General and splanchnic hemodynamics (radioactive microspheres), renal function, spontaneous and histamine-mediated vasopermeability and albumin distribution space were studied in conscious control and nonascitic cirrhotic rats, before and after a moderate and sustained saline infusion (3% of body weight per 30 min + repletion of urinary losses). In basal conditions, cirrhotic rats showed lower fractional sodium excretion than did control rats (0.09 ± 0.01 vs. 0.15 ± 0.01%, p < 0.005). In addition, cirrhotic animals showed higher cardiac output (161.4 ± 12.8 ml per min) and lower total peripheral resistance (0.63 ± 0.05 mm Hg-min per ml) and mean arterial pressure (102.9 ± 3.9 mm Hg) than did control rats (cardiac output: 89.0 ± 7.6; total peripheral resistance: 1.31 ± 0.11; mean arterial pressure: 117.5 ± 5.11; p < 0.005). No differences in portalsystemic shunt rate or vasopermeability between both groups were observed. After saline infusion, fractional sodium excretion increased to 4.31 ± 0.16% in controls but only 2.11 ± 0.02% in cirrhotic animals. In this group, cardiac output decreased by 49.6 ± 5.1% whereas mean arterial pressure and total peripheral resistance increased by 7.1 ± 0.6 and 112 ± 10%, respectively. In control rats, no significant hemodynamic changes were observed. Blood gases did not change after expansion in any group. Saline infusion induced an increase in histamine-mediated vasopermeability in cirrhotic rats but not in control rats. Also albumin distribution space increased more in cirrhotic than in control animals. Heart weight was higher in cirrhotic rats.
These results suggest that the lack of adequate natriuretic response to saline infusion in cirrhotic animals is a multifactorial phenomenon. An ineffective replenishment of the vascular tree produced by increased vasopermeability and the probable existence of cardiomyopathy in cirrhotic rats could also explain the experimental findings.