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 less than 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 less than 0.005). No differences in portal-systemic 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Rats with CCl4-induced cirrhosis of the liver show histological and clinical features that closely resemble those of the disease in humans. Metabolic cages were used and hemodynamic studies (15-micrograms radioactive microspheres) were performed on 10 conscious, nonascitic, cirrhotic rats and in 10 control rats. Compared with control animals, cirrhotic rats showed lower sodium excretion (0.80 +/- 0.07 vs. 1.01 +/- 0.07 meq/day), total solute excretion (12.52 +/- 0.79 vs. 19.38 +/- 3.7 mosmol/day), and increased aldosterone excretion. No differences were observed in urinary epinephrine and norepinephrine excretion. Cirrhotic rats showed also slight hypotension, increased cardiac output (48.97 +/- 3.94 vs. 26.97 +/- 2.3 ml X min-1 X 100 g-1) without tachycardia, and decreased total peripheral resistance, which was mainly attributed to reduced renal and skeletal muscle resistances with increased blood flow throughout these areas. Cirrhotic rats showed increased hepatic vascular resistances by both portal and arterial inputs with portal hypertension (16.15 +/- 1.01 vs. 9.60 +/- 0.77 cmH2O) but without differences in total hepatic blood flow or portal-systemic shunt rate with respect to control rats. Plasma renin content was not significantly different between the groups of rats. From these data it can be concluded that nonascitic, cirrhotic rats show a hyperdynamic circulatory state, which seems to be caused by a peripheral vasodilation of unknown mechanism; portal-systemic shunting does not seem to be a necessary condition for the hyperdynamic status at this early stage of the hemodynamic disturbances.

Portal hypertension was produced experimentally in rats by partial constriction of the portal vein. Twelve rats were injected daily with indomethacin, 4 mg/kg body weight, and 12 with the vehicle (80% ethanol, 0.5 ml/day). There were no differences in portal-systemic shunts nor systemic or splanchnic haemodynamics between indomethacin-treated and untreated rats. These results suggest that cyclo-oxygenase products do not play a significative role in haemodynamic alterations shown by portal-ligated rats.

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Kidney function and tubular handling of water and sodium by superficial nephrons, packed cell volume, total plasma proteins and albumin distribution space were studied in control and cirrhotic rats before and after a moderate and sustained saline infusion (3% body weight per 30 min + reposition of urinary losses). Tubular fluid samples were obtained from late proximal, early distal and late distal convolutions of superficial nephrons using micropuncture. Protein distribution was assessed by intravenous injection of 0.5 muCi of (125I)-albumin. In basal conditions, both groups of rats showed similar glomerular filtration rate and renal plasma flow, but cirrhotic animals had lower sodium excretion (fractional excretion of sodium = 0.04 +/- 0.01% vs. 0.22 +/- 0.02%, p less than 0.05) and urinary volume (4.31 +/- 0.41 vs. 7.57 +/- 0.53 microliter per min; p less than 0.05). After saline infusion, total plasma proteins decreased more in cirrhotic than in control rats (-18.5 +/- 2.7 vs. -12.9 +/- 2.2%, p less than 0.05). The opposite was observed for albumin distribution space (34.5 +/- 6.1 vs. 22.1 +/- 3.5%, p less than 0.05). Fractional sodium excretion increased to 2.98 +/- 0.15% in control rats but only to 0.61 +/- 0.080% in cirrhotic rats. The ratio single nephron glomerular filtration rate/glomerular filtration rate increased from 19.6 +/- 0.7 to 21.2 +/- 1.0 (X10(-6), p less than 0.005) in control animals but did not change in cirrhotic rats. These animals were unable to decrease adequately fractional fluid reabsorption in the proximal tubule and the loop of Henle.(ABSTRACT TRUNCATED AT 250 WORDS)