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首页> 外文期刊>Frontiers in bioscience: a journal and virtual library >PKC and Rho in vascular smooth muscle: activation by BOXes and SAH CSF.
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PKC and Rho in vascular smooth muscle: activation by BOXes and SAH CSF.

机译：血管平滑肌中的PKC和Rho：被BOXes和SAH CSF激活。

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摘要

Cerebral vasospasm (CV) remains a significant cause of delayed neurological deficit and ischemic damage after subarachnoid hemorrhage (SAH), despite intensive research effort. The current lack of an effective therapeutic approach is somewhat due to our lack of understanding regarding the mechanism by which this pathological constriction develops. Recent evidence implicates bilirubin oxidation products (BOXes) in the etiology of CV after SAH: BOXes are found in cerebrospinal fluid from SAH patients with symptomatic or angiographically visible vasospasm (CSFV) but not in CSF from SAH patients with no vasospasm (CSFC). We have previously published research suggesting that the etiology of CV comprises two components: a physiological stimulation to constrict and a pathological failure to relax. Both these components are elicited by CSFV, but not CSFC, and BOXes synthesized in the laboratory potentiate physiological constriction in arterial smooth muscle in vitro, and elicit contraction in pial arteries in vivo. In this paper, we will present our results concerning the action of BOXes on arterial smooth muscle constriction, compared with CSFV. We will also present evidence implicating temporal changes in PKC isoforms and Rho expression in both BOXes- and CSFV-elicited smooth muscle responses.
机译：尽管进行了大量的研究，但蛛网膜下腔出血（SAH）后脑血管痉挛（CV）仍然是延迟神经功能缺损和缺血性损伤的重要原因。当前缺乏有效的治疗方法是由于我们对这种病理性收缩发展的机理缺乏了解。最近的证据表明SAH后CV的病因涉及胆红素氧化产物（BOXes）：在有症状或血管造影可见的血管痉挛（CSFV）的SAH患者的脑脊液中发现BOXes，而在没有血管痉挛（CSFC）的SAH患者的CSF中没有发现BOX。我们以前发表过的研究表明，CV的病因包括两个部分：生理刺激收缩和病理性放松。这两种成分都是由CSFV引发的，而不是由CSFC引发的，而实验室合成的BOXs可以在体外增强动脉平滑肌的生理收缩，并在体内诱发动脉的收缩。在本文中，与CSFV相比，我们将介绍有关BOXes对动脉平滑肌收缩作用的结果。我们还将提供证据表明在BOXes和CSFV引起的平滑肌反应中PKC亚型和Rho表达随时间变化。

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