Blunted hypoxic pulmonary vasoconstriction by increased lung vascular pressures.
We tested the hypothesis that increased pressures within the lung vessels would inhibit hypoxic pulmonary vasoconstriction at all levels of alveolar CO2 tension. Selective hypoxia of the left lower lobe of the lung in open chested dogs caused the electromagnetically measured blood flow to the lobe to decrease 51 plus or minus 4 (SE) percent and its vascular resistance to increase 132 plus or minus 13 percent. Pressure and blood flow in the main pulmonary artery and left atrial pressure did not change during the hypoxic response. Stepwise increments in left artrial and pulmonary arterial pressures induced either by inflating a left atrial balloon or infusing dextran, progressively diminished the vasoconstrictive response to hypoxia. The response was usually abolished when left atrial pressure reached 25 mmHg. For all vascular pressures, hypoxic vasoconstriction was blunted by hypocapnic alkalosis but not enhanced by hypercapnia. We conclude that the redistribution of blood flow away from an hypoxic lobe of the lung to lobes with high Po2 was greatly attenuated by increasing pressures within lung vessels or by inducing respiratory alkalosis.
D000472:Alkalosis, Respiratory / Q000503:physiopathology; D000818:Animals; D016275:Atrial Function; D001794:Blood Pressure; D001810:Blood Volume; D003911:Dextrans / Q000494:pharmacology; D004285:Dogs; D005260:Female; D006935:Hypercapnia / Q000503:physiopathology; D000860:Hypoxia; D008297:Male; D011651:Pulmonary Artery / Q000502:physiology; D011652:Pulmonary Circulation; D012039:Regional Blood Flow; D012119:Respiration; D014655:Vascular Resistance
D003911:Dextrans