Yoshida S, Inoh S, Asano T, Sano K, Shimasaki H, Ueta N
J Neurochem. 1983 May;40(5):1278-86. doi: 10.1111/j.1471-4159.1983.tb13567.x.
Brain free fatty acids (FFAs) and brain water content were measured in gerbils subjected to transient, bilateral cerebral ischemia under brief halothane anesthesia (nontreated group) and pentobarbital anesthesia (treated group). Mortality in the two groups was also evaluated. In nontreated animals, both saturated and mono- and polyunsaturated FFAs increased approximately 12-fold in total at the end of a 30-min period of ischemia; during recirculation, the level of free arachidonic acid dropped rapidly, while other FFAs gradually decreased to their preischemic levels in 90 min. In treated animals, the levels of total FFAs were lower than the nontreated group during ischemia, but higher at 90 min of reflow, and the decrease in the rate of free arachidonic acid was slower in the early period of reflow. Water content increased progressively during ischemia and recirculation with no extravasation of serum protein, but the values were consistently lower in the treated group. None of the nontreated animals survived for 2 weeks; in contrast, survival was 37.5% in the treated group. It is suggested that barbiturate protection from transient cerebral ischemia may be mediated by the attenuation of both membrane phospholipid hydrolysis during ischemia and postischemic peroxidation of accumulated free arachidonic acid.
在短暂氟烷麻醉(未治疗组)和戊巴比妥麻醉(治疗组)下,对遭受短暂双侧脑缺血的沙鼠进行脑游离脂肪酸(FFA)和脑含水量的测量。同时评估两组的死亡率。在未治疗的动物中,在30分钟缺血期结束时,饱和脂肪酸、单不饱和脂肪酸和多不饱和脂肪酸的总量均增加了约12倍;在再灌注期间,游离花生四烯酸水平迅速下降,而其他游离脂肪酸在90分钟内逐渐降至缺血前水平。在治疗的动物中,缺血期间总游离脂肪酸水平低于未治疗组,但在再灌注90分钟时更高,且再灌注早期游离花生四烯酸的下降速率较慢。缺血和再灌注期间含水量逐渐增加,无血清蛋白外渗,但治疗组的值始终较低。未治疗的动物无一存活2周;相比之下,治疗组的存活率为37.5%。提示巴比妥类药物对短暂性脑缺血的保护作用可能是通过减轻缺血期间膜磷脂水解和缺血后积累的游离花生四烯酸的过氧化作用来介导的。