Walus K M, Gustaw P, Konturek S J
Prostaglandins. 1980 Dec;20(6):1089-102. doi: 10.1016/0090-6980(80)90062-3.
Experiments were carried out on anesthetized dogs to compare the effects of prostaglandin E2 (PGE2), prostacyclin (PGI2) and arachidonic acid (AA) administered intraarterially on gastric blood flow and oxygen consumption during constant arterial pressure perfusion and constant flow perfusion of the stomach. Both PGE2 and PGI2 increased total blood flow and oxygen consumption both in the resting stomach and following histamine stimulation although the effects of PGE2 on the oxygen consumption in stimulated stomach were not statistically significant. On the contrary, AA decreased both gastric blood flow and oxygen consumption in the histamine stimulated stomach. To determine if these compounds can influence gastric oxygen consumption independently of their effects on blood flow, the experiments with constant flow perfusion were performed. Both PGE2 and PGI2 decreased both the perfusion pressure and oxygen consumption in the resting as well as in the histamine-stimulated stomach whereas AA increased perfusion pressure and decreased oxygen consumption during histamine administration. Effects of AA were blocked by indomethacin suggesting that not AA itself but some of its metabolites, most likely thromboxanes were responsible for the hemodynamic and metabolic changes resulting from the contraction of gastric arterioles and precapillary sphincters. On the contrary, both PGE2 and PGI2 caused gastric hyperemia and an increase in oxygen consumption in the resting stomach, but decreased the latter parameter in the stimulated stomach, most probably as a result of secretory inhibition overcoming direct vascular effects of these compounds.
在麻醉犬身上进行了实验,以比较在胃的恒压灌注和恒流灌注期间,动脉内给予前列腺素E2(PGE2)、前列环素(PGI2)和花生四烯酸(AA)对胃血流量和氧消耗的影响。PGE2和PGI2均增加了静息胃以及组胺刺激后的总血流量和氧消耗,尽管PGE2对受刺激胃中氧消耗的影响无统计学意义。相反,AA降低了组胺刺激胃中的胃血流量和氧消耗。为了确定这些化合物是否能独立于其对血流量的影响而影响胃氧消耗,进行了恒流灌注实验。PGE2和PGI2均降低了静息胃以及组胺刺激胃中的灌注压和氧消耗,而AA在给予组胺期间增加了灌注压并降低了氧消耗。AA的作用被吲哚美辛阻断,这表明不是AA本身,而是其某些代谢产物,很可能是血栓素,导致了胃小动脉和毛细血管前括约肌收缩引起的血流动力学和代谢变化。相反,PGE2和PGI2均导致静息胃充血和氧消耗增加,但在受刺激胃中降低了后者参数,最可能是由于分泌抑制克服了这些化合物的直接血管作用。