The pathophysiology and treatment of postischemic hypoperfusion after complete cerebral ischemia

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We studied the influences of no-reflow phenomenon and postischemic delayed hypoperfusion (PDH) on recovery of brain functions after transient complete cerebral ischemia using dogs. Cerebral ischemia was produced by clamping of ascending aorta with aorto-atrial bypass formation.No-reflow phenomenon: 100-200 ml of colloidal carbon was injected through aortic arch with 100 mmHg-pressure clamping ascending and descending aorta. The ratio of no-reflow was calculated by measuring the area of colloidal carbon staining on surfaces of coronary section of brain. The formation of no-reflow phenomenon was observed after 15 min of ischemia. Dilution of blood of the brain by physiological saline immediately after aortic clamping resulted in decrease in the no-reflow area. Three min after start of recirculation it was 10% of the surface of coronary section in the dilution group, but more than 70% in the control. After 5 min it was less than 10% in both groups. The brain functions were better in dilution group after 24-48 h. The efficacy of dilution was demonstrated also in histological examination of hippocampal CAl pyramidal cells.PDH: After 15 min of ischemia 20-40% decrease in blood flow in both cerebral cortex and brain stem was observed for 6-10 h following postischemic reactive hyperemia. The administration of Nicardipine 1 ug/kg/min corrected the PDH resulting in improvement of brain functions.Conclusion: We confirmed that 15 min of complete cerebral ischemia brings about both no-reflow phenomenon and PDH, that both contribute deterioration of brain functions, and that treatment of them results in the improvement of postischemic brain functions.