Effects of hypoxia and hypercapnia on capillary flow velocity in the rat cerebral cortex.

The velocity of red blood cells (RBC) in individual capillaries of the rat cerebral cortex was assessed using direct, intravital video microscopy under normal conditions and during systemic hypoxia or hypercapnia. The movement of RBC in capillaries within 50-microm depth of the parietal cortex was visualized with the aid of fluorescent labeling of RBC in a closed cranial window preparation in pentobarbital-anesthetized, artificially ventilated adult rats. Hypoxia was produced by lowering the concentration of oxygen in the inspired gas from 30 to 15% for 5 min. Hypercapnia was achieved by increasing the inspired CO2 concentration (FiCO2) from 0 to 5% and then to 10% for 5 min at each level. The mean arterial pressure was maintained constant during both maneuvers. Under control conditions, fast and heterogeneous RBC flow in multioriented, tortuous capillaries was observed. During hypoxia, RBC velocity increased from 0.61 +/- 0.06 to 0.82 +/- 0.10 mm/sec (35% change). During hypercapnia, RBC velocity increased from 0.73 +/- 0.05 to 1.07 +/- 0. 11 mm/sec (46% change) at 5% CO2 and to 1.19 +/- 0.11 mm/sec (63% change) at 10% CO2. Corresponding changes in regional blood flow as assessed by laser-Doppler flowmetry during hypercapnia were 69 +/- 7 and 128 +/- 21%, respectively. The RBC velocity increased in almost all capillaries during hypoxia and during moderate hypercapnia. However, a substantial number of capillaries showed no change or a small decrease in RBC velocity during severe hypercapnia. A significant negative correlation between the velocity change at 10% CO2 and the normocapnic resting velocity was found in a group of capillaries isolated by cluster analysis. These results suggest that the dominant component of cerebral hyperemic response to hypoxia and to moderate hypercapnia is an increase in capillary RBC flow velocity. A more complex change in the velocity distribution occurs during severe hypercapnia and results in increased homogeneity of RBC perfusion in the cerebrocortical capillary network.