A review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage

Dorsch, Nicholas W.C.

doi:10.1016/0967-5868(94)90080-9

Cited by 38 publications

(10 citation statements)

References 57 publications

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“…Delayed ischemic neurological deficit secondary to vasospasm represents the most frequent cause of disability and death. Without a proper therapy, cerebral vasospasm is associated with a 34% permanent disability and 30% mortality [7,25].…”

Section: Discussionmentioning

confidence: 99%

Milrinone as a Rescue Therapy for Symptomatic Refractory Cerebral Vasospasm in Aneurysmal Subarachnoid Hemorrhage

et al. 2008

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Section: Discussionmentioning

confidence: 99%

Milrinone as a Rescue Therapy for Symptomatic Refractory Cerebral Vasospasm in Aneurysmal Subarachnoid Hemorrhage

et al. 2008

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“…Subarachnoid haemorrhage (SAH) most commonly follows the rupture of an aneurysm of the cerebral arteries 1 . Cerebral vasospasm is one of the most critical complications that contributes to the high morbidity and mortality associated with SAH 2,3 . Many substances have been involved in the development of cerebral vasospasm following SAH, but the complex mechanism of this arterial narrowing is not yet fully understood 1,4 .…”

Section: Introductionmentioning

confidence: 99%

Participation of Vasopressin in the Development of Cerebral Vasospasm in a Rat Model of Subarachnoid Haemorrhage

Trandafir

Nishihashi

Wang

et al. 2004

Clin Exp Pharma Physio

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1. Previous studies have suggested the involvement of arginine vasopressin (AVP) and inflammation in the development of cerebral vasospasm after subarachnoid haemorrhage (SAH). The aim of the present study was to clarify the role of AVP in the arterial narrowing following cerebral haemorrhage by examining the effect of SR 49059 (a V(1) receptor antagonist) on the diameter of rat basilar artery exposed to SAH. The effect of the 5-lipoxygenase inhibitor ZM 230487 on AVP-induced contraction of rat basilar arteries was also investigated. 2. After 1 h and 2 days from SAH induction, brains were removed and pictures of the basilar arteries were taken. The external diameter of the basilar artery was measured in the presence and absence of SR 49059 (1 mg/kg, i.v.). For in vitro experiments, the basilar arteries isolated from control and SAH rats (at 1 h and at 2 days from SAH induction) were cut into spiral preparations and the AVP (0.3 nmol/L)-induced contraction in the presence of ZM 230487 was investigated. Each group analysed (i.e. control, SAH 1 h and SAH 2 days) consisted of eight rats. 3. The diameter of rat basilar arteries decreased by 43 and 25% at 1 h and 2 days from SAH induction, respectively, compared with control. The administration of SR 49059 significantly reduced cerebral vasospasm. After SAH induction, the diameter of the basilar artery in SR 49059-treated groups decreased by only 22% (at 1 h) and by 3% (at 2 days) compared with the control group (P < 0.01). In basilar arterial strips, ZM 230487 attenuated the vasopressin-induced contraction in both control and SAH groups. However, SAH groups showed a significant resistance of the AVP-induced contraction in the presence of ZM 230487 compared with control (P < 0.05). 4. The results suggest that the cerebral vasospasm in SAH rats is due, at least in part, to endogenous AVP and may involve an increase in the activity of 5-lipoxygenase. SR 49059 may represent a potential therapeutic strategy for the treatment of cerebral vasospasm.

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“…azem, 79 or other calcium antagonists 24,33,75,76 were excluded. Eligibility for inclusion was based solely on trial methodology, without consideration of trial size or results.…”

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confidence: 99%

Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis

Barker¹,

Ogilvy²

1996

Journal of Neurosurgery

314

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The authors report findings from a metaanalysis of all published randomized trials of prophylactic nimodipine used in patients who have experienced subarachnoid hemorrhage (SAH). Seven trials were included with a total of 1202 patients suitable for evaluation. Eight outcome measures were examined, including good versus other outcome, good or fair outcome versus other outcome, overall mortality, deficit and/or death attributed to vasospasm, infarction rate as judged by computerized tomography (CT), and deficit and/or death from rebleeding. Nimodipine improved outcome according to all measures examined. The odds of good and of good plus fair outcomes were improved by ratios of 1.86:1 and 1.67:1, respectively, for nimodipine versus control(p<0.005 for both measures). The odds of deficit and/or mortality attributed to vasospasm and CT-assessed infarction rate were reduced by ratios of 0.46:1 to 0.58:1 in the nimodipine group (p<0.008 for all measures). Overall mortality was slightly reduced in the nimodipine group, but the trend was not statistically significant. The rebleeding rate was not increased by nimodipine. A metaregression yielded findings indicating that the treatment effect of nimodipine in individual trials was positively correlated with the severity of SAH in enrolled patients. Although the majority of individual trials examined did not have statistically significant results at the p<0.01 level according to most outcome measures, the metaanalyses confirmed the significant efficacy of prophylactic nimodipine in improving outcome after SAH under the conditions used in these trials.

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A review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage

Cited by 38 publications

References 57 publications

Milrinone as a Rescue Therapy for Symptomatic Refractory Cerebral Vasospasm in Aneurysmal Subarachnoid Hemorrhage

Milrinone as a Rescue Therapy for Symptomatic Refractory Cerebral Vasospasm in Aneurysmal Subarachnoid Hemorrhage

Participation of Vasopressin in the Development of Cerebral Vasospasm in a Rat Model of Subarachnoid Haemorrhage

Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis

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