Hudetz A G
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Microcirculation. 1997 Jun;4(2):233-52. doi: 10.3109/10739689709146787.
Capillary perfusion in the brain is characterized by an essentially continuous flow of erythrocytes and plasma in almost all capillaries. Rapid fluctuations and spatial heterogeneity or red blood cell (RBC) velocity (0.5-1.8 mm/s) within the capillary network are present. In addition, low-frequency (4-8 cpm) synchronous oscillations in RBC velocity in the capillary network emerge when perfusion to cerebral tissue is challenged. Despite the tortuous, three-dimensional architecture of microvessels, functional intercapillary anastomoses are absent. At rest, red cells travel through the capillary network in 100-300 ms along 150- to 500-micron-long paths. Physiological challenges elicit sizable changes in RBC velocity with a minor role for capillary recruitment, change in capillary diameter, or flow shunting. During acute hypoxia, RBC velocity increases in all capillaries; the corresponding response to hypereapnia is more complex and involves redistribution of capillary flow toward more homogeneous perfusion. The response of capillary flow to decreased perfusion pressure reflects autoregulation of cerebral blood flow but also involves intranetwork redistribution of RBC flow between two populations of capillaries, postulated as thoroughfare channels and exchange capillaries. Flow reserve may be provided by the thoroughfare channels and may help maintain flow velocity and capillary exchange and protect the microcirculation from perfusion failure. Isovolemic hemodilution increases RBC velocity three- to fourfold and increases RBC flux to a moderate degree with a relatively small decrease in capillary hematocrit, under normal and compromised arterial blood supply. In cerebral ischemia, leukocyte adhesion is enhanced and appears reversible when the ischemia is moderate but may be progressive when the injury is severe. The observed flow behavior suggests the presence of a physiological regulatory mechanism of cerebral capillary flow that may involve communication among various microvascular and parenchymal cells and utilize locally acting endothelial and parenchymal mediators such as endothelium-derived relaxing factor or nitric oxide.
脑内的毛细血管灌注特点是几乎所有毛细血管中红细胞和血浆基本持续流动。毛细血管网络内存在红细胞（RBC）速度的快速波动和空间异质性（0.5 - 1.8毫米/秒）。此外，当脑组织灌注受到挑战时，毛细血管网络中红细胞速度会出现低频（4 - 8次/分钟）同步振荡。尽管微血管具有曲折的三维结构，但不存在功能性毛细血管间吻合。静息时，红细胞沿150至500微米长的路径在100 - 300毫秒内穿过毛细血管网络。生理刺激会引起红细胞速度的显著变化，而毛细血管募集、毛细血管直径变化或血流分流起的作用较小。急性缺氧时，所有毛细血管中的红细胞速度都会增加；对高碳酸血症的相应反应更为复杂，涉及毛细血管血流重新分布，趋向于更均匀的灌注。毛细血管血流对灌注压降低的反应反映了脑血流的自身调节，但也涉及红细胞流在两类毛细血管（假定为直捷通路和交换毛细血管）之间的网络内重新分布。直捷通路可能提供血流储备，有助于维持血流速度和毛细血管交换，并保护微循环免受灌注衰竭。在正常和动脉血供受损的情况下，等容性血液稀释会使红细胞速度增加三到四倍，并在毛细血管血细胞比容相对小幅降低的情况下适度增加红细胞通量。在脑缺血时，白细胞黏附增强，在中度缺血时似乎是可逆的，但在严重损伤时可能会进展。观察到的血流行为表明存在脑毛细血管血流的生理调节机制，可能涉及各种微血管和实质细胞之间的通讯，并利用局部作用的内皮和实质介质，如内皮衍生舒张因子或一氧化氮。
