Hypoxic vasoconstriction in blood and plasma perfused lungs.

Isolated lungs of pigs, cats and rats were perfused in situ with blood and with plasma at constant flow rate. The experiments were specifically designed to compare the intensity of the hypoxic pressor response (HPR) during blood and plasma perfusion. Ventilation of the lungs with 6.0% O2 during perfusion with blood, elevated the inflow pressure (Pa) from 18.9 +/- 1.5 to 35.8 +/- 2.0 mm Hg in pig lungs, from 12.9 +/- 0.5 to 17.9 +/- 1.1 mm Hg in rat lungs, and from 12.6 +/- 0.8 to 19.2 +/- 1.5 mm Hg in cat lungs. In comparison during perfusion of the lungs with plasma, the HPR was larger in pig lungs (Pa increased from 16.9 +/- 2.0 to 42.3 +/- 2.7 mm Hg), smaller in rat lungs (Pa increased from 10.2 +/- 0.9 to 11.4 +/- 1.2 mm Hg), and also smaller in cat lung (Pa increased from 9.9 +/- 1.2 to 11.9 +/- 1.2 mm Hg). The site of HPR in blood perfused cat lobes was primarily in the middle segment (arterial and venous technique) and remained in the middle segment (although blunted) during plasma perfusion. The vascular pressure-flow relationship in pig lungs showed that during blood perfusion, both the slope and intercept rose during hypoxia; these changes were similar but greater during plasma perfusion. Measurement of thromboxane A2 and prostacyclin in the lung effluent revealed no relation to intensity of the HPR or to the difference in the HPR in blood and plasma perfused lungs. Thus the absence of red blood cells (RBCs) may have been responsible for the difference in the HPR during blood and plasma perfusion; in rats and cats, RBCs appear to be essential for the full expression of the HPR, in contrast, the HPR in pigs does not require the presence of the RBCs. Possible explanations for these differences are suggested.