Nidip - Nidip is in a group of drugs called calcium channel blockers. Nidip relaxes (widens) blood vessels and improves blood flow.
Nidip is used to prevent brain damage caused by reduced blood flow to the brain resulting from aneurysm (AN-yor-iz-m), a dilated or ruptured blood vessel in the brain.
Nidip may also be used for purposes other than those listed here.
Pharmacology: Inhibits movement of calcium ions across cell membrane in systemic and coronary vascular smooth muscle and myocardium. Has greater effect on cerebral arteries than on other arteries.
Indication: Improvement of neurologic deficits caused by vasospasm after subarachnoid hemorrhage from ruptured intracranial berry aneurysms.
Nidip belongs to the class of pharmacological agents known as calcium channel blockers. Nidip is indicated for the improvement of neurological outcome by reducing the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage from ruptured congenital aneurysms who are in good neurological condition post-ictus (e.g., Hunt and Hess Grades I-III). The contractile processes of smooth muscle cells are dependent upon calcium ions, which enter these cells during depolarization as slow ionic transmembrane currents. Nidip inhibits calcium ion transfer into these cells and thus inhibits contractions of vascular smooth muscle. In animal experiments, Nidip had a greater effect on cerebral arteries than on arteries elsewhere in the body perhaps because it is highly lipophilic, allowing it to cross the blood brain barrier.
Nidip helps to improve blood circulation in the brain in people who have a burst blood vessel in the brain. Nidip relaxes the blood vessels and this helps the blood to flow more smoothly. Improved brain circulation will help the brain tissue to heal better.
Oral Prophylaxis of neurological deficit following subarachnoid haemorrhage
Adult: 60 mg every 4 hr beginning within 4 days of onset of haemorrhage and continued for 21 consecutive days. Hepatic impairment: 30 mg every 4 hr in hepatic cirhosis. Intravenous Ischaemic neurological deficits following subarachnoid hemorrhage
Adult: Initially, 1 mg/hr infusion for 2 hr given via bypass into a central vein, increase to 2 mg/hr if no severe decrease in BP is observed. For <70 kg body weight or unstable BP: Initial dose: ≤500 mcg/hr. Treatment is started at once and continued for 5-14 days. Total duration should not exceed 21 days if patient has received oral treatment. Hepatic impairment: Initial dose: ≤500 mcg/hr. Special Populations: Patients with impaired hepatic function: Prophylaxis of neurological deficit: ½ of the usual dose with close BP monitoring. Patients with unstable BP and hepatic impairment: Prophylaxis of neurological deficit in cerebral ischaemia following aneurysmal or traumatic haemorrhage: Initially, 500 mcg/hr or less.
Adult: PO Prophylaxis of neurological deficit following subarachnoid haemorrhage 60 mg 4 hrly for 21 days beginning w/in 4 days of onset of haemorrhage. IV Ischaemic neurological deficits following subarachnoid haemorrhage Initial: 1 mg/hr for 2 hr, up to 2 mg/hr if no severe decrease in BP is observed. Start treatment at once and continue for 5-14 days. Total duration should not exceed 21 days if patient has received oral treatment.