DEDUCTION OF PULMONARY MICROVASCULAR HEMATOCRIT FROM INDICATOR DILUTION CURVES

We have developed a new model describing the relationship between plasma and red cell tracers flowing through the lung. The model is the result of an analysis of the transport of radiolabeled plasma albumin between two flowing phases and shows that differences between red cell and plasma tracer curves are related to microvascular hematocrit. The model was tested in an isolated, blood-perfused dog lung preparation in which we injected Cr-51-labeled red cells and I-125-labeled plasma albumin into the pulmonary artery. From the tracer concentration time curves at the venous outflow, we calculated h(r), the ratio of microvascular hematocrit to large-vessel hematocrit. In 18 baseline experiments, h(r) = 0.92 +/- 0.01 (mn +/- sem) at a blood flow rate of 10.7 +/- 0.3 ml s-1. We determined the effects of (a) glass bead embolization, (b) alloxan, and (c) lobe ligation on h(r). Embolization attenuated the separation between plasma and red cells (increased h(r)), probably as a consequence of passive vasodilation. Alloxan enhanced separation of plasma and red cells (decreased h(r)), possibly as a result of arteriolar vasoconstriction. Ligation of a fraction of the perfused tissue at constant flow did not cause significant change in hr in the remaining perfused tissue. The model assumes that large-vessel transit times are uniform and that all dispersion occurs in the microvasculature. A theoretical analysis apportioning dispersion between large and small vessels disclosed that the error associated with these assumptions is likely to be less than 15% of the measured h(r). We conclude from this study that the microvascular hematocrit model describes experimental plasma and red cell curves. The results imply that h(r) can be readily deduced from tagged red cells and plasma and can be accounted for in calculating permeability-surface area in diffusing tracer experiments.