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Whole organ studies suggest that venous resistance increases as blood flow falls and decreases when blood flow increases. In experiments on skeletal muscle we tested the hypotheses that these resistance changes may be due to changes in venous diameter, changes in the number of venules with blood flow, and/or changes in the shear rate of blood in venules. The hypotheses were tested by measuring diameter and red cell velocity in cat sartorius muscle venules (7-200 microns diam) during arterial pressure reduction and muscle contraction. There was no observable change in venular diameter and an insignificant change in the number of venules with blood flow during these perturbations. There was a significant decrease in the normalized velocity (bulk velocity/vessel diameter) of blood from a mean of 13 s-1 under control conditions to 5 s-1 during arterial pressure reduction to 20 mmHg. Combining these blood velocity data with published in vivo viscosity data, it is deduced that apparent blood viscosity in venules would increase 100% when blood flow was reduced 60%. During postcontraction hyperemia the normalized velocity of blood in venules increased from 16 to 38 s-1, suggesting that apparent blood viscosity in venules would fall 54%.

It has been suggested from whole organ studies that the viscosity of blood in skeletal muscle venules varies inversely with flow over physiological flow ranges. If this is the case, the hydrostatic pressure gradient in venules should change less than flow as flow is altered. To test this hypothesis, pressure in venules of cat sartorius muscle was measured during stepwise arterial pressure reduction to 20 mmHg. Large vein pressure remained constant at about 5 mmHg. Average pressures in the large venules (40-185 microns) ranged from 13.6 to 10.0 mmHg. The difference between pressure in these venules and large vein pressure fell in proportion to the reduction in blood pressure and blood flow. Pressures in the smallest venules studied (25 microns) averaged 19.7 +/- 6.2 (SD) mmHg. The pressure difference between the smallest venules and the large vein fell less than the arteriovenous pressure difference or blood flow when arterial pressure was reduced. During reactive hyperemia the pressure gradient between the smallest venules and the large vein rose proportionately less than blood flow. The stability of pressure in the smallest venules is consistent with the hypothesis that blood viscosity varies inversely with flow rate.

The arteriovenous distributions of volumetric flow (Q), microvessel hematocrit (Hctmicro), and estimates of red cell volumetric flux (QRBC) were obtained under control conditions in rat cremaster muscle. The results demonstrate a monotonic fall in the ratio of Hctmicro/Hctsystemic from 0.86 in 70-microns arterioles to 0.48 in capillaries followed by a subsequent rise to 0.79 in 98-microns venules. To assess the roles of Hctmicro and Q in red blood cell delivery following a period of reduced oxygen transport, tissue ischemia was produced by occluding the first order arteriole. During the occlusion, arteriolar and large venular hematocrits fell 15-30%, whereas small venular hematocrits increased 24%. After release of the occlusion, a reactive hyperemia ensued with Q, QRBC, and QHctmicro increasing significantly above control values in arterioles, capillaries, and venules. All Hctmicro returned to their control values within 10 s following resumption of flow. Based on the relationship between blood viscosity and Hctmicro, at low shear rate, these transient alterations in Hctmicro were estimated to have a profound effect on blood viscosity, and hence the resistance to blood flow. Such changes may affect recovery from an ischemic episode, although not adversely affecting the oxygen-carrying capacity of blood and convective transport of oxygen.

The purpose of this study was to examine changes in the microcirculation that might explain the rise in vascular resistance during hemorrhagic hypotension. Diameter and red blood cell velocity of microcirculatory vessels in exteriorized cat sartorius muscles were studied during 4 h of hemorrhagic hypotension at 60 mmHg. During hypotension, vascular resistance of the muscles rose approximately 70% while calculated volume flow in arterioles and venules fell to about the same degree. Average red blood cell velocity for all capillaries showed a comparable decline. Red blood cell flow stopped in approximately 60% of capillaries, but the extent of stoppage varied greatly among capillary fields. Arterioles larger than 45 microns constricted 9-29%, with the largest arterioles showing the greatest constriction. Arterioles smaller than 45 microns dilated 34-56%, with the smallest arterioles showing the greatest dilation. Venular diameter did not change with hemorrhage. The predominance of arteriolar dilation, especially in the later stages of hypotension, should lead to a fall in vascular resistance of the muscle. This effect may be offset by constriction of arteries outside the microcirculatory field observed and blockage of capillaries or venules by formed elements.