title: Vasodilatory state of decompensated cirrhosis: relation to hepatic dysfunction, ascites, and vasoactive substances.
abstract: The objective of this study was to determine the relations between the hallmark circulatory finding of decompensated cirrhosis, a reduced systemic vascular resistance (SVR), and the indices of hepatic decompensation, the accumulation of ascites, and the concentrations of various vasoactive substances. At a university-affiliated teaching hospital, eighteen hospitalized patients with cirrhosis and 18 age- and sex-matched healthy subjects were used. This was a case-control study. Measurements included cardiac dimensions and indices derived from echocardiograms and Doppler studies, abdominal ultrasound estimates of ascites, indices of hepatic function, and various serum (S) and urinary (U) substances. Results showed that cirrhotics had increased left atrial and left ventricular dimensions, left ventricular mass, heart rate, cardiac output (CO), transvalvular velocities, and a decreased SVR. SVR was related to hepatic dysfunction, as reflected by an abnormal prothrombin time ratio (r = -0.64, p = 0.006), and also related to overall severity of liver disease as estimated by the Child-Pugh score (r = -0.53, p = 0.044). Although cirrhotics with ascites generally had a reduced SVR, estimates of ascites were directly related to SVR (r = 0.57, p = 0.03) and inversely related to CO (r = -0.53, p = 0.04). Concentrations of S and U digoxin-like immunoreactive substance (DLIS) were also increased, but the concentrations of S glucagon and estradiol were not elevated. The accumulations of S and U DLIS, S glucagon, and S estradiol were all related to hepatic dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, Long Island College Hospital, Brooklyn, NY 11201, USA.
authors.forename: H S
authors.initials: HS
authors.lastname: Friedman
authors.forename: N
authors.initials: N
authors.lastname: Cirillo
authors.forename: F
authors.initials: F
authors.lastname: Schiano
authors.forename: P
authors.initials: P
authors.lastname: Nathan
authors.forename: S
authors.initials: S
authors.lastname: Khan
authors.forename: H
authors.initials: H
authors.lastname: Rosero
authors.forename: M
authors.initials: M
authors.lastname: Vaseghi
authors.forename: T
authors.initials: T
authors.lastname: Sacchi
authors.forename: B
authors.initials: B
authors.lastname: Vasavada
authors.forename: L
authors.initials: L
authors.lastname: Bjornson
mesh_terms: D000328:Adult; D001201:Ascites / Q000000981:diagnostic imaging / Q000503:physiopathology; D001798:Blood Proteins / Q000378:metabolism*; D002298:Cardenolides; D004077:Digoxin; D004452:Echocardiography; D015150:Echocardiography, Doppler; D004958:Estradiol / Q000097:blood*; D005260:Female; D005934:Glucagon / Q000097:blood*; D006439:Hemodynamics / Q000502:physiology; D006501:Hepatic Encephalopathy / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D008104:Liver Cirrhosis, Alcoholic / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008111:Liver Function Tests; D008297:Male; D008875:Middle Aged; D012503:Saponins; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology; D014882:Water-Electrolyte Balance / Q000502:physiology
chemical_list: D001798:Blood Proteins; D002298:Cardenolides; D012503:Saponins; C034504:digoxin-like factors; D004958:Estradiol; D004077:Digoxin; D005934:Glucagon