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Increased cerebral infarction by cyclic flow reductions: studies in the guinea pig MCA thrombosis model

Department of Pharmacology, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan We have developed a photochemical model of thrombotic middle cerebral artery (MCA) occlusion in the guinea pig for investigating factors contributing to the development of cerebral infarction. In this mode...

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Published in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 1998-11, Vol.275 (5), p.1578-R1583
Main Authors: Kawano, Ken-Ichi, Ikeda, Yasuhiko, Kondo, Kazunao, Umemura, Kazuo
Format: Article
Language:English
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Summary:Department of Pharmacology, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan We have developed a photochemical model of thrombotic middle cerebral artery (MCA) occlusion in the guinea pig for investigating factors contributing to the development of cerebral infarction. In this model, cyclic flow reductions (CFRs) after recanalization of the MCA are a common observation and might contribute to the development of cerebral infarction. Therefore, we sought to measure the time course of recanalization of the guinea pig MCA after the artery had been occluded by a thrombus. Thrombotic occlusion of the MCA was induced by photochemical reaction between intravenously administered rose bengal and transluminal green light for 10, 15, 20, or 30 min. After the thrombotic occlusion of MCA and subsequent spontaneous thrombolysis, blood flow in the MCA gradually recovered to preocclusion level but with frequent CFRs. The recovery of MCA blood flow or duration of CFRs was dependent on the duration of photochemical reaction (extent of endothelial injury); thus, for a 30-min photochemical reaction, CFRs were still observed 24 h after photochemical reaction. In separate experiments, we also investigated the effect of permanent occlusion of the MCA, which was induced by electrocoagulation in the vessel on cerebral infarction. The infarct volume in the permanent occlusion model was smaller than the maximum value in the thrombotic occlusion model (12.5 vs. 17.4%; P  
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.1998.275.5.r1578