Aneurysmal subarachnoid hemorrhage: Prevention of delayed ischemic dysfunction with intravenous nimodipine

Ljunggren, Bengt; Brandt, Lennart; Säveland, Hans; Romner, Bertil; Ryman, Torsten; Andersson, Karl‐Erik

doi:10.1007/bf01781947

Cited by 7 publications

(5 citation statements)

References 51 publications

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“…Unfortunately, the prevention or reversal of cerebral vasospasm in patients with SAH has not been documented angiographically to date in controlled studies (32,87,(96)(97)(98), and nimodipine has improved neurologic outcome in patients regardless of the angiographic presence or absence of cerebral vasospasm prior to therapy (87,99). Other mechanisms, such as preferential dilation of small pial resistance vessels not detectable angiographycally (6,11,100,101) and subsequent increases in collateral blood flow to ischemic tissues, may contribute to the drug's clinical benefit in patients with SAH (32,97,98,100,(103)(104)(105)(106).…”

Section: Subarachnoid Hemorrhagementioning

confidence: 97%

“…SAH resulting from rupture of saccular arterial aneurysms at the base of the brain frequently leads to clot formation in the basal subarachnoid cisterns, and this promotes subsequent cerebral vasospasm (29,101,115,119). Delayed cerebral vasospasm with neurologic deficits occurs in approximately 30% of patients with SAH within 3-4 days after the event (29,90,105,119,120).…”

Section: Subarachnoid Hemorrhagementioning

confidence: 99%

See 1 more Smart Citation

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Tomassoni

Lanari

Silvestrelli

et al. 2008

Clinical and Experimental Hypertension

120

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Nimodipine is a 1,4-dihydropyridine-derivative Ca(2+)-channel blocker developed approximately 30 years ago. It is highly lipophilic, crosses the blood-brain barrier, and reaches brain and cerebrospinal fluid. Early treatment with nimodipine reduces the severity of neurological deficits resulting from vasospasm in subarachnoid haemorrhage (SAH) patients. In SAH, nimodipine reduced spasm-related deficits of all severities, but no spasm-unrelated deficits. This paper has reviewed preclinical studies on the influence of nimodipine in various animal models of cerebral ischemia, with particular attention toward investigations published in the last 10 years. These studies further support the main indication of nimodipine, by clarifying some mechanisms of the anti-ischemic activity of the compound. Papers reporting a possible role of nimodipine in epileptogenesis were also examined. Clinical studies on nimodipine were grouped into subarachnoid hemorrhage, acute ischemic stroke, cerebral ischemia without stroke, dementia disorders, and migraine. Clinical investigations have shown that the drug improves neurological outcome by reducing the incidence and severity of ischemic deficits in patients with SAH from ruptured intracranial berry aneurysms regardless of their post-ictus neurological condition. No relevant effects of treatment with nimodipine were reported for acute ischemic stroke, cerebral ischemia without stroke, and migraine, except than for cluster headache. The less pronounced cardiovascular effects of nimodipine compared to other dihydropyridine-type Ca(2+)-channel blockers probably accounts for its use out of label for treating patients affected by chronic cerebral ischemia and vascular cognitive impairment. However, the blood pressure-lowering effects of nimodipine should not be minimized, as clinical studies have documented lowering blood pressure in small groups of patients, including cases of withdrawn due to pronounced hypotension induced by nimodipine administration. In the area of vascular cognitive impairment, short-term benefits of nimodipine do not justify its use as a long-term anti-dementia drug, and benefits obtained in elderly patients affected by subcortical vascular dementia require to be confirmed by other groups and in larger scale trials. In conclusion, nimodipine is a safe drug with an important place in pharmacotherapy and with the main documentation for reduction in the severity of neurological deficits resulting from vasospasm in SAH patients.

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Section: Subarachnoid Hemorrhagementioning

confidence: 97%

Section: Subarachnoid Hemorrhagementioning

confidence: 99%

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Tomassoni

Lanari

Silvestrelli

et al. 2008

Clinical and Experimental Hypertension

120

View full text Add to dashboard Cite

show abstract

“…1) is a dihydropyridine calcium channel blocker that acts by relaxing the arterial smooth muscle. Able to cross the blood-brain barrier, nimodipine can dilate the cerebral arterioles [1,2]; thus it is used currently to prevent and treat the ischemic damage caused by cerebral arterial spasm in subarachnoid hemorrhage [3]. Nimodipine has also been used in other cerebrovascular disorders, such as ischemic stroke [4] and multi-infarct dementia [5].…”

Section: Introductionmentioning

confidence: 99%

Determination of nimodipine in human plasma by a sensitive and selective liquid chromatography–tandem mass spectrometry method

Qiu

Chen

et al. 2004

Journal of Chromatography B

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“…Nimodipine (NMD) is a dihydropyridine calcium channel blocker and is currently used to prevent and treat the ischemic damage caused by cerebral arterial spasm in subarachnoid hemorrhage [1] . NMD has also been used in other cerebrovascular disorders, such as ischemic stroke [2] and multi-infarct dementia [3] .…”

Section: Introductionmentioning

confidence: 99%

Effect of baicalin and berberine on transport of nimodipine on primary-cultured, rat brain microvascular endothelial cells

Zhang

Liu

Xie

et al. 2007

Acta Pharmacologica Sinica

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Aim: To investigate whether baicalin and berberine affects the transport of nimodipine (NMD) across the blood-brain barrier (BBB). Methods: Primarycultured, rat brain microvascular endothelial cells (rBMEC) were used as an in vitro model of the BBB. When cells became confluent, the steady-state uptake of NMD by rBMEC with or without baicalin and berberine was measured. The effects of baicalin and berberine on the efflux of NMD from rBMEC were also studied. Results: Baicalin (2-5 µg/mL) increased the uptake of NMD, and baicalin (10-20 µg/mL) decreased the uptake. The steady-state uptake of NMD was higher than that of control group in the presence of 0.01-1 µg/mL berberine, but was lower in the presence of 2-10 µg/mL berberine. Conclusion: The bidirectional effect of baicalin and berberine on the uptake of NMD by rBMEC was found. Higher concentration showed an inhibitory effect, and lower concentration demonstrated an increasing effect.

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Aneurysmal subarachnoid hemorrhage: Prevention of delayed ischemic dysfunction with intravenous nimodipine

Cited by 7 publications

References 51 publications

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Determination of nimodipine in human plasma by a sensitive and selective liquid chromatography–tandem mass spectrometry method

Effect of baicalin and berberine on transport of nimodipine on primary-cultured, rat brain microvascular endothelial cells

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