Nitroprusside-induced hypotension and cerebrovascular autoregulation in the anesthetized pig.

The influence of sodium nitroprusside (SNP) on cerebral blood flow and cerebrovascular autoregulation at doses that produced 36% +/- 3% (slight) and 52% +/- 4% (moderate) reductions of mean arterial blood pressure (MABP) was evaluated in mechanically ventilated fentanyl/N2O-anesthetized pigs. The blood flow of the frontal hemispheres was evaluated by sagittal sinus outflow, which was determined by an electromagnetic method. Integrity of cerebral autoregulation was evaluated by two formal tests: one hypertensive challenge with an angiotensin infusion (n = 12) and one hypotensive challenge with reduced venous return to the heart (blockade of the vena cava, n = 7). The tests were performed before, during, and after hypotension. Cerebral blood flow tended to increase during hypotension, but this change was not significant. Impaired autoregulation was seen in both tests during slight hypotension (MABP = 89 +/- 3 mm Hg) with an SNP infusion of 12 +/- 3 micrograms.kg-1.min-1. Cerebral autoregulation was completely abolished at both tests during moderate hypotension (MABP = 61 +/- 2 mm Hg with an SNP infusion of 38 +/- 7 micrograms.kg-1.min-1). Despite a posthypotensive increase in cerebral blood flow without rebound hypertension, the autoregulatory response to angiotensin-induced hypertension was restored within 15-25 min. The autoregulatory response to a decrease in MABP was impaired for more than an hour after discontinuation of the SNP infusion. No acidosis was observed. The authors conclude that during slight and moderate SNP-induced hypotension, there was a dose-dependent impairment of cerebral autoregulation. Further, the autoregulatory response to the hypotensive challenge after SNP hypotension was markedly delayed, whereas the response to hypertension was rapidly restored.