[Cerebral hemodynamics of post-ischemic delayed hypoperfusion (PDH) and the effects of nicardipine on the PDH].

Post-ischemic delayed cerebral hypoperfusion (PDH) is considered to be one of the most critical factors limiting brain recovery after cerebral ischemia. This experiment was designed to determine the characteristics of PDH and the effects of nicardipine on the PDH. Twenty-four dogs underwent complete cerebral ischemia for 15 min using aortic clamping method with aorto-atrial bypass formation, and cerebral cortical blood flow (c-CBF), brain stem blood flow (s-CBF), intracranial pressure (ICP), and perfusion pressure (PP) were measured for 48h. Eight dogs (1 microgram group) received nicardipine 1 microgram.kg-1.min-1 for 4 h following 10 micrograms bolus iv injection 5 min after declamping of aorta. Another 8 dogs (2 micrograms group) received 10 micrograms + 2 micrograms.kg-1.min-1 nicardipine in the same manner as in group 1. The remaining 8 served as controls. In the control group c-CBF and s-CBF decreased to 60% and 55% of pre-ischemic values, respectively 1 hour after declamping of aorta, and returned to pre-ischemic values 10 and 6 h later, respectively, in spite of no significant changes in PP's. 1 microgram group and 2 micrograms group maintained pre-ischemic CBF value throughout the experimental period, and the values were significantly higher than in control group between 1st and 5th h post-ischemia. There were no significant differences in ICP's among the 3 groups throughout the experiment. In conclusion, PDH appears to be a phenomenon always accompanying transient complete cerebral ischemia, and it is assumed to be caused by constriction of cerebral vessels. Nicardipine improved PDH, indicating that the underlying mechanism of PDH must be related to a disorder in Ca2+ metabolism of cerebral vessels after ischemia.