Kazda S
Neurochirurgia (Stuttg). 1985 May;28 Suppl 1:70-3. doi: 10.1055/s-2008-1054106.
In isolated vessels in vitro nimodipine inhibits spasms induced by depolarization independently of the vessel's origin. The spasms induced by spasmogenic agonists such as serotonin, catecholamines, histamine, thromboxane, or whole blood are inhibited only in the cerebral vessels and not in the peripheral vessels. In vivo, nimodipine inhibits cerebrovascular spasms and brain damage in acute and chronic animal experiments. In chronic studies on stroke-prone, spontaneously hypertensive rats, nimodipine prevents cerebral tissue damage and prolongs the survival time without affecting the high blood pressure. Nimodipine inhibits the transmembraneous calcium influx in the smooth muscle cells of the cerebral vessels and thus prevents cerebral hypoperfusion after spasmogenic stimulation. In chronic cerebrovascular stress nimodipine prevents harmful calcium overloading and thus ensures the integrity of the cerebral parenchyma.
在体外分离的血管中，尼莫地平可抑制由去极化诱导的痉挛，且与血管来源无关。由5-羟色胺、儿茶酚胺、组胺、血栓素或全血等致痉激动剂诱导的痉挛，仅在脑血管中受到抑制，而在外周血管中不受抑制。在体内，在急性和慢性动物实验中，尼莫地平可抑制脑血管痉挛和脑损伤。在对易中风的自发性高血压大鼠的慢性研究中，尼莫地平可预防脑组织损伤并延长存活时间，而不影响高血压。尼莫地平抑制脑血管平滑肌细胞中的跨膜钙内流，从而防止致痉刺激后的脑灌注不足。在慢性脑血管应激状态下，尼莫地平可防止有害的钙超载，从而确保脑实质的完整性。
