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.

Total cerebral blood volume calculated from a model of [99mTc]pertechnetate distribution in the head.

A method for calculation of the blood volume from the internal carotid and vertebral arteries to the internal jugular veins [total cerebral blood volume (TCBV)] was validated. This was achieved noninvasively in anesthetized rats from the time-activity curve recorded over the head after [99mTc]pertechnetate (Tc) intravenous bolus injection. Tc had the advantage over many other tracers in that it rapidly and evenly distributed in blood cells and plasma. Tc was found to behave in the head according to a two-parallel-compartment model containing a fast cerebral compartment and a slow extracerebral compartment. This model was mathematically described by a sum of two lagged normal density curves (LNDC) that fitted the head curve adequately. Responses of the LNDC parameters to flow and volume variations were first tested on a hydraulic setup. TCBV was calculated from the LNDC parameters of the cerebral fast compartment and the simultaneously determined cardiac output. In normocapnic rats, TCBV amounted to 49 +/- 7 (SD) microliters/g, distributed approximately two-thirds in the extra-parenchymal and one-third in the intraparenchymal cerebral vasculatures