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首页> 外文期刊>Neurosurgery >Molecular keys to the problems of cerebral vasospasm.
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Molecular keys to the problems of cerebral vasospasm.

机译：解决脑血管痉挛问题的分子关键。

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摘要

The mechanisms responsible for subarachnoid hemorrhage (SAH)-induced vasospasm are under intense investigation but remain incompletely understood. A consequence of SAH-induced vasospasm, cerebral infarction, produces a nonrecoverable ischemic tissue core surrounded by a potentially amenable penumbra. However, successful treatment has been inconsistent. In this review, we summarize the basic molecular biology of cerebrovascular regulation, describe recent developments in molecular biology to elucidate the mechanisms of SAH-induced vasospasm, and discuss the potential contribution of cerebral microcirculation regulation to the control of ischemia. Our understanding of the pathogenesis of SAH-induced vasospasm remains a major scientific challenge; however, molecular biological techniques are beginning to uncover the intracellular mechanisms involved in vascular regulation and its failure. Recent findings of microvascular regulatory mechanisms and their failure after SAH suggest a role in the development and size of the ischemia. Progress is being made in identifying the various components in the blood that cause SAH-induced vasospasm. Thus, our evolving understanding of the underlying molecular mechanism may provide the basis for improved treatment after SAH-induced vasospasm, especially at the level of the microcirculation.
机译：蛛网膜下腔出血（SAH）引起的血管痉挛的机制正在深入研究，但仍不完全清楚。 SAH诱发的血管痉挛的结果是脑梗塞，产生了不可恢复的局部缺血性组织核心，周围被潜在的半影包围。但是，成功的治疗一直是不一致的。在这篇综述中，我们总结了脑血管调节的基本分子生物学，描述了分子生物学的最新进展，以阐明SAH诱导的血管痉挛的机制，并讨论了脑微循环调节对缺血控制的潜在作用。我们对SAH诱导的血管痉挛的发病机理的理解仍然是一个重大的科学挑战;然而，分子生物学技术开始揭示涉及血管调节及其衰竭的细胞内机制。最近发现的微血管调节机制及其在SAH后的衰竭提示了缺血的发展和大小中的作用。在鉴定引起SAH诱导的血管痉挛的血液中各种成分方面正在取得进展。因此，我们对潜在分子机制的不断发展的理解可能为改善SAH诱发的血管痉挛后治疗提供基础，尤其是在微循环水平上。

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