PIAL MICROVASCULAR HEMODYNAMICS IN ANEMIA

Isovolemic hemodilution and subsequent anemia increase cerebral blood flow (CBF). We hypothesized that pial microvascular pressure also incr eases with hemodilution and that arteriolar diameter varies concurrent ly as a myogenic autoregulatory response. First- and second-order arte rioles (31-92 mum, n = 29) and large venules (65215 mum, n = 17) were studied in thiopental-anesthetized rats. Microvascular pressure was de termined using the servo-null technique, and vessel diameters were obt ained directly from a video monitoring system. We measured the increas e in CBF (radiolabeled microspheres) that accompanies hemodilution in a separate group of animals (n = 20). Hematocrit was reduced to 16-36% with homologous plasma (hemodilution group, n = 13) or held constant with homologous whole blood (control group, n = 4). In control animals , arteriolar and venular diameter varied +/-1-2 mum from baseline valu es, and microvascular pressure remained unchanged from baseline. In th e hemodilution group, CBF increased, but there was no systematic pial vasodilation. Furthermore, intraluminal pressure did not increase in p ial microvessels, suggesting that proximal vasodilation was negligible even at the lowest hematocrit studied. Vascular resistance fell propo rtionately in both large vessel and microvascular segments. We conclud e that experimental anemia does not produce alterations in microvascul ar pressure in rats, and the hyperemia accompanying hemodilution is la rgely viscosity mediated.