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The cardiovascular response to stroke in normal and hypertensive rats ‐ therapeutic or pathological?
Author(s) -
McBryde Fiona,
Thakkar Pratik,
McGregor Ailsa,
Paton Julian,
Barrett Carolyn
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1011.3
Subject(s) - medicine , penumbra , stroke (engine) , blood pressure , cardiology , pathological , anesthesia , ischemia , mechanical engineering , engineering
Over 80% of ischemic stroke patients show an abrupt increase in blood pressure (BP) in the hours and days following stroke; yet whether post‐stroke hypertension is beneficial or harmful remains controversial, and the underlying physiological basis is unclear. We propose that one reason for this uncertainty may be a difference in the cardiovascular response to stroke between normotensive subjects compared to those with pre‐existing hypertension. We hypothesized that hypertensive subjects may be less able to increase blood pressure after stroke. To investigate the dynamic cardiovascular response to stroke, Wistar (n=6, 393±34g) and spontaneously hypertensive (SH) rats (n=6, 377±29g) were placed under isofluorane anaesthesia (~3%), and instrumented with radio telemeters to record BP, ICP and brain tissue oxygen (p0 2 ) in the region of the future stroke penumbra. After a 1‐week recovery period, an ischemic stroke was induced via transient middle cerebral artery occlusion on Day 0, and recordings continued for 10 days after stroke. In both Wistar and SH rats, penumbra p0 2 decreased to less than half baseline levels during the 2‐hour occlusion period, but rapidly recovered to baseline levels within minutes of reperfusion. In Wistar rats, BP increased rapidly (+37±4 mmHg above baseline of 108±6 mmHg; p<0.01) within 48 hours of stroke, before returning to baseline levels by Day 4. The magnitude of the post‐stroke blood pressure increase was similar in SH rats, (+34±3 mmHg above a hypertensive baseline of 145±5 mmHg; p<0.01), however SH rats showed a more gradual return to baseline levels by Day 7 (p=0.0459). ICP reflects cerebral oedema, and was also increased after stroke in both groups, peaking at 16±5 mmHg (p=0.035) on Day 3 in Wistars, with a slightly but significantly smaller increase of 7±1 mmHg (p<0.01) in SH rats. Following re‐perfusion, penumbra p02 tended to remain at or above baseline levels for the full recording period in both rat groups. Contrary to our hypothesis, we found that ischemic stroke was associated with very similar patterns of elevated blood pressure and intracranial pressure, and steadily maintained penumbra tissue oxygen content, in both normotensive and hypertensive rats. That this post‐stroke surge in blood pressure persists even in subjects with pre‐existing hypertension, suggests that it may play a fundamental role in the defensive response to stroke. Future studies will determine the impact of preventing post‐stroke hypertension on the recovery from stroke, in particular the ability to maintain penumbra p02. Support or Funding Information Supported by the Health Research Council of New Zealand, the EU IRSES scheme and Royal Society Newton Fellowship Alumni funding.