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全脑缺血、前列环素缺乏与治疗可能性

Complete cerebral ischemia, prostacyclin deficiency, and therapeutic possibilities.

作者信息

Pluta R

机构信息

Department of Neuropathology, Medical Research Centre, Polish Academy of Sciences, Warsaw.

出版信息

Acta Neurochir Suppl (Wien). 1994;60:303-6. doi: 10.1007/978-3-7091-9334-1_81.

Abstract

This report summarizes the results of our studies on the effects of prostacyclin (PGI2) on the outcome of global cerebral ischemia (GCI). GCI was produced for 15 and 20 min. In vivo dialysis of the hippocampus was used to determine the changes in extracellular concentrations of calcium (Ca/2e) and blood-brain barrier (BBB) permeability. Moreover, EEG and general physiological parameters were recorded. This was combined with morphological observations. PGI2 was infused continuously i.v. at a rate of 2 micrograms/kg/min. Rabbits with untreated GCI served as reference. Treatment with PGI2 significantly enhanced EEG recovery and normalization during recirculation, and reduced both the decrease in Ca+2e, and the BBB leakage. The number of ischemic neurons in the PGI2-treated rabbits was significantly lower than in the non-treated ones. PGI2 reduced brain edema. These data suggest that PGI2 may protect against postischemic brain damage, in part by inhibiting excessive calcium influx to neurons and in part by tightening of BBB.

摘要

本报告总结了我们关于前列环素(PGI2)对全脑缺血(GCI)结局影响的研究结果。全脑缺血持续15分钟和20分钟。采用海马体内透析法测定细胞外钙浓度(Ca²⁺e)的变化以及血脑屏障(BBB)的通透性。此外,记录脑电图(EEG)和一般生理参数,并结合形态学观察。以2微克/千克/分钟的速率持续静脉输注PGI2。未治疗的全脑缺血兔作为对照。PGI2治疗显著促进了再灌注期间脑电图的恢复和正常化,并减少了Ca²⁺e的降低以及血脑屏障的渗漏。接受PGI2治疗的兔中缺血神经元的数量显著低于未治疗的兔。PGI2减轻了脑水肿。这些数据表明,PGI2可能通过部分抑制过多钙流入神经元以及部分通过收紧血脑屏障来预防缺血后脑损伤。

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