Relationships between plasma atrial natriuretic peptide concentrations and hemodynamics and hematocrit in patients with cirrhosis

✍ Scribed by Dr. Richard Moreau; Antoine Hadengue; Eric Pussard; Olivier Soubrane; Philippe Sogni; Christophe Gaudin; Didier Lebrec

• Publisher: John Wiley and Sons
• Year: 1991
• Tongue: English
• Weight: 632 KB
• Volume: 14
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840140615

✦ Synopsis

W e studied the relationships in 29 patients with Cirrhosis between pulmonary arterial atrial natriuretic peptide concentrations and the following: sys- temic and splanchnie hemodynamics, the hematmrit, arterial oxyhemoglobin saturation, oxygen tension and the severity of cirrhosis. Plasma atrial natriuretic peptide concentrations ranged from 21 to 208 pg/d and averaged 78 f 8 pg/ml (mean f S.E.M.). Simple regression analysis showed significant correlations between plasma atrial natriuretic peptide concentration and the following: hematocrit, mean pulmonary arterial pressure, wedged hepatic venous pressure, free hepatic venous pressure, pulmonary wedged pressure and serum bilirubin concentrations.

No significant correlations were found between plasma atrial natriuretic peptide concentrations and all other hemodynamic values, arterial oxyhemoglobin saturation and oxygen tension. Multiple stepwise regression analysis showed that the hematocrit, mean pulmonary arterial pressure and wedged hepatic venous pressure were significant and independent predictors of pulmonary artery plasma atrial natriuretic peptide concentrations (R2 = 0.69). Partial regression coefficients were -0.74 (p < 0.001), 0.61 (p < 0.001) and 0.44 (p < 0.05) for the hematocrit, the mean pulmonary arterial pressure and the wedged hepatic venous pressure, respectively. In conclusion, in patients with cirrhosis, increased plasma atrial natriuretic peptide concentrations were related to the degree of hemodilution, increased pulmonary arterial preywe and the degree of portal hypertension. Plasma atlnal natriuretic peptide concentrations were not influenced by the arterial oxygenation levels. (HEPA-