Bruix J, Bosch J, Kravetz D, Mastai R, Rodés J
Gastroenterology. 1985 Feb;88(2):430-5. doi: 10.1016/0016-5085(85)90503-7.
The role of prostaglandins in the pathogenesis of the circulatory abnormalities of cirrhosis was investigated by studying the effects of prostaglandin inhibition with indomethacin (50 mg/8 h for 24 h) on the systemic and splanchnic hemodynamics in 13 patients with cirrhosis of the liver. Indomethacin administration significantly reduced cardiac output (from 7.44 +/- 0.7 to 6.78 +/- 0.7 L/min, p less than 0.05) and increased peripheral vascular resistance (from 990 +/- 104 to 1155 +/- 140 dyn X s X cm-5, p less than 0.05). Arterial pressure was not modified. These changes in systemic hemodynamics were associated with a significant reduction in hepatic blood flow (from 1.88 +/- 0.43 to 1.48 +/- 0.3 L/min, p less than 0.05) and with a slight decrease of portal pressure (from 18.8 +/- 1.3 to 17.5 +/- 1.4 mmHg, p less than 0.05). These results suggest that endogenous prostaglandins contribute to the increased cardiac output and diminished vascular resistance observed in cirrhosis of the liver. In addition, by promoting splanchnic vasodilation, prostaglandins may contribute to increased portal pressure in these patients.
通过研究用吲哚美辛(50毫克/8小时,共24小时)抑制前列腺素对13例肝硬化患者全身和内脏血流动力学的影响,探讨了前列腺素在肝硬化循环异常发病机制中的作用。给予吲哚美辛后,心输出量显著降低(从7.44±0.7降至6.78±0.7升/分钟,p<0.05),外周血管阻力增加(从990±104增至1155±140达因×秒×厘米⁻⁵,p<0.05)。动脉压未改变。全身血流动力学的这些变化与肝血流量显著减少(从1.88±0.43降至1.48±0.3升/分钟,p<0.05)以及门静脉压力略有降低(从18.8±1.3降至17.5±1.4毫米汞柱,p<0.05)有关。这些结果表明,内源性前列腺素有助于肝硬化患者心输出量增加和血管阻力降低。此外,通过促进内脏血管舒张,前列腺素可能导致这些患者门静脉压力升高。