Cerebral blood flow during dihydralazine-induced hypotension in hypertensive rats.

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Abstract
The cerebrovascular effects of graded, controlled dihydralazine-induced hypotension were studied in rats with renal hypertension (RHR) and spontaneous hypertension (SHR). Repeated measurements of cerebral blood flow (CBF) were made using the intraarterial 133Xe injection technique in anesthetized normocapnic animals. Dihydralazine was administered in single increasing i.v. doses (0.1-2 mg/kg), and CBF measured after each dose when a stable blood pressure was reached. From a resting level of 145 .+-. 7 mm Hg in RHR and 138 .+-. 11 mm Hg in SHR, mean arterial pressure (MAP) fell stepwise to a minimum of around 50 mm Hg. CBF was preserved during dihydralazine induced hypotension, and remained at the resting level of 79 .+-. 13 ml/100 g per min in RHR and 88 .+-. 16 ml/100 g per min in SHR. Following 2 h hypotension at the lowest pressure reached, the rats were sacrificed by perfusion fization and the brains processed for light microscopy. Evidence of regional ischemic brain damage was found in 4 of 11 animals: in 2 cases the damage appeared to be accentuated in the arterial boundary zones. Although the lower limit of CBF autoregulation in these rats is around 100 mm Hg during hemorrhagic hypotension, dihydralazine brought MAP to around 50 mm Hg without any concomitant fall in CBF. This was interpreted as being due to direct dilatation of cerebral resistance vessels. The combination of low pressure and direct dilatation may have resulted in uneven perfusion, thus accounting for the regional ischemic lesions.