27 research outputs found
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Limitations of diazoxide reversal of vasospasm
Diazoxide failed to safely relieve cerebral vasospasm by intracisternal injections in dogs and by intracarotid injections in monkeys despite in vitro documentation of arterial relaxation with this agent. Administration of the drug frequently produced hypotension and, in the presence of vasospasm, was associated with a high mortality rate
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Reversal of experimental cerebral vasospasm by intravenous nitroprusside therapy
Cerebral vasospasm was induced in dogs by intracisternal injection of blood. After angiographic demonstration of spasm, sodium nitroprusside was infused intravenously and its effect on the diameter of the basilar artery was studied angiographically. Ten experiments were performed within 90 minutes of the induction of spasm and nine experiments were performed 24 or 48 hours later. Significant dilatation of the basilar artery was achieved in all cases and it persisted for as long as the infusion of nitroprusside continued. The drug produced a modest degree of systemic hypotension. In six experiments it was possible to avoid hypotension by a simultaneous infusion of dopamine
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Effect of intravenous sodium nitroprusside on cerebral blood flow and intracranial pressure
Local cerebral blood flow was measured with the hydrogen clearance technique during intravenous infusion of nitroprusside in monkeys. Concentrations of the drug required to reduce the mean arterial blood pressure by less than 40% resulted in no significant change or only a slight increase in regional cerebral blood flow. Larger doses, however, produced a loss of cerebral autoregulation, thereby inducing a drop in cerebral blood flow. Intracranial pressure rose proportionately to the nitroprusside dose during the infusion