Microvascular hematocrit and red cell flux in rat cremaster muscle

The arteriovenous distributions of volumetric flow (Q̇), microvessel hematocrit (Hct(micro)), and estimates of red cell volumetric flux (Q̇(RBC)) were obtained under control conditions in rat cremaster muscle. The results demonstrate a monotonic fall in the ratio of Hct(micro)/Hct(systemic) from 0.86 in 70-μm arterioles to 0.48 in capillaries followed by a subsequent rise in 0.79 and 98-μm venules. To assess the roles of Hct(micro) and Q̇ 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 Q̇, Q̇(RBC), and Q̇Hct(micro) increasing significantly above control values in arterioles, capillaries, and venules. All Hct(micro) returned to their control values within 10 s following resumption of flow. Based on the relationship between blood viscosity and Hct(micro), at low shear rate, these transient alterations in Hct(micro) 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.