To ascertain whether infarction and noninfarction outcomes to rapid occlusion of the middle cerebral artery (MCA) are differentiated by alteration of the systolic blood pressure (BP), rats under the following conditions were tested: normal Wistar rats (NW) made acutely hypertensive with deoxycorticosterone acetate (DOCA)-salt, spontaneously hypertensive stroke-prone rats (SHRSP) receiving captopril antihypertensive medication for 7 weeks, and SHRSP with captopril withdrawn 2 weeks prior to the occlusion test. Eleven of 13 acutely DOCA-salt hypertensive NW were protected from infarction. Adequate collateral circulation was preserved in NW vessels initially formed under normotensive conditions but tested during acute DOCA-salt hypertension. Since all SHRSP tested had infarcts, SHRSP were more susceptible to infarction than NW made acutely DOCA-salt hypertensive. SHRSP with captopril medication withdrawn for 2 weeks had higher BP and larger infarcts than SHRSP maintained on the drug. Results suggest that the mechanism causing elevated BP or one secondary to it adversely alters the collateral supply in SHRSP. An increase in collateral vascular resistance initiated during anatomical development of the anastomoses very early in life may predispose SHRSP to infarct after rapid MCA occlusion later in life.
- Copyright © 1984 by American Heart Association