Wiśniewski H M, Maślińska D
New York State Institute for Basic Research in Developmental Disabilities, Department of Pathological Neurobiology, Staten Island, NY, USA.
Folia Neuropathol. 1996;34(2):65-71.
Brain of twelve, 44-78 years old non-demented patients affected by total ischemia after cardiac arrest, were used in the study. All of them were resuscitated within a few minutes after cardiac arrest and they survived for 3 to 36 days afterward. In all cases, after cardiac arrest, beta PP overexpression was found by immunocytochemical methods in many cortical and subcortical neurons as well as in ependymal and choroid plexus cells. This overexpression of beta PP, was concomitant with formation of many A beta nonfibrillar (thioflavine-negative) plaques in the neuropil. Because of a break in the blood-brain barrier around many vessels, weakly A beta-immunoreactive material was also found. The data presented provided strong evidence that the total brain ischemia resulting from cardiac arrest is a risk factor for beta-amyloidosis.
该研究使用了12名年龄在44至78岁之间、心脏骤停后发生全脑缺血的非痴呆患者的大脑。他们均在心脏骤停后几分钟内被复苏，并在之后存活了3至36天。在所有病例中，心脏骤停后，通过免疫细胞化学方法在许多皮质和皮质下神经元以及室管膜和脉络丛细胞中发现了β淀粉样前体蛋白（beta PP）的过表达。βPP的这种过表达与神经毡中许多β淀粉样蛋白（Aβ）非纤维状（硫黄素阴性）斑块的形成同时出现。由于许多血管周围血脑屏障的破坏，还发现了弱阳性的Aβ免疫反应性物质。所呈现的数据提供了强有力的证据，表明心脏骤停导致的全脑缺血是β淀粉样变性的一个危险因素。
