Yamane K, Shima T, Okada Y, Csiba L, Uozumi T
Department of Neurosurgery, Chugoku Rousai Hospital, Kure, Japan.
Surg Neurol. 1994 Oct;42(4):352-7. doi: 10.1016/0090-3019(94)90409-x.
To investigate the mechanism of acute brain swelling after cerebral embolism in rats, the authors evaluated the regional changes in tissue pH, ATP, blood-brain barrier function, and water content. The deep cerebrum--thalamus, hypothalamus, and hippocampus--had alkaline change in tissue pH accompanied with the disruption of the blood-brain barrier, decrease of ATP, and increase of water content. The cortex and the caudate putamen, on the other hand, did not show edema though acidic change and ATP decrease were seen. These results suggest that an early vasogenic edema in the deep cerebrum is a main factor for evolving acute brain swelling in this embolization model of rats.
为研究大鼠脑栓塞后急性脑肿胀的机制，作者评估了组织pH值、三磷酸腺苷（ATP）、血脑屏障功能及含水量的局部变化。大脑深部——丘脑、下丘脑及海马体——组织pH值呈碱性变化，同时伴有血脑屏障破坏、ATP减少及含水量增加。另一方面，尽管皮质及尾状核壳核出现酸性变化及ATP减少，但未出现水肿。这些结果表明，在该大鼠栓塞模型中，大脑深部早期的血管源性水肿是急性脑肿胀进展的主要因素。
