Induced response to hypercapnia in the two-compartment total cerebral blood volume: influence on brain vascular reserve and flow efficiency.

This study was undertaken to investigate the mechanisms of CBF increase as induced by hypercapnia. It was achieved in anesthetized rats by determining total cerebral blood volume (TCBV), parenchymal blood (CBV), plasma (CPV), erythrocyte (CEV) volumes and cerebral hematocrit (CHct) as well as CBF at about 40, 60, and 80 mm Hg PaCO2. TCBV was measured by a noninvasive blood dilution method using [99mTc]pertechnetate. CBV, CPV, and CEV were measured on isolated brain by 125I-serum albumin and 51Cr-erythrocytes. CBF was measured by both [131I/14C]iodoantipyrine and 57Co-microsphere extractions. The extraparenchymal blood volume (ECBV) was evaluated by subtracting CBV from TCBV. Under normocapnia, ECBV was 2.8 times larger than CBV. Under moderate hypercapnia, ECBV increased by 44%, CBV was not modified, and CBF increased by 52%. These results demonstrate that the main site of vasodilation is located in the extraparenchymal vasculature, which thus acts as a vascular reserve. By contrast, under severe hypercapnia, ECBV remained unchanged, whereas CBV then increased by 17%; CBF simultaneously showed an additional augmentation of either 52 or 309% when diffusible tracer or microspheres were used. This important increase in CBF cannot be explained either by capillary recruitment of closed capillaries or by active diameter lengthening of already open capillaries. The concomitant and great increase in capillary blood velocity was also shown to reduce cerebral flow efficiency, a situation consistent with a "luxury perfusion."