Hypertensive Response to Ischemic Stroke in the Normotensive Wistar Rat

Abstract

Background and Purpose— Over 80% of ischemic stroke patients show an abrupt increase in arterial blood pressure in the hours and days following ischemic stroke. Whether this poststroke hypertension is beneficial or harmful remains controversial and the underlying physiological basis is unclear. Methods— To investigate the dynamic cardiovascular response to stroke, adult Wistar rats (n=5–8 per group, 393±34 g) were instrumented with telemeters to blood pressure, intracranial pressure, renal sympathetic nerve activity, and brain tissue oxygen in the predicted penumbra (P o 2 ). After 2 weeks of recovery, cardiovascular signals were recorded for a 3-day baseline period, then ischemic stroke was induced via transient middle cerebral artery occlusion, or sham surgery. Cardiovascular signals were then recorded for a further 10 days, and the functional sensorimotor recovery assessed using the cylinder and sticky dot tests. Results— Baseline values of all variables were similar between groups. Compared to sham, in the 2 days following stroke middle cerebral artery occlusion produced an immediate, transient rise above baseline in mean blood pressure (21±3 versus 2±4 mm Hg; P <0.001), renal sympathetic nerve activity (54±11% versus 7±4%; P =0.006), and cerebral perfusion pressure (12±5 versus 1±4; P ≤0.001). Intracranial pressure increased more slowly, peaking 3 days after middle cerebral artery occlusion (14±6 versus −1±1 mm Hg; P <0.001). Treating with the antihypertensive agent nifedipine after stroke (1.5–0.75 mg/kg per hour SC) ameliorated poststroke hypertension (12±3 mm Hg on day 1; P =0.041), abolished the intracranial pressure increase (3±1; P <0.001) and reduced cerebral perfusion pressure (10±3 mm Hg; P =0.017). Preventing poststroke hypertension affected neither the recovery of sensorimotor function nor infarct size. Conclusions— These findings suggest that poststroke hypertension is immediate, temporally matched to an increase in sympathetic outflow, and elevates cerebral perfusion pressure for several days after stroke, which may enhance cerebral perfusion. Preventing poststroke hypertension does not appear to worsen prognosis after stroke in young, normotensive, and otherwise healthy rats. Visual Overview— An online visual overview is available for this article.