References

The effects of varying rates of alcohol infusion (0.015–0.12 mg/g body weight/ min) on hepatic haemodynamics were studied in male Wistar rats. An infusion of 0.015 mg/g body weight/min alcohol had no significant effect on portal pressure (PP) or wedged hepatic venous pressure (WHVP). However, increasing rates of infusion of alcohol (0.03–0.12 mg/g body weight/min) progressively increased PP and WHVP, the maximum increase in PP occurring following an infusion of 0.12 mg/g body weight/min (6.5 ± 0.5 – 10.3 ± 0.6 mm Hg). The effect of varying rates of alcohol infusion on portal venous flow and liver blood flow was biphasic. Thus following an infusion of 0.03 mg/g body weight/min alcohol, liver blood flow (40.6 ± 4.9–54.3 ± 5.8 ml/100g/min) and portal venous flow (28.6 ± 2.9–41.3 ± 4.1 ml/min) were increased. However, following infusions of 0.06 and 0.12 mg/g body weight/min alcohol, liver blood flow and portal venous flow were decreased. The results suggest that previous conflicting reports on the effects of alcohol on hepatic haemodynamics may be related to the dose of alcohol administered.

The effects of systemic and intraportal administration of propranolol on hepatic haemodynamics were studied in cirrhotic and non-cirrhotic rats. In the non-cirrhotic rat systemic infusion of 4 micrograms (kg body wt)-1 min-1 propranolol significantly decreased portal pressure, wedged hepatic venous pressure, portal venous flow and liver blood flow without affecting heart rate. Similar changes were observed in the cirrhotic rat following an infusion of 2 micrograms (kg body wt)-1 min-1 propranolol. Higher rates of propranolol infusion produced greater reductions in portal pressure, wedged hepatic venous pressure, portal venous flow and liver blood flow in cirrhotic and non-cirrhotic rats but these changes were accompanied by a bradycardia. The reduction in portal pressure effected by propranolol was accompanied by an increased splanchnic vascular resistance. Intraportal injection of propranolol resulted in a rapid but transient fall in portal pressure. The decrease in portal pressure was sustained if propranolol was infused intraportally. The results indicate that propranolol effects a reduction in portal pressure via a combination of increased splanchnic vascular resistance, increased hepatic arterial resistance and reduced cardiac output. The observation that propranolol can significantly reduce portal pressure without affecting heart rate may be clinically important in the long-term management of portal hypertension. Furthermore, the rapid reduction in portal pressure following intravenous administration suggests that propranolol may be of value in the acute control of variceal haemorrhage.

No abstract

hepatic encephalopathy does not affect GABA uptake by the brain. These data were confirmed by assay of GABA levels in the brain of comatose rats. Using the most reliable and sensitive technique for assay of GABA, the gas chromatograph-mass spectrometer technique, we demonstrated that GABA levels in the brain are not increased during hepatic coma in rats and thus far, no evidence has been provided that GABA is increased in the brain in experimental hepatic encephalopathy. We also stressed that assay of GABA levels does not reflect levels of GABA in the GABAergic nerve terminals since there are at least three different pools of GABA in the brain. The best index to changes in GABA synthesis in nerve terminals is assay of glutamic acid decarboxylase activity which is decreased in hepatic encephalopathy (2).These data support the concept of upregulation of GABA receptors in hepatic encephalopathy (3). Zeneroli ML, IulianoE, Racagni G, et al. Metabolism and brain uptake of y-aminobutiric acid in galactosamine-induced hepatic encephalopathy in rats. J Neurochem 1982; 381219-1222. 3. Baraldi M, Zeneroli ML. Experimental hepatic encephalopathy: changes in the binding of y-aminobutyric acid. Science 1982; 216:427-428.