Reduced RBC versus plasma microvascular flow due to endotoxin.

The microvascular circuits traversed by red blood cells (RBCs) and plasma from first-order arterioles to first-order venules are complicated by variations in hemodynamic, rheologic, and dimensional parameters. Escherichia coli endotoxin causes microcirculatory derangements expected to alter RBC and plasma transport through these circuits. Wistar male rats were anesthetized with pentobarbital; the left cremaster muscle was spread over an optical port in a Krebs solution bath and administered endotoxin (6 mg/kg) iv over a 1-h period. The right femoral artery was cannulated for measurement of aortic pressure (Pm) and ia bolus injections of fluorescent DTAF-RBC and FITC-dextran. Fluorescence epi-illumination videomicroscopy and densitometry were used to obtained time-concentration curves (TCCs) in arterioles and venules. Control Pm averaged 106 +/- 8 mm Hg and progressively decreased during the 150-min observation period following endotoxin infusion. Arteriolar and venular diameters decreased approximately 50% during the 150-min observation period. At control DTAF-RBC flow velocity exceeded FITC-dextran velocities but by 90 min postendotoxin, even though both velocities were greatly reduced, plasma velocity, significantly exceeded red cell velocity. The control mean transit times for FITC-dextran exceeded the DTAF-RBC times in all vessels; 90 min postendotoxin the DTAF-RBC mean transit times significantly exceeded the FITC times and cell aggregates were in venous blood. The data suggest that cell aggregation, vasoconstriction and use of longer alternate parallel vascular circuits occur in endotoxin shock, restricting red cell flow. Plasma bypasses RBCs, flowing more rapidly than red cells in terminal shock.