Plasma catecholamines in patients with presinusoidal portal hypertension: Comparison with cirrhotic patients and nonportal hypertensive subjects

Abstract

During a hemodynamic study, plasma catecholamine concentrations were measured in the pulmonary artery and in the hepatic vein in 18 presinusoidal portal hypertensive patients. Results were compared with those in 15 nonportal hypertensive subjects and in 24 cirrhotic patients in good condition (grade A, according to Pugh's classification). Plasma norepinephrine concentrations in the pulmonary artery or in the hepatic vein were not significantly different between nonportal hypertensive subjects (mean +/- S.E.M.: 271 +/- 36 and 83 +/- 11 pg/ml, respectively) and presinusoidal portal hypertensive patients (273 +/- 33 and 84 +/- 11 pg/ml, respectively). These concentrations were, however, elevated in cirrhotic patients (408 +/- 47 and 256 +/- 45 pg/ml, p less than 0.05 in comparison with the two other groups). These differences suggest that increased sympathetic nervous activity in cirrhosis is associated with the presence of liver disease or increase in sinusoidal pressure. Differences in plasma epinephrine concentrations were not significant among the three groups of patients. However, the existence of a significant correlation between pulmonary artery plasma epinephrine concentration and cardiac index (r2 = 0.46, p less than 0.01) in patients with presinusoidal portal hypertension suggests that the adrenal medulla could play a role in the pathophysiology of the hyperkinetic syndrome of these patients.

High-density lipoproteins reduce the effect of endotoxin on cytokine production and systemic hemodynamics in cirrhotic rats with ascites

“…However, in those cases with extremely high plasma and ascitic fluid levels of cytokines, a decrease in cardiac function also develops, thus leading to severe arterial hypotension, marked activation of the endogenous vasoconstrictor systems and multiorgan failure [38]. Different mediators have been proposed for this hemodynamic derangement associated with septic shock, including NO [33], CO [39], glucagon, adenosine, calcitonin gene-related peptide [40], cathecolamines [41], platelet activating factor [6], prostacyclin [42] parathyroid hormone-related protein (PTH-rP) [43], and atrial natriuretic peptide [44] among others.…”

A Spatial Model of Hepatic Calcium Signaling and Glucose Metabolism Under Autonomic Control Reveals Functional Consequences of Varying Liver Innervation Patterns Across Species

“…An increase in blood flow serves as a proxy for simulating hepatic Ca 2+ and glycogenolytic dynamics in cases with increase in portal hypertension. Consistent with clinical findings (Joly et al, 1967;Gaudin et al, 1991), we simulated equal rates of catecholamine secretion from the adrenal glands for normotensive and portal hypertensive cases and focused our analysis on the interplay of innervation and blood flow to modulate hepatic glycogenolysis in the two cases.…”