Effect of hypoxia on erythrocyte deformability in different species.

The contribution of erythrocyte deformability to the pulmonary vascular resistance during hypoxia in different animal species has not been examined. We hypothesized that the increase in pulmonary vascular resistance during hypoxia was partially due to erythrocytes (RBC's) becoming less deformable during hypoxia, and therefore their transit in the capillaries becomes restricted. To test this, we measured an index of deformability of RBC's from six animal species (dog, pig, cat, rabbit, hamster, rat) during normoxic and hypoxic condition, and compared the changes in deformability with the pulmonary hypoxic pressor response (HPR) which has been reported in the same species. Deformability was indexed as the resistance that a Hemafil polycarbonate membrane (Nucleopore filter, 4.7 micron pores) offers to a 10% suspension of RBC's. The RBC suspension was either normoxic (PO2 = 150 torr) or hypoxic (PO2 = 50 torr). We found that hypoxia decreased RBC deformability; the largest decrease occurred in rat RBC's, a small but significant decrease was observed in the RBC's of cats, rabbits and hamsters, but no change was detected in RBC's of dogs or pigs. In general, such changes in deformability do not correlate well with the HPR in intact or in isolated lungs, for example the pig, had the largest HPR but the smallest change in RBC deformability. In some species, however, there was a positive correlation between RBC deformability and HPR, for example rats, rabbits and cats are usually better responders than dogs and hamsters, similarly the deformability of RBC's in rats, rabbits and cats were also more influenced by hypoxia than RBC's from dogs. The limiting factors in this relationship are the artificial conditions which were used to measure deformability and HPR, both may be different than in the intact conditions. Nevertheless the present data show that erythrocytes of some species can become less flexible during hypoxia, and hence may impede the transit in the capillaries. Therefore we propose that the hypoxic pressor response in the pulmonary vasculature may be partly due to smooth muscle contraction (vasoconstriction) and partly due to a decrease in erythrocyte deformability (capillary obstruction). Both components are likely to be species dependent.