Nimodipine
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Nimodipine
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| Systematic (IUPAC) name | |
| 2-methoxyethyl1-methylethyl2,6-dimethyl-4-(3-nitrophenyl) -1,4-dihydropyridine-3,5- dicarboxylate | |
| Identifiers | |
| CAS number | |
| ATC code | C08 |
| PubChem | |
| DrugBank | |
| Chemical data | |
| Formula | C21H26N2O7 |
| Mol. mass | 418.44 g/mol |
| Physical data | |
| Melt. point | 7 °C (45 °F) |
| Pharmacokinetic data | |
| Bioavailability | 100% (Intravenous) 13% (Oral) |
| Protein binding | 95% |
| Metabolism | Hepatic |
| Half life | 8-9 hours |
| Excretion | ? |
| Therapeutic considerations | |
| Pregnancy cat. |
C: (USA) |
| Legal status | |
| Routes | Intravenous, Oral |
Nimodipine (marketed by Bayer as Nimotop) is a dihydropyridine calcium channel blocker originally developed for the treatment of high blood pressure. It is not frequently used for this indication, but has shown good results in preventing a major complication of subarachnoid hemorrhage (a form of cerebral hemorrhage) termed vasospasm; this is now the main use of nimodipine.
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[edit] Dosage
The regular dosage is 60 mg tablets every four hours. If the patient is unable to take tablets orally, it was previously given via intravenous infusion at a rate of 1-2 mg/hour (lower dosage if the body weight is <70 kg or blood pressure is too low),[1] but since the withdrawal of the IV preparation, administration by nasogastric tube is an alternative.
[edit] Usage
Because it has some selectivity for cerebral vasculature, nimodipine's main use is in the prevention of cerebral vasospasm and resultant ischemia, a complication of subarachnoid hemorrhage (a form of cerebral bleed). Its administration begins within 4 days of a subarachnoid hemorrhage and is continued for three weeks. If blood pressure drops by over 5%, dosage is adjusted. There is still controversy regarding the use of intravenous nimodipine on a routine basis.[2][1]
A 2003 trial (Belfort et al) found nimodipine was inferior to magnesium sulfate in preventing seizures in women with severe preeclampsia.[3]
[edit] Mode of action
Nimodipine binds specifically to L-type voltage-gated calcium channels. There are numerous theories about its mechanism in preventing vasospasm, but none are conclusive.[4]
[edit] Contraindications & side-effects
Nimodipine is associated with low blood pressure, flushing and sweating, edema, nausea and other gastrointestinal problems. It is contraindicated in unstable angina or an episode of myocardial infarction more recently than one month.
While nimodipine was occasionally administered intravenously in the past, the FDA released an alert in January 2006 warning that it had received reports of the approved oral preparation being used intravenously, leading to severe complications; this was despite warnings on the box that this should not be done.[5]
[edit] References
- ^ a b Janjua N, Mayer SA (2003). "Cerebral vasospasm after subarachnoid hemorrhage". Current opinion in critical care 9 (2): 113–9. doi:. PMID 12657973.
- ^ Allen GS, Ahn HS, Preziosi TJ, et al (1983). "Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage". N. Engl. J. Med. 308 (11): 619–24. PMID 6338383.
- ^ Belfort MA, Anthony J, Saade GR, Allen JC (2003). "A comparison of magnesium sulfate and nimodipine for the prevention of eclampsia". N. Engl. J. Med. 348 (4): 304–11. doi:. PMID 12540643.
- ^ Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-44307-145-4.
- ^ Information for Healthcare Professionals: Nimodipine (marketed as Nimotop). Retrieved on 2007-10-10.
[edit] External links
- Nimotop (manufacturer's website)
- Nimodipine (patient information)
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