Role of erythrocyte deformability in the acute hypoxic pressor response in the pulmonary vasculature.

To assess the importance of erythrocyte deformability in the pulmonary hypoxic pressor response (HPR) we examined whether alterations in erythrocyte deformability are related to the differences between the brisk HPR in rats vs the small HPR in hamsters, and between the HPR in low altitude rats vs high altitude rats (10 days in 10% oxygen). Deformability of the erythrocytes (RBC) was assessed by filtering equal volume of RBC suspension through Nucleopore filters (4.7 micron) using the same pressure head across the filter. The results show that during hypoxia, rat RBC become relatively nondeformable compared to hamster's RBC. This finding is consistent with a large HPR in rats but a small HPR in hamsters. Furthermore, the deformability of RBC from high altitude rats became unaffected by hypoxia and was associated with blunting in the HPR in isolated lungs from high altitude rats. The HPR in isolated lungs from low altitude rats was larger when they were perfused with blood from normal rats (= 86% increase in resistance) than when perfused with blood from high altitude rats (= 36% increase in resistance). This finding further supports the possible role of RBC deformability in HPR. Inconsistent with the importance of deformability, however, was the finding that high altitude rat lungs had a blunted HPR whether they were perfused with normal rat blood or high altitude rat blood. This may be due to restructuring of the pulmonary microvascular bed in the lung from high altitude rats. The results favor the idea that changes in erythrocyte deformability may be responsible for the difference between the HPR in low altitude rats and hamsters, and between the HPR in low and high altitude rats. We suggest that 'obstruction' of the capillaries by less deformable erythrocyte is another factor, besides smooth muscle contraction, responsible for the hypoxic pressor response in the pulmonary vasculature.