ARTERIAL UNDERFILLING DOES NOT CAUSE SODIUM RETENTION IN CIRRHOSIS

PURPOSE: To test the peripheral arterial vasodilation hypothesis of so dium retention in cirrhosis. This states that sodium retention is trig gered by arterial underfilling and predicts that development of sodium retention will be associated with significant and related declines in indices of arterial filling that reverse when sodium retention resolv es. DESIGN: Longitudinal evaluation of a cohort of patients with alcoh olic liver disease. PATIENTS AND METHODS: Eighteen men, 8 of whom were studied twice, 3 three times, 2 four times, and 5 rive times (40 betw een-study comparisons). Between 23 studies, the patients were ascites- free (Group NN). Ascites spontaneously disappeared between seven studi es (Group YN), appeared between six studies (Group NY), and remained p resent between four studies (Group YY). Between-study changes in blood volume, arterial blood pressure, cardiac output, systemic vascular re sistance, left atrial volume, left ventricular diastolic diameter, aor tic root diameter, aortic blood velocity, plasma norepinephrine and at rial natriuretic factor concentrations, plasma renin activity, and uri nary sodium excretion were evaluated by paired t-tests. These changes were also compared among groups by analysis of variance. In addition, correlations among the changes were sought. RESULTS: Systolic, diastol ic, and mean arterial pressures, left ventricular diastolic diameter, aortic root diameter, stroke volume, cardiac output, plasma norepineph rine concentration, and systemic vascular resistance were unchanged be tween studies. Left atrial volume increased between studies in Group N Y. Pulse pressure fell more in Group NY than in Groups NN and YN, prin cipally as a result of a decline in systolic blood pressure. Plasma no repinephrine concentration, plasma renin activity, and blood volume ro se more in Group NY than in Groups NN, YN, and YY. Changes in both sys tolic and pulse pressures were directly correlated with the change in sodium excretion but unrelated to the change in plasma norepinephrine concentration. Changes in plasma norepinephrine concentration and plas ma renin activity were unrelated to changes in blood pressure, systemi c vascular resistance, and urinary sodium excretion. CONCLUSIONS: None of the indices of arterial filling tested except pulse pressure were related to sodium retention. Reduced pulse pressure is inconsistent wi th arterial underfilling, as peripheral vasodilation instead increases pulse pressure by increasing diastolic run-off. These data do not sup port the hypothesis that arterial underfilling is the stimulus for sod ium retention in alcoholic cirrhosis.