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The hypertensive rat and predisposition to cerebral infarction.

S ince the 1930s, when animal models of focal ischemic stroke were first developed, there has been a great deal of variability in the degree of ischemia and histologic damage produced by occluding a major cerebral artery. This bedeviling interspecies and intraspecies variability has seriously hampered progress in experimental stroke research. It was therefore a welcome development when the spontaneously hypertensive rat (SHR) and its strokeprone relative (SHRSP) were shown to have much larger and less variable infarcts after middle cerebral artery (MCA) occlusion than most, if not all, other animal models of focal stroke." Not only could pathophysiological investigations and drug testing be conducted with greater statistical power and a reasonable number of inexpensive animals, but now the relation of hypertension to stroke could be directly studied as well. One potential drawback, however, was that the severity of ischemia was so great that otherwise useful therapies might prove ineffective in the SHR. That the hypertensive rat can differ from its normotensive counterpart in its sensitivity to drug therapy is evidenced in a study by Roussel et al reported in this issue. These authors demonstrated that the noncompetitive JV-methyl-D-aspartate antagonist MK-801 given 30 minutes before permanent MCA occlusion, results in a 32% infarct reduction 48 hours later in normotensive rats but not in SHR. The lack of efficacy in the SHR may be due to their single dose schedule or, as they suggest, inadequate power to exclude a 25% reduction in infarct volume. However, they rightly point out that it is generally more difficult to achieve pharmacological protection against focal ischemia in SHR than in normotensive rats. Since several laboratories have already shown definitively that MK-801 protects the focally ischemic brain,the effectiveness of MK-801 is not at issue, but the question arises as to why and how the presence of hypertension modifies the drug response by the focalry ischemic brain. It has long been thought that arterial hypertrophy induced by chronic hypertension infringes on the