Endogenous opioid system activity following temporary focal cerebral ischemia.

Endogenous opioid system activity following temporary focal cerebral ischemia.
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暂时性局灶性脑缺血后的内源性阿片类系统活性。

DOI:
10.1007/978-3-7091-9334-1_67
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发表时间:
1994
期刊:
Acta neurochirurgica. Supplementum
影响因子:
--
通讯作者:
Krumins,S
Krumins,S
中科院分区:
--
文献类型:
--
作者:
Ting,P;Xu,S;Krumins,S

文献摘要

被引文献

相似文献

用非选择性阿片受体拮抗剂[~ 3 H]二丙诺啡与μ、δ、κ受体的高选择性配体序贯置换,研究了猫大脑中动脉暂时闭塞(MCAO)时阿片受体(μ、δ、κ)浓度的变化。阈值脑缺血(rCBF <10 ml/100 g/min)后,释放MCAO后10 min,三种阿片受体亚型浓度均增加2 ~ 3倍。此外,56%的猫描绘了早期缺血后充血BBB开放,在1小时和3小时后释放闭塞,与脑水肿的显着后续进展。我们认为脑内阿片活性的增强可能与缺血后早期血脑屏障开放引起的神经元损伤有关。
We studied changes in opioid receptors (μ,δ, κ) concentrations during temporary middle cerebral artery occlusion (MCAO) in cats by sequential displacement of unselective opioid antagonist, [3H]diprenorphine with highly selective ligands for μ, δ and κ, subsites. Following threshold cerebral ischemia (rCBF < 10ml/100 g/min) there was a 2 to 3 fold increase in the 3 opioid receptor subtype concentrations at 10 min following the release of MCAO. Further, 56% of the cats depicted early postischemic hyperemia BBB opening, at 1 h and 3 h following the release of occlusion, with significant subsequent progression of brain edema. We believe that the enhanced brain opioid activity may be relevant to the neuronal damage caused by the early postischemic BBB opening.