Subarachnoid hemorrhage, from ruptured intracranial berry aneurysms (Hunt and Hess Grades I-V)

Nimodipine is a calcium channel antagonist for the improvement of neurological deficits due to cerebral artery spasm following subarachnoid hemorrhage.

Oral bioavailability: 5-15%, due to the extensive first-pass metabolism; Protein binding: >95%; It crosses the blood-brain barrier, but concentrations in CSF are lower than those in plasma. Metabolism: Extensively hepatic via the CYP450 3A4 enzyme；Terminal elimination half-life: approximately 9 hr

hypersensitivity to nimodipine; Intravenous doses of nimodipine > 1mcg/kg/min (0.06 mg/kg/hr) may cause significant decreases in blood pressure and should be used with caution.

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Enters breast milk/not recommended

Primary side effects are GI disturbance (diarrhea, nausea, and abdominal cramps). Reduction in blood pressure may also occur.

For oral use, 60 mg ORALLY on empty stomach every 4 hr for 21 consecutive days; therapy should begin within 96 hours of subarachnoid hemorrhage. Dosage should be reduced in patients with hepatic function impairment.

Nimodipine is sensitive to light. Nimodipine solution can bind to polyvinyl chloride (PVC) tubing; non-PVC infusion equipment should be used. Nimodipine solution must not be added to an infusion bag or bottle, or be mixed with other drugs.