Reversal of cerebral arterial spasm by intrathecal administration of a calcium antagonist (nimodipine).
Specific antagonists to the influx of calcium, necessary for the excitation-contraction coupling process in arterial smooth muscle, are potentially useful in the treatment of cerebral vasospasm but systemic hypotension might limit their clinical applicability. We studied the effect of the calcium antagonist nimodipine (BAY e 9736) on cerebral arterial spasm, intraventricular pressure and blood pressure (BP), when administered into the cerebral ventricles of the dog. Cerebral vasospasm was produced by the injection of autologous blood into the cisterna magna. In a group of 8 dogs, 100 micrograms of nimodipine was injected into the lateral ventricle. The effect of the drug on the basilar artery was monitored angiographically. Nimodipine always relieved spasm, and often the relaxation surpassed the resting vessel diameter. In a control group, the injection of placebo did not relax the spastic arteries. Determinations using gas chromatography of nimodipine in CSF and blood demonstrated that a concentration of 1 microgram/ml in cisternal CSF was sufficient to reduce spasm while concomitant plasma concentrations of 0.004 micrograms/ml did not result in significant BP reduction.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000008:administration & dosage* / Q000627:therapeutic use; D004285:Dogs; D005260:Female; D007278:Injections, Spinal; D007427:Intracranial Pressure / Q000187:drug effects; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D009539:Nicotinic Acids / Q000008:administration & dosage* / Q000627:therapeutic use; D009553:Nimodipine; D013345:Subarachnoid Hemorrhage / Q000150:complications
D002121:Calcium Channel Blockers; D009539:Nicotinic Acids; D009553:Nimodipine