J.Jpn. Surg. Soc.. 80(12): 1598-1601, 1979

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Report on the annual meeting

PATHOPHYSIOLOGICAL STUDY IN EXPERIMENTAL CEREBRAL INFARCTION

Difficulties in achieving focal temporary cerebral ischemia in experimental animals have delayed the study of the prevention and treatment of cerebral infarction. We have succeeded in producing focal cerebral infarction by temporary occlusion of brain arteries. Infarction confined to the anterior portion of the thalamus was obtained by simultaneous occlusion of the 4 cerebral arteries: internal carotid, anterior cerebral, middle cerebral and posterior communicating arteries for 60 and 120 minutes. This experimental model in dogs is unique, since thalamic infarction can be produced with high frequency, and the dogs can be kept alive and managed for sufficient periods after temporary artery clipping. The thalamus EEG increased detection of experimental cerebral infarction, and was useful in predicting ischemic regions or infarction. The electrophysiological recordings in this animal model, with constant infarction in all dogs, showed diminution of the fast wave component and attenuation of voltage in the ipsilateral thalamic lead. Using this model, the relationship between EEG change and cerebral blood flow have been clarified. In studies on the restoration of blood flow in acute cerebral infarction, thalamic infarction was examined by rCBF and electron microscopical studies. With this model it is possible to investigate cerebral infarction not only from the pathophysiological viewpoint, but also from the viewpoint of prevention and treatment of cerebral infarction in man. Investigation on whether or not mannitol can prevent infarctions in ischemic brain tissue have been carried out utilizing the thalamic infarction model in dogs. Finally, the protective effect of mannitol in cerebral infarction was presented by means of various experimental studies.

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