Arachidonic acid and postprandial intestinal hyperemia.

Arachidonic acid and postprandial intestinal hyperemia.
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花生四烯酸与餐后肠道充血。

DOI:
10.1152/ajpgi.1984.246.5.g521
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发表时间:
1984
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Chou,CC
Chou,CC
中科院分区:
--
文献类型:
--
作者:
Mangino,MJ;Chou,CC

文献摘要

被引文献

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在麻醉犬空肠中研究了前列腺素合成对食物诱导的肠血流量和O2摄取增加的影响。静脉(40 μ g × kg ~(-1)× min ~(-1))或动脉(0.8-1.6 μ g × min ~(-1))输注和腔内放置(6.5 × 10 ~(-4)M或200 μ g/ml)花生四烯酸(AA)可显著减轻食物诱导的空肠充血。此外,腔内放置AA显着衰减食物诱导的空肠O2摄取增加。血流量和O2摄取的变化在花生四烯酸给药前后均显著相关。虽然静脉输注AA降低了血流量,但在自由流动条件下,动脉内输注和腔内放置AA并没有显著改变静息血流量。在另一系列实验中,在恒定流量条件下静脉输注AA产生了双相反应:当局部血液AA浓度升高至1至6微克/毫升血液时,血管阻力上升,当浓度升高至8至12微克/毫升血液时,血管阻力下降。这项研究表明,前列腺素的合成有显着的影响,对静息肠血流量和餐后肠充血。充血的减弱可能是由于其减弱了食物诱导的肠氧化代谢增加。
The effects of prostaglandin synthesis on food-induced increases in intestinal blood flow and O2 uptake were examined in the jejunum of anesthetized dogs. Intravenous (40 micrograms X kg-1 X min-1) or intra-arterial (0.8-1.6 microgram X min-1) infusions and luminal placement (6.5 X 10(-4) M or 200 micrograms/ml) of arachidonic acid (AA) significantly attenuated the food-induced jejunal hyperemia. Furthermore, luminal placement of AA significantly attenuated the food-induced increase in jejunal O2 uptake. Changes in blood flow and O2 uptake were significantly correlated both before and after arachidonic acid administration. Although intravenous infusion of AA decreased blood flow, intra-arterial infusion and luminal placement of AA did not significantly alter resting blood flow under free-flow conditions. In another series of experiments, intravenous infusions of AA under constant-flow conditions produced a biphasic response: vascular resistance rose when local blood AA concentration was raised to the range between 1 and 6 micrograms/ml blood and fell when the concentration was raised between 8 and 12 micrograms/ml blood. This study indicates that prostaglandin synthesis has a marked effect on both resting intestinal blood flow and postprandial intestinal hyperemia. The attenuation of the hyperemia may be due to its attenuation of the food-induced increase in intestinal oxidative metabolism.