Mongolian Gerbilにおける一時的脳虚血後の脳障害に関する研究

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Studies on cerebral changes during recirculation after temporary ischemic insult were carried out in the Mongolian Gerbil which frequently shows anomaly of the circle of Willis. In this animal, occlusion of one side of the common carotid artery resulted in a large focal ischemia of the ipsilateral hemisphere in about 30%. Animals susceptive to ischemia could be selected by neurological symptoms observed soon after the carotid occlusion. Following temporary ischemia of 15, 30 mins., 1 hr., 3, 6 and 9 hrs., the cerebral circulation was resumed by releasing the carotid occlusion for different time lengths. A multidisciplinary and comparative approach which included a) histopathological study, b) morphological assessment on Blood-Brain Barrier (BBB) damage by Evans Blue for protein leakage and on edema, c) morphological evaluation of "no-reflow phenomenon" by injection of carbon black, d) contact autoradiographic assays on regional cerebral blood flow (rCBF) with ^<14>C-antipyrine was made. 1. The histopathological change is related to the duration of ischemia and recirculation. The ischemic lesion appears to progress (or mature) after re-establishment of the circulation. The rate of "maturation" is related to the intensity of the ischemic insult, i.e. the shorter the occlusion time, the later the onset of tissue damage. Neuronal recovery was suggested by time course histological study. 2. The incidence and time of appearance of the BBB lesions following recirculation is related directly to the duration of the ischemic insult. When the duration of ischemia was 30 mins., BBB damage was demonstrated in 50% of animals only at 20 hours after re-establishment of the circulation. On the other hand, BBB damage was always seen in all animals at one hour after recirculation, when the duration of ischemia was 6 hours. 3. Although the duration of "no-reflow phenomenon" relates to the length of ischemia, the phenomenon is transient and lasts about 10 minutes in animals suffering from temporary ischemia up to 6 hours. 4. Following cerebral ischemia for one hour, bi-phasic, reactive hyperemia which includes oligemic phase in between was observed. Later hyperemia associates una voce with the appearance of severe tissue damage, which progressed continuously following release of carotid occlusion. The breakdown of BBB accompanied both severe tissue damage and local increase of rCBF. The histopathological changes as well as BBB damage for protein tracer appears and progresses concurrently after recirculation. Increased rCBF (luxury perfusion) was always noted when the tissue damage was severe.

Mongolian Gerbilにおける一時的脳虚血後の脳障害に関する研究

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