The galactose elimination capacity, a measure of the functional liver cell mass, and liver volume were measured in 50 normal subjects of five different age groups (less than 50, 51 to 60, 61 to 70, 71 to 80 and greater than 81 years). The volume of the liver was evaluated by ultrasonography. All subjects had normal routine liver function tests and no history of liver disease. Galactose elimination progressively decreased from 3.05 +/- 0.58 (S.D.) mmoles per min in younger subjects to 1.83 +/- 0.24 mmoles per min in subjects over 81 (p less than 0.00003), without any change in the apparent volume of distribution of the sugar. Similarly, the estimated volume of the liver decreased from 110 +/- 14 units to 75 +/- 13 units with increasing age (p less than 0.0002). Both galactose elimination capacity and the estimated liver volume inversely correlated with age (r = -0.728 and r = -0.579, respectively) whereas a positive correlation was observed between galactose elimination and the estimated liver volume (r = 0.520). Part correlation analysis confirmed that age, when entered in a multiple regression already containing body weight and estimated liver volume as independent variables, had a significant effect on liver function, whereas no significant independent effect of liver volume was present. Both age and body weight had a significant independent effect on the estimated liver volume. The maximum functional capacity of the liver, measured by galactose elimination, is reduced in the elderly. Although several factors may play a role, our data suggest that aging is associated with a slight decline in the intrinsic metabolic activity of the hepatic parenchyma.

Blood flow in the splanchnic veins was studied in cirrhotics and matched controls by means of a system that combines a mechanical sector scanner with a pulsed Doppler. The measurements were validated in an in vitro model. Echo-doppler studies could be carried out reproducibly in only approximately two-thirds of cases because of poor echo transmission or incomplete cooperation. Portal blood velocity was significantly reduced in cirrhotics (10.5 +/- 0.6 cm/s versus 16.0 +/- 0.5 in controls; p less than 0.001), but portal blood flow was normal because of enlarged portal caliber. A complete hemodynamic evaluation of the splenic and superior mesenteric veins was possible in only a few subjects. In selected patients the technique may prove relevant in the study of hemodynamic effects of drugs and surgery on portal blood flow.

The drugs currently under investigation in the prevention of recurrent gastrointestinal bleeding in cirrhosis are likely to decrease the portal pressure by means of a primary reduction of portal blood flow. The hemodynamic effects of beta-blocking agents and vasodilatory drugs were noninvasively measured in eight patients with cirrhosis by means of pulsed echo-doppler equipment. Portal caliber, blood velocity and flow were recorded hourly after a single dose of propranolol (40 mg p.o.) or atenolol (100 mg p.o.), and every 5 min after treatment with isosorbide dinitrate (5 mg sublingually). The drugs were administered at random with an interval of 2 days or more. The portal caliber decreased after atenolol, but did not change after propranolol and isosorbide. The blood velocity decreased by 29 +/- 2% 3 hr after propranolol, by 26 +/- 2% 3 hr after atenolol and by 31 +/- 3% 15 min after isosorbide. The portal blood flow decreased by 0.29 +/- 0.03 liters per min after propranolol, by 0.34 +/- 0.06 after atenolol and by 0.26 +/- 0.03 after isosorbide, without any difference among the various treatments. beta-blockers and vasodilatory drugs have comparable effects on portal blood flow. beta 1-selective and nonselective beta-blockers are similarly effective in keeping with the hypothesis that changes in portal blood flow are mainly due to the block of beta 1-receptors.