ channels causing membrane depolarisation causing calcium ion influx and smooth muscle contraction
• Endothelium-derived vasoactive substances:

• Nitric oxide - formed from L-arginine via catalysis by endothelial NO synthase (eNOS)
• Activates soluble guanylate cyclase causing synthesis of cyclic GMP, leading to smooth muscle relaxation
• NO synthase inhibitors cause vasoconstriction, and inhaled NO reduces hypoxic pulmonary vasoconstriction

• This is vital in utero - hypoxic pulmonary vasoconstriction maintains high PA pressure

• This diverts blood through the ductus arteriosus, with <15% perfusing lung
• At birth, gasping markedly decreases PA resistance by radial traction and increased P_aO2
• Decreased pH also causes vasoconstriction and increased O₂ sensitivity