N-acetylcysteine prevents vasospasm after subarachnoid hemorrhage

Güney, Önder; Erdi, Fatih; Esen, Hasan; Kiyici, Aysel; Kocaoğullar, Yalçın

doi:10.1016/j.surneu.2009.06.003

Cited by 19 publications

(11 citation statements)

References 36 publications

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“…Concordantly, antioxidants have been shown to attenuate arterial narrowing in experimental SAH produced by autologous blood injection [50, 51]. There have been several mechanisms proposed to explain how ROS may contribute to cerebral vasospasm after SAH.…”

Section: Hbo and Mechanisms Of Prolonged Vasoconstrictionmentioning

confidence: 99%

Hyperbaric Oxygen for Cerebral Vasospasm and Brain Injury Following Subarachnoid Hemorrhage

Ostrowski

Zhang

2011

Transl. Stroke Res.

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The impact of acute brain injury and delayed neurological deficits due to cerebral vasospasm (CVS) are major determinants of outcomes after subarachnoid hemorrhage (SAH). Although hyperbaric oxygen (HBO) had been used to treat patients with SAH, the supporting evidence and underlying mechanisms have not been systematically reviewed. In the present paper, the overview of studies of HBO for cerebral vasospasm is followed by a discussion of HBO molecular mechanisms involved in the protection against SAH-induced brain injury and even, as hypothesized, in attenuating vascular spasm alone. Faced with the paucity of information as to what degree HBO is capable of antagonizing vasospasm after SAH, the authors postulate that the major beneficial effects of HBO in SAH include a reduction of acute brain injury and combating brain damage caused by CVS. Consequently, authors reviewed the effects of HBO on SAH-induced hypoxic signaling and other mechanisms of neurovascular injury. Moreover, authors hypothesize that HBO administered after SAH may “precondition” the brain against the detrimental sequelae of vasospasm. In conclusion, the existing evidence speaks in favor of administering HBO in both acute and delayed phase after SAH; however, further studies are needed to understand the underlying mechanisms and to establish the optimal regimen of treatment.

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Section: Hbo and Mechanisms Of Prolonged Vasoconstrictionmentioning

confidence: 99%

Hyperbaric Oxygen for Cerebral Vasospasm and Brain Injury Following Subarachnoid Hemorrhage

Ostrowski

Zhang

2011

Transl. Stroke Res.

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“…There were also drugs with anti-apoptotic effects, including proanthocyanidin, N-acetylcysteine, mexiletine, immunoglobulin, telmisartan, 2,2 0 -dipyridyl, recombinant human erythropoietin, human tissue kallikrein, alpha lipoic acid and so on. 6,[42][43][44][45][46][47][48][49][50] Signalling pathways participating in the anti-apoptotic effects include the Akt pathway, JAK2/STAT3 pathway, and others. Based on the above results, we could conclude that anti-apoptotic and anti-inammatory mechanisms play an important role in the attenuation of CVS aer SAH.…”

Section: Discussionmentioning

confidence: 99%

Ethyl pyruvate attenuates delayed experimental cerebral vasospasm following subarachnoid haemorrhage in rats: possible role of JNK pathway

et al. 2018

RSC Adv.

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“…The method for cerebral vasospasm induction was similar with our previous studies [4,5]. The head of the rabbit was extended in the prone position.…”

Section: Cerebral Vasospasm Modelmentioning

confidence: 97%

Alterations of the thioredoxin system during subarachnoid hemorrhage-induced cerebral vasospasm

et al. 2015

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N-acetylcysteine prevents vasospasm after subarachnoid hemorrhage

Cited by 19 publications

References 36 publications

Hyperbaric Oxygen for Cerebral Vasospasm and Brain Injury Following Subarachnoid Hemorrhage

Hyperbaric Oxygen for Cerebral Vasospasm and Brain Injury Following Subarachnoid Hemorrhage

Ethyl pyruvate attenuates delayed experimental cerebral vasospasm following subarachnoid haemorrhage in rats: possible role of JNK pathway

Alterations of the thioredoxin system during subarachnoid hemorrhage-induced cerebral vasospasm

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