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兔脑和小脑皮质压迫性缺血后的早期超微结构改变

The early ultrastructural alterations in the rabbit cerebral and cerebellar cortex after compression ischaemia.

作者信息

Kalimo H, Paljärvi L, Vapalahti M

出版信息

Neuropathol Appl Neurobiol. 1979 May-Jun;5(3):211-23. doi: 10.1111/j.1365-2990.1979.tb00620.x.

Abstract

The ultrastructural alterations in the rabbit cerebral and cerebellar cortex resulting from 30 minutes complete, permanent cerebral ischaemia were studied. The ischaemia was induced by raising the intracranial pressure (ICP) above the systolic arterial pressure (compression ischaemia). Immediately after releasing the ICP the brain was fixed by intravascular glutaraldehyde perfusion. Samples from the cerebral and cerebellar cortex were processed for electron microscopy. The ultrastructural changes were relatively minor; there was a generalised, slight intracellular oedema, most prominent in the subpial area; the nuclear chromatin was clumped, the endoplasmic reticulum and cisternae of the golgi apparatus became somewhat dilated, the inner matrix of the slightly swollen mitochondria showed increased electron lucency, and microtubules and ribosomes began to loose their compact structure. These changes, unaccompanied by any extensive volumetric change of any cellular compartment, agree well with the recently presented hypothesis of two different types of anoxic-ischaemic nerve cell injury. This cellular reaction to complete, permanent compression ischaemia represents the type of injury that is seen resulting from ischaemic insults during which no flow of fluid irrigates the ischaemically injured cells.

摘要

研究了兔脑和小脑皮质在30分钟完全性、永久性脑缺血后的超微结构改变。通过将颅内压(ICP)升高至收缩期动脉压以上(压迫性缺血)诱导缺血。释放颅内压后立即通过血管内戊二醛灌注固定大脑。取大脑和小脑皮质样本进行电子显微镜检查。超微结构变化相对较小;存在全身性、轻度细胞内水肿,在软膜下区域最为明显;核染色质聚集,内质网和高尔基器的池稍有扩张,轻度肿胀的线粒体内部基质电子透明度增加,微管和核糖体开始失去紧密结构。这些变化未伴随任何细胞成分的广泛体积变化,与最近提出的两种不同类型的缺氧缺血性神经细胞损伤假说非常吻合。这种对完全性、永久性压迫性缺血的细胞反应代表了在缺血性损伤期间没有液体流动灌溉缺血性损伤细胞时所见到的损伤类型。

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