Bruckner G, Infante J, Combs G F, Kinsella J E
J Nutr. 1983 Sep;113(9):1884-9. doi: 10.1093/jn/113.9.1884.
This study was initiated to examine the role of prostanoids (thromboxane) in the development of nutritional encephalomalacia (NE). Chicks were fed diets deficient in or supplemented with vitamin E in the presence or absence of a known prostaglandin inhibitor, acetylsalicylic acid (ASA). When the incidence of NE was approximately 50% in the vitamin E--deficient group without ASA supplement, the chicks were killed, and serum thromboxane B2 (TxB2) and serum and brain fatty acid (FA) composition were determined. The incidence of NE was not altered by ASA treatment. Plasma arachidonate levels were increased by ASA treatment on the vitamin E--deficient diet. Furthermore, the serum TxB2 levels in vitamin E--deficient versus vitamin E--adequate chicks, unlike changes noted for rats, were decreased. Aspirin treatment drastically reduced TxB2 levels in all groups but did not alter the incidence of NE. Therefore, it is unlikely that the development of NE is a result of thromboxane-mediated thrombosis.
开展本研究以检测前列腺素（血栓素）在营养性脑软化（NE）发展过程中的作用。在存在或不存在已知前列腺素抑制剂乙酰水杨酸（ASA）的情况下，给雏鸡饲喂缺乏维生素E或补充了维生素E的日粮。当未补充ASA的维生素E缺乏组中NE的发生率约为50%时，将雏鸡处死，并测定血清血栓素B2（TxB2）以及血清和脑脂肪酸（FA）组成。ASA处理未改变NE的发生率。在维生素E缺乏日粮中，ASA处理可提高血浆花生四烯酸水平。此外，与大鼠的变化不同，维生素E缺乏雏鸡与维生素E充足雏鸡相比，血清TxB2水平降低。阿司匹林处理大幅降低了所有组的TxB2水平，但未改变NE的发生率。因此，NE的发展不太可能是血栓素介导的血栓形成的结果。
