| Literature DB >> 497053 |
S Tanaka, T Yoshimoto, T Sakamoto, H Seki, J Suzuki.
Abstract
Experimental brain infarction in model animals should most ideally be constant in the site of occurrence, be of severity that is controllable by the occlusion time of blood flow and, moreover, be reproducible at a high rate to desired extent and severity. However, among infarction models elaborated in animals so far, only thalamus infarction model in dogs which were reported by us previously have been proven to satisfy almost all of these requirements. In experiments with these model dogs we found that an extensive infarction can be produced at a high frequency in the involved hemisphere by a transient occlusion of blood flow at such intracranial levels as the internal carotid artery, the junction of the anterior cerebral artery and ophthalmic artery, the middle cerebral artery, the origin of the segment A2 of the anterior cerebral artery, and the junction of the posterior communicating artery and posterior cerebral artery. During about one hour following the releasing of the arteries approximately 2 hours occlusion, the development of severe brain edema resulted involving the whole hemisphere on the affected side invariably in all cases. This method for experimental production of brain infarction permits to control the degree of resultant brain edema by changing the duration of occlusion of blood flow, requires simple manipulations only and ensures production of a constant lesion. With these advantage it can be anticipated to prove of great benefit in the study of postischemic brain edema.Entities:
Mesh:
Year: 1979 PMID: 497053
Source DB: PubMed Journal: No To Shinkei ISSN: 0006-8969