Disease relevance of Vasospasm, Intracranial

• Rho and Rho-kinase have attracted increasing clinical interest as a result of emerging evidence for their roles in the pathogenesis of several cardiovascular disorders, including hypertension, coronary and cerebral vasospasm, atherosclerosis and diabetes, and are now considered important future therapeutic targets [1].
• Following successful clipping of the aneurysm she developed a left hemiplegia associated with focal cerebral vasospasm, which markedly improved when systemic blood pressure was raised with intravenous dopamine infusion [2].
• BACKGROUND AND PURPOSE: Tirilazad mesylate has been used in the attempt to prevent cerebral vasospasm after subarachnoid hemorrhage (SAH), although the actual targets of this agent in vivo have thus far been controversial [3].
• Intrathecal sodium nitroprusside improves cerebral blood flow and oxygenation in refractory cerebral vasospasm and ischemia in humans [4].
• CONCLUSIONS: In addition to the marked luminal narrowing of large arteries detected as severe angiographic vasospasm, microcirculatory changes detected as prolonged peripheral CCT affected cerebral ischemia during cerebral vasospasm [5].

High impact information on Vasospasm, Intracranial

• Heme oxygenase-1 gene induction as an intrinsic regulation against delayed cerebral vasospasm in rats [6].
• These findings suggest that NPY may be involved in the cerebral vasospasm which follows subarachnoid haemorrhage and in the maintenance of normal vascular tone [7].
• In this article, the effects of ET receptor antagonists and ECE-1 inhibitors on the prevention and reversal of SAH-induced cerebral vasospasm in preclinical animal models are reviewed [8].
• Endothelin and subarachnoid hemorrhage-induced cerebral vasospasm: pathogenesis and treatment [8].
• The findings suggest that cilostazol is an interesting candidate for future clinical trials of delayed cerebral vasospasm [9].

Chemical compound and disease context of Vasospasm, Intracranial

• Prevention of cerebrovascular spasms with nimodipine [10].
• Effect of selective inhibitor of thromboxane A2 synthetase on experimental cerebral vasospasm [11].
• Several reports have indicated that hemoglobin is a potent cerebral vasoconstrictor and therefore is considered to be an active principle in the genesis of cerebral vasospasm [12].
• These actions of haemolysate and 5-HT may be involved in the cerebral vasospasm observed following subarachnoid haemorrhage [13].
• Further investigation of the effects of nitroglycerin on cerebral vasospasm is warranted [14].

Biological context of Vasospasm, Intracranial

• Intracranial pressure monitoring during intraarterial papaverine infusion for cerebral vasospasm [15].
• Influence of blood volume on cerebrospinal fluid levels of arachidonic acid metabolites after subarachnoid hemorrhage: experimental study on the pathogenesis of cerebral vasospasm [16].
• Endothelin-1 (ET-1) is a 21 amino acid peptide that has been closely linked to cerebral vasospasm and more recently to oxidative stress after traumatic brain injury [17].
• Acutely, cocaine can induce cerebral vasoconstriction, cerebrovascular spasm, cerebral vasculitis and intracerebral haemorrhage [18].
• Somatosensory evoked potentials quantify clinical improvement of cerebral vasospasm after intravenous administration of nimodipine [19].

Anatomical context of Vasospasm, Intracranial

• Endothelin-1, a peptide exhibiting extremely potent cerebral vasoactive properties, is elevated in the cerebrospinal fluid after hemorrhagic stroke and implicated in cerebral vasospasm [20].
• Clentiazem protects against chronic cerebral vasospasm in rabbit basilar artery [21].
• The results suggest that due to its potent calcium-blocking activity on cerebral arteries, PN 200-110 might be of value for the prevention and treatment of cerebrovascular spasms following subarachnoid hemorrhage [22].
• These data support the association of dihydropyridine-sensitive Ca2+ channels with mitogenesis in vascular smooth muscle, and suggest an alternate mechanism of action for the beneficial effect of dihydropyridines in prophylaxis of cerebral vasospasm [23].
• This study was designed primarily to determine the efficacy of nimodipine given intracisternally in reversing the cerebral vasospasm produced in dogs by the injection of 4 ml of autogenous blood into the cisterna magna [24].

Gene context of Vasospasm, Intracranial

• Ro 61-1790, a new hydrosoluble endothelin antagonist: general pharmacology and effects on experimental cerebral vasospasm [25].
• Increased serum vWF, MMP-9, and VEGF levels could accurately predict the onset of cerebral vasospasm after SAH [26].
• CONCLUSION: The development of cerebral vasospasm after SAH was preceded by increases in serum vWF, MMP-9, and VEGF levels [26].
• Endothelin-1 (ET-1) induced cerebral vasospasm is inhibited by ETA receptors specific antagonist-BQ-123; this protects the neurons from ischemic damage [27].
• Therefore, the chemical nature of the cerebroarterial ECE activity must be further elucidated before rational development of efficient ECE inhibitors for treatment of cerebral vasospasm becomes possible [28].

Analytical, diagnostic and therapeutic context of Vasospasm, Intracranial

• Intraarterial infusion of papaverine in experimental cerebral vasospasm [29].
• METHODS: Thirty-eight patients enrolled as part of the North American trial of tirilazad in aneurysmal SAH underwent transluminal angioplasty for symptomatic cerebral vasospasm [30].
• Immunohistochemistry of leukotriene C4 in experimental cerebral vasospasm [31].
• In the long-term infusion experiment, the effect of a 14-day intravenous infusion of saline (control group, five animals) or L-arginine (10(-3) M; six animals) on the occurrence and degree of cerebral vasospasm was examined in monkeys [32].
• The authors summarize the effects of calcium entry blockers, review the pharmacology of nimodipine, and discuss both the known and possible interactions of oral nimodipine with physical and pharmacological interventions that neuroanesthesiologists employ for patients with cerebral vasospasm during craniotomy for aneurysm clipping [33].

References