Effect of erythrocyte heat treatment on pulmonary vascular resistance.

The effect of red blood cell deformability on the pulmonary vascular resistance was studied in isolated dog and rat lungs. Blood cells were incubated at 49 degrees C for 1 hr, to render them rigid. The resistance to blood flow in the lung was assessed either by calculating the pulmonary vascular resistance (PVR = arterial - venous pressure difference divided by flow rate) or by examining the vascular pressure-flow relationship for changes in slope and intercept. The resistance in the lung was first assessed during perfusion with normal blood and again during perfusion with rigid cells. The results showed that PVR in dog lungs increased by 15% during perfusion with heat-treated blood and that this increase in PVR was associated with a significant increase in the middle segment resistance (arterial-venous occlusion technique) and with an increase in critical closing pressure (pressure intercept of the pressure-flow curve). In contrast to the small effect in dog lungs, the PVR in rat lungs rose more than 400% during perfusion with heat-treated blood. The marked increase of PVR in rat lungs was prevented with papaverine (PVR increased only 58%), suggesting that vasoconstriction was a primary event in rat lungs. The rise in vascular resistance in rat lungs was further shown to be primarily due to the presence of rigid erythrocytes (RBC). The increase in PVR in the rat lungs was not due to mechanical obstruction of the vasculature but rather to constriction of arteries and veins (double occlusion technique). The conclusion from this study is that RBC deformability plays an important role in the pulmonary vasculature, primarily because of release of vasoactive substances and partially because of the potential mechanical obstruction of capillaries. These events are apparently species dependent and are attributed mostly to red blood cell deformability which decreases during heat treatment.