Abstract

CEREBRAL AUTOREGULATION, THE physiological regulatory mechanism that maintains a constant cerebral blood flow (CBF) over wide ranges of arterial blood pressure, was investigated in normotensive and spontaneously hypertensive rats by means of laser-Doppler flowmetry. Systemic arterial hypertension was produced at rates ranging from 0.02 mm Hg/second to 11 mm Hg/second by constant infusion of epinephrine and norepinephrine. Systemic arterial hypotension was produced at rates ranging from −0.03 mm Hg/second to −12 mm Hg/second, either by bleeding the animals into a reservoir or by compressing the abdomen. In those cases with a low rate of change in systemic arterial blood pressure (SABP), the measurements lasted for 5 ± 2 minutes, and in those with a high rate of change in SABP, measurements lasted for 40 ± 30 seconds. The purpose was to record the time of onset and course of autoregulation in the basal ganglia in response to slow or rapid changes in SABP. CBF in the basal gray matter remained at baseline values (i.e., autoregulation was functioning) if the rate of increase of SABP did not exceed a critical value (0.10 mm Hg/second in the normotensive rats; 0.35 mm Hg/second in the spontaneously hypertensive rats). When hypertension was produced at faster rates, CBF followed arterial blood pressure passively, and no autoregulatory response was observed for 2 ± 1 minutes. Hypotension did not change the baseline CBF when it was not produced at a rate faster than −0.4 mm Hg/second in normotensive rats and −0.15 mm Hg/second in spontaneously hypertensive rats. If the rate of decrease of SABP exceeded these values, CBF followed the changes in SABP passively, and no sign of autoregulation was observed for 2 ± 1 minutes. In conclusion, functioning of autoregulation was found to depend on the rate of change in SABP, even within the known autoregulatory pressure range (60–160 mm Hg). The autoregulatory limit, defined as the change in CBF in response to the rate of change in SABP, was significantly different in normotensive and spontaneously hypertensive rats, the latter having a higher value at the upper end and a smaller value at the lower end of autoregulation. Further elucidation of this aspect of autoregulation may have consequences in clinical settings such as hypotensive anesthesia and the hypertensive treatment of ischemia.

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