Kidooka M, Matsuda M, Handa J
Department of Neurosurgery, Shiga University of Medical Science, Japan.
Surg Neurol. 1987 Dec;28(6):437-40. doi: 10.1016/0090-3019(87)90226-6.
Using a model of global cerebral ischemia in rats, we examined the effects of a dihydropyridine Ca2+ antagonist, nicardipine, on the liberation of free fatty acids (FFAs). After decapitation of the animals, FFAs showed a rapid progressive increase for a whole experimental period of up to 60 minutes without reaching a plateau. Nicardipine in a dosage of 1 mg/kg effectively attenuated the liberation of FFAs, particularly that of arachidonic acid which is known as the precursor of prostaglandins, thromboxanes, and leukotrienes. The FFAs of the brain have been known as one of the biochemical markers that indicate ischemic damage of the brain cell membrane. The results of the present study support a possible protective effect of Ca2+ antagonist against cerebral ischemia.
利用大鼠全脑缺血模型,我们研究了二氢吡啶类钙拮抗剂尼卡地平对游离脂肪酸(FFA)释放的影响。动物断头后,在长达60分钟的整个实验期间,FFA呈快速渐进性增加,且未达到平台期。剂量为1mg/kg的尼卡地平有效减弱了FFA的释放,尤其是花生四烯酸的释放,花生四烯酸是已知的前列腺素、血栓素和白三烯的前体。脑FFA一直被认为是指示脑细胞膜缺血损伤的生化标志物之一。本研究结果支持钙拮抗剂对脑缺血可能具有保护作用。