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美国卫生研究院文献>The Journal of Neurology and Psychopathology
>Oral nimodipine reduces prostaglandin and thromboxane production by arteries chronically exposed to a periarterial haematoma and the antifibrinolytic agent tranexamic acid.
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Oral nimodipine reduces prostaglandin and thromboxane production by arteries chronically exposed to a periarterial haematoma and the antifibrinolytic agent tranexamic acid.
The calcium antagonist nimodipine blocks the effects of many vasoconstrictors of cerebrovascular smooth muscle and may reduce the incidence of delayed cerebral ischaemia following subarachnoid haemorrhage though not necessarily by inhibiting the development of angiographic cerebral vasospasm. Post-haemorrhagic CSF contains abnormally large quantities of various eicosanoids that partly reflect enhanced production by cerebral arteries. Does nimodipine affect this process? The extra-arterial and intra-arterial production of PG6 keto-F1 alpha, PGE2, PGF2 alpha and TXB2 were measured in perfused common carotid arteries taken from rabbits in which the arteries had been ensheathed by blood clot in vivo for 7 days. All rabbits were given the antifibrinolytic agent tranexamic acid to retard resolution of the clot, and half were given oral nimodipine (2 mg/kg/day) for 10 days. Nimodipine significantly reduced the extra-arterial production of TXB2 during the third and fourth hours of perfusion and, less consistently, the production of PGF2 alpha, PGE2 and PG6 keto-F1 alpha. Lutrol, the solvent for nimodipine, had no such effect.
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机译:钙拮抗剂尼莫地平阻断了脑血管平滑肌的许多血管收缩剂的作用,并可能降低了蛛网膜下腔出血后迟发性脑缺血的发生率,尽管不一定通过抑制血管造影术脑血管痉挛的发展来实现。出血后脑脊液中含有异常大量的各种类花生酸,部分反映了脑动脉产生的产量增加。尼莫地平会影响这一过程吗?在取自兔子的经灌注的普通颈动脉中测量了PG6酮-F1α,PGE2,PGF2α和TXB2的动脉外和动脉内生成,这些动脉在体内已经被血凝块包裹了7天。给所有兔子抗纤维蛋白溶解剂氨甲环酸以延迟血块的分离,一半给兔子口服尼莫地平(2 mg / kg /天),持续10天。尼莫地平在灌注的第三个和第四个小时内显着降低了TXB2的动脉外生成,并且降低了PGF2α,PGE2和PG6酮-F1α的生成,但不一致。尼莫地平的溶剂Lutrol没有这种作用。
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