Hamm T F, Dorman R V
Department of Biological Sciences, Kent State University, OH 44242.
J Neurosci Res. 1990 Aug;26(4):488-94. doi: 10.1002/jnr.490260412.
Pentobarbital pretreatment may be used to predict biochemical events involved in ischemic brain damage following bilateral carotid artery ligations in the gerbil, since it reduces the subsequent edema and mortality. The effects of this anesthetic on the ischemia-induced modifications of cerebral arachidonic acid metabolism were investigated, in order to correlate observed alterations with tissue damage. Cerebral lipids were radiolabeled in vivo with [3H]arachidonic acid prior to 10 min of cerebral ischemia and 0-120 min of perfusion. Ischemia stimulated a 97.3% increase in unesterified [3H]arachidonate, which was due to the loss of label from choline, inositol, and ethanolamine glycerophospholipids. Tissue reperfusion stimulated further reductions in [3H]choline and [3H]inositol glycerophospholipids, while ethanolamine glycerophospholipid and triglyceride labeling increased. Inositol glycerophospholipid, but not choline glycerophospholipid, labeling returned to control level by 60 min of reperfusion. Pentobarbital pretreatment reduced the accumulation of [3H]arachidonate by 56.2% during ischemia. It increased the recovery of [3H]ethanolamine glycerophospholipids during the ischemic period and [3H]choline glycerophospholipids during the first 5 min of reperfusion. These effects accounted for the reduction of unesterified [3H]arachidonate observed during ischemia and reperfusion.
戊巴比妥预处理可用于预测沙鼠双侧颈动脉结扎后缺血性脑损伤所涉及的生化事件，因为它能降低随后的脑水肿和死亡率。研究了这种麻醉剂对缺血诱导的脑花生四烯酸代谢改变的影响，以便将观察到的变化与组织损伤联系起来。在脑缺血10分钟和灌注0 - 120分钟之前，用[3H]花生四烯酸在体内对脑脂质进行放射性标记。缺血刺激未酯化的[3H]花生四烯酸盐增加了97.3%，这是由于胆碱、肌醇和乙醇胺甘油磷脂中标记物的丢失。组织再灌注刺激了[3H]胆碱和[3H]肌醇甘油磷脂的进一步减少，而乙醇胺甘油磷脂和甘油三酯的标记增加。再灌注60分钟时，肌醇甘油磷脂而非胆碱甘油磷脂的标记恢复到对照水平。戊巴比妥预处理在缺血期间使[3H]花生四烯酸盐的积累减少了56.2%。它增加了缺血期间[3H]乙醇胺甘油磷脂以及再灌注最初5分钟内[3H]胆碱甘油磷脂的恢复。这些作用解释了在缺血和再灌注期间观察到的未酯化[3H]花生四烯酸盐的减少。
