[Hyperammonemia induced by propranolol in cirrhotic patients. Role of the kidney and influence of the severity of the cirrhosis].

The effect of the intravenous injection of 0.1 mg/kg of propranolol on arterial ammonemia was studied in 30 patients with alcoholic cirrhosis comparatively with 10 healthy volunteers. Moreover, in 20 patients in the cirrhotic group (10 were Pugh's grade A or B and 10 others were grade C), left renal vein catheterization was performed to follow the changes in ammonemia and glutaminemia levels simultaneously with those occurring in arterial blood. After 30 min, arterial ammonemia was significantly increased in the controls (p less than 0.02) and in the cirrhotic patients (p less than 0.001). The renal venous ammonemia was also significantly increased in all of the cirrhotic patients (p less than 0.01). In the grade A and B patients, the increase in ammonemia was more marked in the renal vein as compared with that in arterial blood (p less than 0.001). In contrast, in the grade C patients, the increase in ammonemia did not differ significantly between the two sectors. The difference in ammonia concentration between arterial and renal venous blood increased significantly after 30 min in the grade A and B patients (p less than 0.001) whereas it was stable in the grade C patients. The changes of glutaminemia in arterial and renal venous blood were not significantly different in the two groups of cirrhotic patients. These data show that, in our experimental conditions, propranolol induces arterial hyperammonemia in cirrhotic patients and that the kidney could interfere with the mechanism of hyperammonemia, at least in grade A and B patients.