Mechanism of increased sensitivity to cerebral ischemia following carotid artery occlusion in stroke-prone spontaneously hypertensive rats: importance of genetic factors.

Abstract

Neurological symptoms and cerebral metabolism following bilateral carotid artery occlusion (BCAO) were observed in stroke-prone spontaneously hypertensive rats (SHRSP), stroke-resistant SHR (SHRSR), normal Wistar-Kyoto rats (WKY) and the F1 and F2 hybrids between SHRSP and SHRSR or WKY. Systolic blood pressure recorded before BCAO was found to rank in the following order: SHRSP greater than F1 (SHRSP X SHRSR) greater than SHRSR greater than F1 (SHRSP X WKY) greater than WKY. The effect of BCAO in these rats tended to be proportional to the blood pressure. F1 (SHRSP X WKY) was more sensitive to brain ischemia than SHRSR. In addition, though none of the SHRSR (average blood pressure 155 mm Hg) developed acute stroke symptoms, many animals of the F2 generation, in which the blood pressure was equal to or lower than that of SHRSR, developed stroke symptoms. Lactate and ATP changes in the F2 generations did not correlate with the blood pressure. The results suggest that genetic factors may play an important role in susceptibility to brain ischemia in the stroke-prone rats.