Survey of clinical experience with nimodipine in patients with subarachnoid hemorrhage.

The present studies show that nimodipine prevents and/or improves permanent ischemic neurological deficits in patients with subarachnoid hemorrhage. This was particularly marked in four double-blind, placebo-controlled studies in which statistically significant reductions in mortality and morbidity as consequence of cerebral vasospasm were found. The drug has been shown to increase cerebral blood flow, to reduce vasoconstriction, although not to fully prevent angiographic vasospasm, and to improve central conduction time.

Calcium agonists and antagonists of the dihydropyridine type: antinociceptive effects, interference with opiate-mu-receptor agonists and neuropharmacological actions in rodents.

The calcium antagonist dihydropyridine derivative nimodipine and its enantiomers BAY N 5247, BAY N 5248, as well as BAY R 4407 (calcium antagonist (+)-enantiomer of the calcium agonist dihydropyridine BAY K 8644) do not exert antinociceptive effects in the rat as measured by the vocalization test in doses up to 100 micrograms/kg IV, and in the mouse as measured by the hot plate test in oral doses up to 100 mg/kg. The calcium agonists BAY K 8644 and BAY R 5417 ((-)-enantiomer of BAY K 8644) are also ineffective in the rat vocalization test but BAY K 8644 increases reaction time in the hot plate test (mouse) dose-dependently (1-10 mg/kg PO). mu-receptor agonist (fentanyl) antinociceptive effects are potentiated by simultaneous IV administration of the calcium antagonists, the (-)-enantiomer of nimodipine BAY N 5248 being the most potent.

Blood pressure and heart rate during treatment with nimodipine in patients with subarachnoid hemorrhage.

Careful observation of blood pressure and heart rate in patients with subarachnoid hemorrhage during therapy with nimodipine showed that blood pressure decreases mainly in hypertensive patients during the first hours of therapy or when treatment is started immediately with 2 mg per hour instead of the recommended initial dose of 1 mg per hour. Predominantly mild or moderate reversible falls in blood pressure were reported as side effects in 21/421 patients (5%). Electrocardiographic abnormalities such as tachycardia, bradycardia, arrhythmia or extrasystoles were reported as side effects during treatment with nimodipine in 18 patients (4,3%).

Overview on pharmacokinetics of nimodipine in healthy volunteers and in patients with subarachnoid hemorrhage.

The pharmacokinetics of Nimodipine were studied in healthy volunteers and in patients with subarachnoid hemorrhage (SAH) following cerebral aneurysm rupture. Nimodipine was absorbed rapidly. After an oral dose of 120 mg an average maximal plasma concentration 106 micrograms/l was recorded 45 to 60 minutes later.