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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||1 (21/1)|
|State||Published - 1987|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)