Description: Nimodipine has been used as an accessory to improve the neurologic outcome following subarctic hemorrhage (SAH) from ruptured cranial aneurism. It acts as a calcium channel blocking agent. It goes into the brain and works by barricading the entrance of extracellular calcium in nerve cell. Being highly lipotropic, nimodipine has greater action on the intellectual vessels. Nimodipine is isopropyl 2–methoxyethyl 1, 4–dihydro–2, 6–dimethyl–4– (m-nitrophenyl) –3, 5–pyridinedicarboxylate.

Pharmacological effects: Nimodipine is a calcium channel blocker. The contractile processes of smooth muscle cells are dependent upon calcium ions, which enter these cells during depolarization as slow ionic transmembrane currents. Nimodipine inhibits calcium ion transfer into these cells and thus inhibits contractions of vascular smooth muscle. In animal experiments, Nimodipine had a greater effect on cerebral arteries than on arteries elsewhere in the body perhaps because it is highly liphophilic, allowing it to cross the blood-brain barrier; concentrations of Nimodipine as high as 12.5 ng/mL have been detected in the cerebrospinal fluid of Nimodipine-treated subarachnoid hemorrhage (SAH) patients.

Indications: Nimodipine treatment is efficacious in overthrowing vasospasm in experimental SAH. Nimodipine infusion was found more effective application in basilar artery. Applications of nimodipine were effective in vertebral artery, which demonstrates the powerful vasodilator effect of the drug. Intra artery nimodipine infusion was found more effective in both vertebral and basilar arteries. Nimodipine treatment can be considered as an alternative technique for the treatment of vasospasm due to SAH. 

Adverse reaction: Hepatitis, Itching, Diaphoresis, Vomiting, Anemia, Jaundice, Hematoma, Palpitation, Hypertension, Dizziness, Wheezing, intravascular coagulation, Deep vein thrombos, Congestive heart failure, Light headedness, Neurological deterioration, Phenytoin toxicity, Hyponatremia.