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 (Po2). 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.