Renal prostaglandin E2 and other vasoactive modulators in refractory hepatic ascites: response to peritoneovenous shunting.
To assess the role of renal prostaglandin E2 in the pathogenesis of refractory ascites, in relation to renal sodium handling and circulating levels of vasoconstrictive substances, we studied 12 cirrhotic patients with refractory ascites before and after peritoneovenous shunting. Baseline values for urinary prostaglandin E2 excretion, sodium excretion, and creatinine clearance, as well as serum aldosterone, plasma renin activity, and plasma free norepinephrine, were obtained preoperatively with patients on a sodium- and fluid-restricted diet. Diuretics were also withheld. Similar parameters were measured immediately postoperatively during four consecutive 2-h intervals, then again at 2 wk and 3 mo. In patients with refractory ascites, mean baseline urinary prostaglandin E2 excretion was significantly elevated (2.5 +/- 0.8 pmol/min), compared with that in both normal controls and cirrhotics without ascites (1.3 +/- 0.3 pmol/min). A significant natriuresis occurred immediately postoperatively and persisted at 2 wk and 3 mo. Concomitantly, the elevated levels of preoperative vasoconstrictor substances gradually normalized by 2 wk. Urinary prostaglandin E2 excretion, however, rose transiently in the immediate postoperative period and then fell gradually to within the normal range by 3 mo. Enhanced renal prostaglandin E2 synthesis, therefore, does not play a role in the sustained improvement in sodium homeostasis after peritoneovenous shunting in patients with refractory ascites.[1]References
- Renal prostaglandin E2 and other vasoactive modulators in refractory hepatic ascites: response to peritoneovenous shunting. Shaw-Stiffel, T., Campbell, P.J., Sole, M.J., Greig, P., Wong, P.Y., Blendis, L.M. Gastroenterology (1988) [Pubmed]
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