SLIGHTLY ALTERED PERMEABILITY SURFACE-AREA PRODUCTS IMPLY SOME CEREBRAL CAPILLARY RECRUITMENT DURING HYPERCAPNIA

To test the capillary recruitment hypothesis in brain, cerebral blood flow was raised markedly in rats by exposure to 8% CO2 (hypercapnia), and capillary permeability-surface area (PS) products were measured. L ocal cerebral blood flow (LCBF), volume of radiolabeled blood in paren chymal microvessels (also referred to as the blood space or V-b), plus the local capillary influx rate constants (K-1) and PS products of [C -14]antipyrine and 3-O-[C-14]methyl-D-glucose (3OMG) were estimated in 44 brain areas. Hypercapnia raised PaO2 to 140 mm Hg, elevated LCBF b y two- to threefold through out the brain, and increased V-b from 5 to 33% (mean = 22%) in 42 of 44 brain areas; hypercapnia did not, howeve r, alter microvessel hematocrit. With hypercapnia, the influx of antip yrine was increased by 40-65% in all brain areas, and the PS products of antipyrine were elevated from 0-35% (mean = 17%). The PS products o f antipyrine plus the parenchymal blood spaces suggest modest (< 30%) capillary recruitment in most brain areas as well as some microvessel dilation, mainly in forebrain gray matter and white matter areas. In c ontrast, hypercapnia did not appreciably alter K-1 nor PS of 3OMG; it slightly but not significantly raised the blood levels of glucose. In view of the blood space and antipyrine evidence for modest capillary r ecruitment and vasodilation, the lack of change in PS of 3OMG implies that glucose transporter activity was lowered by hypercapnia, an effec t similar to that reported for high-dose pentobarbital. Finally, the m icrovessel hematocrit and 3OMG data suggest that cerebral capillary pe rmeability (P) was not increased by hypercapnia. Overall, hypercapnia seems to increase LCBF mainly by raising the velocity of blood flow; c apillary recruitment and dilation appear to play relatively minor role s in this flow increase. (C) 1994 Academic Press, Inc.