Lewis, A. J.; Zingg, W.
November 1966
Angiology;Nov1966, Vol. 17 Issue 11, p800
Academic Journal
A method has been described of producing brain lesions in dogs with some regularity. Hypotension was induced by bleeding, together with administration of Arfonad, and cerebral ischemia by a period of head-up tilt during the induced hypotension. Ten of 30 animals survived 5 days or more, and the clinical and neuropathologic sequelae are described. Nine brains showed ischemic lesions of varying degree and distribution, only two being cortical Seven showed centrum ovale lesions only partly explicable on the basis of boundary zones. These lesions showed considerable variation in depth, for which the causes are thus far unclear. They may include the dual nature of the central circulation, closure of small arteries when their internal pressure drops below a critical point, and relative preservation of completely bloodless areas where organic acid formation is minimal. The cause of white matter lesions is considered to be endothelial damage due to local hypoxemia, which provides a mechanism through which arterial hypotension and the classic mechanism of venous stasis may either cause leukomalacia. The shortcomings of the experimental technique are discussed, together with criteria for a better method. A review of reported neuropathologic sequelae of open-heart surgery shows a great variety of lesions, of which hypotension is but one possible cause.


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