BLOOD-FLOW IN THE CEREBRAL CAPILLARY NETWORK - A REVIEW EMPHASIZING OBSERVATIONS WITH INTRAVITAL MICROSCOPY

Capillary perfusion in the brain is characterized by an essentially co ntinuous flow of erythrocytes and plasma in almost all capillaries. Ra pid fluctuations and spatial heterogeneity or red blood cell (RBC) vel ocity (0.5-1.8 mm/s) within the capillar; network are present. In addi tion, 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 mi crovessels, functional intercapillary anastomoses are absent. At rest, red cells travel through the capillary network in 100-300 ms along 15 0- to 500-mu m-long paths. Physiological challenges elicit sizable cha nges in RBC velocity with a minor role for capillary recruitment, chan ge in capillary diameter, or flow shunting. During acute hypoxia, RBC velocity increases in all capillaries; the corresponding response to h ypercapnia is more complex and involves redistribution of capillary fl ow toward more homogeneous perfusion. The response of capillary flow t o decreased perfusion pressure reflects autoregulation of cerebral blo od flow but also involves intranetwork redistribution of RBC flow betw een two populations of capillaries, postulated as thoroughfare channel s and exchange capillaries. Flow reserve may be provided by the thorou ghfare channels and may help maintain flow velocity and capillary exch ange and protect the microcirculation from perfusion failure. Isovolem ic hemodilution increases RBC velocity three- to fourfold and increase s RBC flux to a moderate degree with a relatively small decrease in ca pillary hematocrit, under normal and compromised arterial blood supply . In cerebral ischemia, leukocyte adhesion is enhanced and appears rev ersible 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 m ay involve communication among various microvascular and parenchymal c ells and utilize locally acting endothelial and parenchymal mediators such as endothelium-derived relaxing factor or nitric oxide.