SUMMARY A pathological examination was performed on normotensive rats (NTR) and spontaneously hypertensive rats (SHR) following bilateral common carotid artery ligation. After ligation, diffuse and extensive cerebral infarcts in the carotid artery territory occurred frequently in SHR, while NTR occasionally had wellcircumscribed small infarcts.The posterior communicating arteries, which are the major anastomotic channels connecting the carotid and vertebrobasilar systems, did not show any anomalies and were well developed in SHR and NTR. Vascular changes secondary to hypertension, such as fibrinoid necrosis or thickening of the wall, were not observed in SHR. Because of the paucity of structural difference of the blood vessels, the more diffuse and extensive cerebral infarcts in SHR after carotid occlusion were attributed to the hemodynamic difference rather than the morphological difference between the two groups.The results of the present experiment suggest that hypertension per se, i.e., hemodynamic factors, may be operative for the development of cerebral infarction.Introduction SPONTANEOUSLY hypertensive rats (SHR) had a marked increase in lactate and lactate-pyruvate ratio of the brain following bilateral common carotid artery ligation and an early mortality, while a slight increase in metabolites and a lower mortality were observed in normotensive rats (NTR). 13 To elucidate the cause of the susceptibility of SHR to brain ischemia, a pathological study of the rat brain was performed.

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Effects of• Brain lactate, pyruvate, and arterial acid-base balance were measured in normotensive rats (NTR) and spontaneously hypertensive rats (SHR) 60 minutes after bilateral carotid artery ligation. Brain lactate and lactate-pyruvate ratios were significantly increased in both SHR and NTR following carotid occlusion, although lactate increase in the former was six and one-half times greater than in the latter. These findings suggest that bilateral carotid occlusion in SHR may cause more severe circulatory changes which result in increased anaerobic metabolism. Furthermore, higher brain lactate was concomitant with lower arterial carbon dioxide tension. The mechanism of spontaneous hyperventilation following cerebral ischemia was discussed. Additional Key Wordsspontaneous hyperventilation cerebral ischemia hypocapnia anaerobic metabolism

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