DEDUCTION OF PULMONARY MICROVASCULAR HEMATOCRIT FROM INDICATOR DILUTION CURVES

We have developed a new model describing the relationship between plas ma and red cell tracers flowing through the lung. The model is the res ult of an analysis of the transport of radiolabeled plasma albumin bet ween two flowing phases and shows that differences between red cell an d plasma tracer curves are related to microvascular hematocrit. The mo del was tested in an isolated, blood-perfused dog lung preparation in which we injected Cr-51-labeled red cells and I-125-labeled plasma alb umin into the pulmonary artery. From the tracer concentration time cur ves at the venous outflow, we calculated h(r), the ratio of microvascu lar 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 arterio lar 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 ar e uniform and that all dispersion occurs in the microvasculature. A th eoretical analysis apportioning dispersion between large and small ves sels disclosed that the error associated with these assumptions is lik ely to be less than 15% of the measured h(r). We conclude from this st udy that the microvascular hematocrit model describes experimental pla sma and red cell curves. The results imply that h(r) can be readily de duced from tagged red cells and plasma and can be accounted for in cal culating permeability-surface area in diffusing tracer experiments.