Serum endothelin and atrial natriuretic peptide in cirrhotic patients with ascites and hepatorenal syndrome

BACKGROUND: The pathogenesis of cirrhotic ascites and hepatorenal syndrome remains unresolved. The involvement of both endothelin-1 and atrial natriuretic peptide have recently been suggested. This study investigated the concentrations of serum endothelin and atrial natriuretic peptide in cirrhotic patients. METHODS: Seven healthy subjects and 31 cirrhotic patients were studied. Cirrhotic patients were divided into three groups: Group I, 16 cirrhotic patients without ascites; Group II, 10 cirrhotic patients with ascites, but without hepatorenal syndrome; and Group III, five cirrhotic patients with hepatorenal syndrome and ascites. Their sera were analyzed for endothelin-1 and atrial natriuretic peptide concentrations. RESULTS: Cirrhotic patients with ascites, Group II and Group III, had higher plasma endothelin-1 concentrations (15.9 +/- 2.3 pg/ml and 24 +/- 2.1 pg/ml, respectively) than normal subjects and compensated cirrhotics (3.8 +/- 0.7 pg/ml and 6.4 +/- 1.1 pg/ml, respectively); p < 0.001). Atrial natriuretic peptide concentrations were also significantly higher in cirrhotic patients than in normal subjects (p < 0.025). Plasma endothelin-1 concentration had a negative correlation with creatinine clearance (r = -0.65, p < 0.001), as did atrial natriuretic peptide concentrations (r = -0.44, p = 0.012). Plasma endothelin-1 correlated significantly with atrial natriuretic peptide concentrations (r = 0.38, p = 0.035). CONCLUSIONS: Both endothelin-1 and atrial natriuretic peptide concentrations were elevated in cirrhotic patients with ascites and hepatorenal syndrome. Endothelin-1 may have a negative impact on renal function. Our data also suggested that impaired responsiveness rather than impaired secretion of atrial natriuretic peptide is responsible for sodium retention in cirrhotic patients with ascites.     

Fetal liver volume measurement by three-dimensional ultrasonography: a preliminary study

The effect of all-trans retinoic acid (RA), which is known as a regulator of cell growth and differentiation, was studied during neuronal apoptosis. Apoptosis was induced in primary cultures of chick embryonic neurons by treatment with staurosporine (200 nM) for 24 h which led to a reduction of cellular viability to 40% compared to 83% in untreated cultures as well as to an increase in the number of apoptotic neurons (determined by nuclear staining with Hoechst 33258) to 60% compared to 15% in untreated cultures. RA (1 nM-10 microM) reduced the number of non-viable and apoptotic cells in a concentration-dependent manner and the maximal response was seen at 1 microM RA with 60% cellular viability and 38% apoptotic neurons. The production of mitochondrial reactive oxygen species (ROS, determined by the fluorescent indicator dihydrorhodamine) was elevated 4.4-fold after 4 h of staurosporine-treatment which was reduced to a 2-fold increase in the presence of 10 microM RA. The results indicate that RA was able to reduce apoptotic damage in staurosporine-treated chick embryonic neurons by suppressing the production of ROS.