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膳食脂肪类型和环境氧分压会影响肺部前列腺素的合成潜力。

Dietary fat type and ambient oxygen tension influence pulmonary prostaglandin synthetic potential.

作者信息

Meydani S N, Mathias M M, Schatte C L

出版信息

Prostaglandins Med. 1978 Sep;1(3):241-9. doi: 10.1016/0161-4630(78)90110-6.

Abstract

Chronic hyperoxia produces pathological changes in lung which can be fatal. With an interest in delineating dietary factors which might affect the pulmonary response to hyperoxia, we fed rats a semi-synthetic diet containing polyunsaturated fatty acids (PUFA) as either 5% or 78% of the fat complement. The rats were exposed to pure oxygen at one atmosphere. Half the animals in each diet group were injected with aspirin during the hyperoxic exposure. Radioimmunoassay of lung prostaglandins (PG) F2alpha, E2 and E1 were performed at 0, 24, 48 and 72 hours. The major findings were: (1) Feeding the high PUFA diet elevated lung PG synthetic potential tenfold over that of low PUFA-fed animals. There was no effect of diet on mortality. (2) Hyperoxia significantly increased F2alpha-synthetic potential during the first 24 hours of hyperoxia and moderately increased the synthetic potential of E2 and E1. (3) Aspirin significantly depressed synthetic potential of all three PG prior to oxygen exposure but its effect was overcome during hyperoxia. Aspirin-injected rats showed 80% mortality in oxygen vs. 50% for saline controls.

摘要

慢性高氧会在肺部产生可致命的病理变化。出于确定可能影响肺部对高氧反应的饮食因素的兴趣,我们用一种半合成饮食喂养大鼠,该饮食中多不饱和脂肪酸(PUFA)占脂肪成分的5%或78%。大鼠在一个大气压下暴露于纯氧中。每个饮食组的一半动物在高氧暴露期间注射阿司匹林。在0、24、48和72小时对肺前列腺素(PG)F2α、E2和E1进行放射免疫测定。主要发现如下:(1)喂养高PUFA饮食使肺PG合成潜能比低PUFA喂养的动物提高了十倍。饮食对死亡率没有影响。(2)高氧在高氧暴露的最初24小时内显著增加F2α合成潜能,并适度增加E2和E1的合成潜能。(3)阿司匹林在氧气暴露前显著降低了所有三种PG的合成潜能,但其作用在高氧期间被克服。注射阿司匹林的大鼠在氧气环境中的死亡率为80%,而生理盐水对照组为50%。

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