Spatial features of focal infarction after hydralazine treatment in stroke-prone spontaneously hypertensive rats.
Rapid occlusion of the middle cerebral artery above the rhinal fissure produces a large ischemic infarct in hypertensive rats, but this occlusion results in a minimal lesion in young normotensive rats. Our purpose was to attenuate rising blood pressure in young stroke-prone spontaneously hypertensive rats with hydralazine before the occlusion to determine if the gross infarct volume is smaller, and if it is, to determine whether length, width, depth, or surface area of the infarct changes, which could suggest a mechanism of protection.
Untreated rats (n = 6) and rats receiving hydralazine for 1.5 (n = 6) or 5 (n = 5) weeks were anesthetized, and the middle cerebral artery was rapidly occluded with a ligature. One day later the rats were killed and the brains were fixed in formalin. Fine-grain-release film that is sensitive to spectral properties of the infarct was used to photograph the tissue. Infarcted areas were traced on paper and then digitized for measurements and computations with a microcomputer.
Compared with untreated rats, tail systolic blood pressure (120 +/- 3 versus 138 +/- 4 mm Hg), infarct volume (61 +/- 4 versus 93 +/- 6 mm3), infarct surface area (39 +/- 1 versus 54 +/- 2 mm2), infarct width (3.8 +/- 0.1 versus 4.8 +/- 0.2 mm), and infarct length (6.0 +/- 0.3 versus 8.1 +/- 0.3 mm) were less in rats receiving hydralazine for 5 weeks (p < 0.05). No change was detected in infarct depth.
Treatment of young stroke-prone spontaneously hypertensive rats with hydralazine for 5 weeks before middle cerebral artery occlusion results in a smaller infarct. The narrower, shorter dimensions indicate increased protection against lateral enlargement of the infarct and the possibility that protection was due to increased collateral blood flow through modified blood vessels.
- Copyright © 1993 by American Heart Association