Ventilation Perfusion Matching

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Hypoxic pulmonary vasoconstriction[edit]
  • 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 PaO2
  • Decreased pH also causes vasoconstriction and increased O2 sensitivity