Wernze H, Müller G, Goerig M
Adv Prostaglandin Thromboxane Res. 1980;7:1089-96.
A. No consistent changes in the urine PGE2 and PGF2 alpha related to sodium excretion could be found in hepatic cirrhosis with and without ascites. B. Intensive renal sodium retention in cirrhosis with ascites (urine Natless than 20 mEq/24 hr) is very often associated with increasing PGF/PGE ratio, whereas absolute urine PGE2 can be found low or normal. The PG shift is possibly due to a stimulation of the PGE2-9-keto-reductase. C. Application of saluretics and spironolactone in cirrhosis with ascites normalizes the PGF/PGE ratio in accordance with increasing sodium excretion. D. PG changes observed cannot be considered as a primary factor accounting for deranged renal sodium handling in cirrhosis. Anomalous PG pattern possibly reflects enchanced intrarenal vascular resistance.
A. 在有腹水和无腹水的肝硬化患者中,未发现尿中前列腺素E2(PGE2)和前列腺素F2α(PGF2α)与钠排泄相关的一致性变化。B. 有腹水的肝硬化患者出现强烈的肾钠潴留(尿钠低于20毫当量/24小时)时,常常伴有PGF/PGE比值升高,而尿PGE2绝对值可低或正常。PG的这种变化可能是由于PGE2 - 9 - 酮还原酶受到刺激。C. 对有腹水的肝硬化患者应用利尿剂和螺内酯后,随着钠排泄增加,PGF/PGE比值恢复正常。D. 观察到的PG变化不能被视为肝硬化患者肾钠处理紊乱的主要因素。异常的PG模式可能反映肾内血管阻力增加。