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THE VENULAR NETWORK OF SKELETAL MUSCLE AND MICROCIRCULATORY HOMEOSTASIS.HOUSE, STEVEN DONALD. January 1983 (has links)
It has been deduced from indirect evidence that significant adjustments of vascular resistance take place in the venous network when blood flow changes in a organ. In the following experiments, we attempted to test the hypotheses that changes in postcapillary resistance in skeletal muscle may be due to changes in venous diameter, changes in the number of venules with blood flow, and/or changes in the apparent viscosity of blood in venules. The hypotheses were tested by observing the response of cat sartorius muscle venules (7-200 μm diameter) during arterial pressure reduction and muscle contraction. There was no observable change in venular diameter during any of the above perturbations. There was a significant decrease in the already low normalized velocity of blood in venules from a mean of 13 sec⁻¹ under control conditions to 5 sec⁻¹ during arterial pressure reduction to 20 mm Hg. At very low pressures, the number of venules with blood flow decreased. Combining our findings with Lipowsky's (1975) in vivo viscometry data, it was predicted that resistance in venules would increase 100% as a result of increases in blood viscosity when blood flow was reduced 60%. During post-contraction hyperemia the normalized velocity of blood in venules increased from 16 sec⁻¹ to 38 sec⁻¹ and the number of venules with blood flow increased a modest amount. Combining our observations with Lipowsky's data, we predict that venular resistance would fall 54% when blood flow increased 250% If shear rate changes cause substantial changes in blood viscosity in venules as suggested by the findings cited above, hydrostatic pressure in the small venules should tend to remain relatively constant as flow is altered. To determine whether this is the case, pressures of venules were measured using the servo-null technique during arterial pressure reduction. Pressures in the larger venules were a linear function of blood pressure and blood flow with an intercept not significantly different from the systemic venous pressure. Pressures in the smallest venules studied (24 μm), however, were somewhat insensitive to alterations in blood pressure (intercept of 10.4 mm Hg) and blood flow (intercept of 13.2 mm Hg). The stability of pressure in 40 venules supports the hypothesis that variable blood viscosity maintains the pressure drop in the venous network and the capillary hydrostatic pressure somewhat constant during changes in blood flow.
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