Effect of diltiazem on experimental chronic cerebral vasospasm in the monkey.

@article{Frazee1985EffectOD,
  title={Effect of diltiazem on experimental chronic cerebral vasospasm in the monkey.},
  author={John G. Frazee and Jane Bevan and Rosemary D. Bevan and K R Jones},
  journal={Journal of neurosurgery},
  year={1985},
  volume={62 6},
  pages={
          912-7
        }
}
The influence of diltiazem on chronic cerebral vasospasm was studied following subarachnoid hemorrhage (SAH) in a primate model. The model mimics the human experience including the production of neurological deficits. Six monkeys were pretreated with diltiazem (25 mg/kg twice daily) for 2 days prior to surgical production of an SAH and for 5 days after the hemorrhage. This group was compared with six untreated monkeys that also sustained an SAH. The mean diameter of cerebral arteries measured… 
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26 Citations
Background Citations
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Methods Citations
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26 Citations

Citation Type

Citation Type

Diltiazem protects against functional changes in chronic cerebrovasospasm in monkeys.
Diltiazem given 48 hours before experimental subarachnoid hemorrhage protects the cerebral vasculature of monkeys against the widespread cerebrovascular spasm seen on angiography after 5-6 days and…
The effect of Iloprost on chronic cerebral vasospasm.
Clentiazem Protects Against Chronic Cerebral Vasospasm in Rabbit Basilar Artery
TLDR
The vascular damage associated with chronic cerebral vasospasm is related to calcium entry into the smooth muscle and endothelial cells, and possibly sympathetic nerve terminals, through calcium channels sensitive to clentiazem, which suggests that clent Diazem may be of value in the management of chronic cerebral Vasospasm.
Experimental chronic cerebrovascular spasm in the monkey: an assessment of the functional changes in the cerebral arteries and their protection by diltiazem.
Clentiazem reduces infarct size in rabbit middle cerebral artery occlusion.
TLDR
It is indicated that pretreatment with clentiazem offers cerebral protection and significantly reduces infarct volume as well as arterial wall damage beyond the occlusion and vascular smooth muscle contractility to histamine and relaxation to acetylcholine were significantly enhanced in vessels from treated rabbits.
Evaluation of the calcium-antagonist nimodipine for the prevention of vasospasm after aneurysmal subarachnoid haemorrhage
TLDR
Nimodipine given within four days after the SAH did not prevent vasospasm, but it significantly reduced the severity of the vasoconstriction, especially in high-risk patients, and protects the brain by increasing its tolerance to focal ischaemia.
Endoscopic technique: A new model of subarachnoid hemorrhage in rats
TLDR
A new model of SAH in rat is described that simulates the clinical phenomenon of ruptured intracranial aneurysm that also produces cerebral vasospasm and an endoscopic technique is developed that permits a direct vision of internal carotid artery and puncturing the artery to provoke SAH.
Functional arterial changes in chronic cerebrovasospasm in monkeys: an in vitro assessment of the contribution to arterial narrowing.
TLDR
It is proposed that 5-6 days after experimental subarachnoid hemorrhage in monkeys the change most responsible for persistent narrowing in the larger arteries is an increased rigidity of the vessel wall, which is probably caused by an inflammatory response.
Effect of AT877 on cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Results of a prospective placebo-controlled double-blind trial.
TLDR
This is the first report of a placebo-controlled double-blind trial that has demonstrated a significant reduction in angiographically revealed vasospasm by intravenous drug therapy.
A primate model for acute and late cerebral vasospasm: Angiographic findings
TLDR
The present study has shown that a reproducible biphasic vasospasm can be produced in the squirrel monkey and evaluated by repeated angiographic examinations.
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References

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TLDR
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TLDR
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TLDR
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TLDR
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