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Oxidative stress in subarachnoid haemorrhage: significance in acute brain injury and vasospasm.
Antioxidant therapy has provided neuroprotection and antispasmotic effects in experimental SAH and some therapies have demonstrated improved outcomes in clinical trials, laying a foundation for the use of antioxidants in the treatment of aneurismal SAH.
Protein Kinase C and Cerebral Vasospasm
  • I. Laher, J. Zhang
  • Biology, Medicine
    Journal of cerebral blood flow and metabolism…
  • 1 August 2001
Investigation of PKC in cerebral vasospasm helps explain increased arterial narrowing at the signal transduction level and alters current perceptions that the pathophysiology is caused by a combination of multiple receptor activation, hemoglobin toxicity, and damaged neurogenic control.
Dual effect of HBO on cerebral infarction in MCAO rats.
The results of this study suggest that applying HBO within 6 h of ischemia-reperfusion injury could benefit the patient but that applied HBO 12 h or more after injury could harm the patient.
Improved rat model for cerebral vasospasm studies
Here, an SAH was produced in rats using a 'double hemorrhage' method and following SAH, cerebral arteries showed pathological alterations, significant decreases in luminal perimeter, and increases in arterial wall thickness, over a 7-day post-SAH period.
Mechanism of endothelin-1-induced contraction in rabbit basilar artery.
It is demonstrated that MAPK may be involved in ET-1-induced contraction in rabbit basilar artery, which is downstream of PTK, Src, and Janus tyrosine kinase pathways but may not be downstream of phosphatidylinositol-3 Kinase pathways.
Upregulation of rho A and rho kinase messenger RNAs in the basilar artery of a rat model of subarachnoid hemorrhage.
OBJECT Rho A, a small guanosine triphosphate-binding protein, and rho kinases have been suggested to play an important role in the agonist-induced myofilament Ca++ sensitization and cytoskeletal
Vasospasm in traumatic brain injury.
Vigilant diagnostic surveillance and the prevention of secondary brain damage due to hypotension, hypoxia, and intracranial hypertension, may be more cost effective than attempting to minimize post-traumatic vasospasm.