Keyeux A, Ochrymowicz-Bemelmans D, Charlier A A
Unit of Cardiovascular Physiology, Université Catholique de Louvain, School of Medicine, Brussels, Belgium.
J Cereb Blood Flow Metab. 1995 Nov;15(6):1121-31. doi: 10.1038/jcbfm.1995.139.
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."
本研究旨在探讨高碳酸血症诱导脑血流量（CBF）增加的机制。通过测定麻醉大鼠在约40、60和80mmHg动脉血二氧化碳分压（PaCO₂）时的全脑血容量（TCBV）、实质血容量（CBV）、血浆容量（CPV）、红细胞容量（CEV）和脑血细胞比容（CHct）以及CBF来实现。TCBV采用无创血液稀释法，使用[⁹⁹ᵐTc]高锝酸盐进行测量。CBV、CPV和CEV在离体脑上采用¹²⁵I - 血清白蛋白和⁵¹Cr - 红细胞进行测量。CBF采用[¹³¹I/¹⁴C]碘安替比林和⁵⁷Co - 微球提取法进行测量。通过从TCBV中减去CBV来评估脑外血容量（ECBV）。在正常碳酸血症下，ECBV比CBV大2.8倍。在中度高碳酸血症下，ECBV增加44%，CBV未改变，CBF增加52%。这些结果表明，血管舒张的主要部位位于脑外血管系统，因此其起到血管储备的作用。相比之下，在重度高碳酸血症下，ECBV保持不变，而CBV增加17%；当使用可扩散示踪剂或微球时，CBF同时额外增加52%或309%。CBF的这种显著增加既不能用闭合毛细血管的开放募集来解释，也不能用已开放毛细血管的主动管径延长来解释。同时还表明，毛细血管血流速度的大幅增加会降低脑血流效率，这种情况与“奢侈灌注”一致。
