flunarizine and Cardiovascular-Diseases

flunarizine has been researched along with Cardiovascular-Diseases* in 2 studies

Other Studies

2 other study(ies) available for flunarizine and Cardiovascular-Diseases

Article	Year
A long-term follow-up study of cinnarizine- and flunarizine-induced parkinsonism. Movement disorders : official journal of the Movement Disorder Society, 1997, Volume: 12, Issue:1 The natural course of calcium-entry blocker-induced parkinsonism was evaluated in 13 elderly patients previously exposed to cinnarizine or flunarizine or both for a median period of 7 months. Clinical assessments were carried out before drug discontinuation and twice thereafter over a period lasting < or = 7 years. None of the patients showed a full recovery of extrapyramidal signs, indicating that the long-term prognosis of the parkinsonism is less benign than previously reported. Two main patterns of clinical outcome were recognized (i.e., "remittent" and "persistent and not progressive" parkinsonism), whereas the development of a progressive disorder was observed only in one patient. No significant correlation was found between the patterns of outcome and some clinical variables, such as total duration of exposure to cinnarizine and flunarizine, cumulative drug dosages, and age at onset of parkinsonism. There was no significant difference in terms of family history of essential tremor or parkinsonism or both among patients with the two main patterns of clinical course. Topics: Aged; Calcium Channel Blockers; Cardiovascular Diseases; Cinnarizine; Dose-Response Relationship, Drug; Female; Flunarizine; Follow-Up Studies; Humans; Male; Middle Aged; Neurologic Examination; Parkinson Disease, Secondary; Treatment Outcome	1997
Ca2+ modulators as antidotes to imipramine and neurotransmitter toxicity. Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), 1987, Volume: 185, Issue:4 Flunarizine and nimodipine, Ca2+ modulators which exert antagonist effects against catecholamines and serotonin and have specific action on the brain, were used as antidotes to imipramine toxicity in the rat. Imipramine, a tricyclic antidepressant, inhibits synaptic reuptake of catecholamines and serotonin. Flunarizine administered concurrently with imipramine increased survival time significantly (p less than 0.04). After a lethal dose of imipramine (85 mg/kg) 5 out of 5 animals treated with flunarizine (2.37 +/- 1.21 mg/kg in divided doses) and 4 out of 5 animals treated with nimodipine (0.36 +/- 0.11 mg/kg) survived. The acute toxicity of imipramine might be related, in part, to drug-induced alteration in turnover of excitatory neurotransmitters which will induce intracellular Ca2+ accumulation and damage to vital organs. These toxic effects of endogenously produced neuroamines may be antagonized by nimodipine or flunarizine. Topics: Animals; Antidotes; Calcium; Cardiovascular Diseases; Flunarizine; Imipramine; Male; Neurotransmitter Agents; Nimodipine; Rats; Rats, Inbred Strains	1987

Article

Year

A long-term follow-up study of cinnarizine- and flunarizine-induced parkinsonism.

Movement disorders : official journal of the Movement Disorder Society, 1997, Volume: 12, Issue:1

The natural course of calcium-entry blocker-induced parkinsonism was evaluated in 13 elderly patients previously exposed to cinnarizine or flunarizine or both for a median period of 7 months. Clinical assessments were carried out before drug discontinuation and twice thereafter over a period lasting < or = 7 years. None of the patients showed a full recovery of extrapyramidal signs, indicating that the long-term prognosis of the parkinsonism is less benign than previously reported. Two main patterns of clinical outcome were recognized (i.e., "remittent" and "persistent and not progressive" parkinsonism), whereas the development of a progressive disorder was observed only in one patient. No significant correlation was found between the patterns of outcome and some clinical variables, such as total duration of exposure to cinnarizine and flunarizine, cumulative drug dosages, and age at onset of parkinsonism. There was no significant difference in terms of family history of essential tremor or parkinsonism or both among patients with the two main patterns of clinical course.

Topics: Aged; Calcium Channel Blockers; Cardiovascular Diseases; Cinnarizine; Dose-Response Relationship, Drug; Female; Flunarizine; Follow-Up Studies; Humans; Male; Middle Aged; Neurologic Examination; Parkinson Disease, Secondary; Treatment Outcome

1997

Ca2+ modulators as antidotes to imipramine and neurotransmitter toxicity.

Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), 1987, Volume: 185, Issue:4

Flunarizine and nimodipine, Ca2+ modulators which exert antagonist effects against catecholamines and serotonin and have specific action on the brain, were used as antidotes to imipramine toxicity in the rat. Imipramine, a tricyclic antidepressant, inhibits synaptic reuptake of catecholamines and serotonin. Flunarizine administered concurrently with imipramine increased survival time significantly (p less than 0.04). After a lethal dose of imipramine (85 mg/kg) 5 out of 5 animals treated with flunarizine (2.37 +/- 1.21 mg/kg in divided doses) and 4 out of 5 animals treated with nimodipine (0.36 +/- 0.11 mg/kg) survived. The acute toxicity of imipramine might be related, in part, to drug-induced alteration in turnover of excitatory neurotransmitters which will induce intracellular Ca2+ accumulation and damage to vital organs. These toxic effects of endogenously produced neuroamines may be antagonized by nimodipine or flunarizine.

Topics: Animals; Antidotes; Calcium; Cardiovascular Diseases; Flunarizine; Imipramine; Male; Neurotransmitter Agents; Nimodipine; Rats; Rats, Inbred Strains

1987