Ischemic brain injury: the importance of calcium, lipolytic activities, and free fatty acids.
Ischemic brain injury: the importance of calcium, lipolytic activities, and free fatty acids.
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发表时间：
1982-05
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通讯作者：
T. Wieloch;B. Siesjö
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作者：
T. Wieloch;B. Siesjö
缺血性脑损伤伴随着多种代谢改变。在本综述中，可能对这些损伤的结果很重要的不良反应是那些与磷脂和多不饱和脂肪酸代谢相关的不良反应，这些代谢是由钙离子稳态紊乱以及缺血后的能量消耗所引发的。这些条件导致磷脂酶的活化和磷脂再合成速率的降低，同时游离脂肪酸、特别是花生四烯酸的浓度增加。在再循环阶段，当重新建立氧气供应时，多不饱和花生四烯酸充当环加氧酶和脂氧合酶途径中的底物，导致羟基脂肪酸和氢过氧脂肪酸、前列腺素以及可能还有白三烯的形成。这些物质对细胞膜的完整性产生不利影响，不可逆地改变细胞的功能特性，并且还影响大脑再灌注有效性的血管调节特性。
Ischemic brain insults are accompanied by several metabolic alterations. In the present review, the adverse reactions, which might be important for the outcome of these insults, are those related to phospholipid and polyunsaturated fatty acid metabolism triggered by the disturbed calcium ion homeostasis in combination with energy depletion following ischemia. The conditions lead to an activation of phospholipases and to a decreased rate of phospholipid resynthesis with a concomitant increase in the concentration of free fatty acids, in particular arachidonic acid. During the recirculation phase, when oxygen supply is reestablished, the polyunsaturated arachidonic acid serves as substrate in the cyclo-oxygenase and lipoxygenase pathways leading to the formation of hydroxy-and hydroperoxy fatty acids, prostaglandins and possibly also leukotrienes. These substances have adverse effects on the integrity of cell membranes, irreversibly altering the functional properties of the cells, and also vasomodulator properties influencing the effectiveness of the reperfusion of the brain.