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[Human atrial natriuretic factor (hANF) in liver cirrhosis]
Mean plasma levels of hANF at admission were significantly higher in liver cirrhosis (LC) patients with ascites (93 +/- 11 ng, n = 20; p less than 0.05) than in LC-patients without ascites (32 +/- 14 ng/l, n = 11) or healthy controls (31 +/- 15 ng/l; range: 5-80 ng/l; n = 106). Diuretic treatment of patients with LC and ascites normalised hANF plasma concentrations (44 +/- 14 ng/l; p less than 0.05). Increase of plasma hANF in LC-patients with ascites after acute volume expansion was lower (relative rise: 159%) than in those without ascites (relative rise: 223%). Volume redistribution into the vascular compartment, induced by peritoneovenous shunt implantation in LC-patients with diuretic treatment-refractory ascites, resulted in a sharp increase of plasma hANF levels (344 +/- 87 ng/l = 420% of preoperative concentration). Normal and slightly increased levels of plasma hANF and the appropriate regulation to volume changes suggest an intact control of the hormone in LC-patients. Neither a lack nor an inappropriate secretion of hANF as a cause for sodium retention as postulated by the overflow theory of ascites accumulation could be found in liver cirrhosis.
Mean plasma levels of hANF at admission were significantly higher in liver cirrhosis (LC) patients with ascites (93 +/- 11 ng, n = 20; p less than 0.05) than in LC-patients without ascites (32 +/- 14 ng/l, n = 11) or healthy controls (31 +/- 15 ng/l; range: 5-80 ng/l; n = 106). Diuretic treatment of patients with LC and ascites normalised hANF plasma concentrations (44 +/- 14 ng/l; p less than 0.05). Increase of plasma hANF in LC-patients with ascites after acute volume expansion was lower (relative rise: 159%) than in those without ascites (relative rise: 223%). Volume redistribution into the vascular compartment, induced by peritoneovenous shunt implantation in LC-patients with diuretic treatment-refractory ascites, resulted in a sharp increase of plasma hANF levels (344 +/- 87 ng/l = 420% of preoperative concentration). Normal and slightly increased levels of plasma hANF and the appropriate regulation to volume changes suggest an intact control of the hormone in LC-patients. Neither a lack nor an inappropriate secretion of hANF as a cause for sodium retention as postulated by the overflow theory of ascites accumulation could be found in liver cirrhosis.