2009 Volume 3 Issue 1 Pages 11-16
The effects of nitric oxide (NO) on microflow and capillary red blood cell (RBC) velocity of the cerebral cortex were examined in 5 urethane-anesthetized rats through an open cranial window. Changes in microflow were evaluated with hemodilution technique with in-house Matlab-domain software, KEIO-IS1, presented as a 2-D microflow-map. When FITC-labeled RBCs were injected into the femoral vein, they appeared in the microvasculature of the cerebral cortex including capillaries. Changes in RBC velocity and attendance in single capillaries were determined with a high-speed camera laser scanning confocal fluorescence microscope before, during and after NO administration. The velocity and number of RBCs in the ROI were calculated with KEIO-IS2. Nitroprusside (a NO donor) was administered topically on the exposed brain surface, additionally microinjected into the tissues in 3 rats, and further intravenously in 2 rats. We found that: 1) NO increased microflow markedly regardless of the routes of administration and when limited to the cases of topical application microflow increased by 182±22 % (mean ± SD) of control (P<0.01). 2) RBC velocity in capillaries remained broadly unchanged, whereas RBC number (attendance) decreased in all cases (P<0.05). We interpreted that NO induced an increase in microflow not through nutritional capillaries but via other pathways from artery to veins, e.g., thoroughfare channels. This finding suggests the presence of an independent velocity-impedance mechanism at the level of individual single capillaries in which excessive increase in capillary flow is somehow prevented. [MVRC 3(1): 11-16, 2009]
