Our results provide objective evidence for the amphetamine-like stimulatory effects of khat leaves. These effects were closely similar to those observed after cathinone, 0.5 mg/kg body weight, although peak plasma concentrations of cathinone after khat were delayed.

This study provides evidence for abnormal autonomic functioning in patients with erythrophobia when under mental stress.

Increased levels of natural benzodiazepine receptor agonists, produced in the body (endogenous) or ingested with food (exogenous) have been proposed as one of the factors causing hepatic encephalopathy in both experimental animals and human subjects. However, the divergent response of hepatic encephalopathy to benzodiazepine antagonists sheds doubt on this attractive hypothesis. Acute liver failure was induced in male Sprague-Dawley rats (n = 17) with intraperitoneal thioacetamide (600 mg/kg/day for 3 days) while 14 control rats received vehicle only. Acute liver failure developed in all treated rats (AST: 1,898 +/- 1,359 IU/L vs. controls, 45 +/- 5 IU/L, p < 0.005; bilirubin: 36 +/- 27 mumol/L vs. controls, 1.5 +/- 0.5 mumol/L, p < 0.005; centrizonal necrosis) and grade 3 or 4 hepatic encephalopathy (neurologic assessment and activity monitoring). However, benzodiazepine receptor ligand activity, measured in the supernatant of whole-brain homogenates with a [3H]flumazenil binding competition assay, was clearly increased in only 1 of 17 rats with acute liver failure compared with controls (52.7 +/- 34.1 vs. 44.3 +/- 18.9 ng diazepam equivalents/gm; NS). To evaluate whether the reported increase in benzodiazepine receptor ligand activity could be due to prolonged residence of exogenous benzodiazepine-like substances, additional rats with acute liver failure and controls were treated with diazepam (five doses of 0.5 mg/kg at 12-hr intervals by gavage). Benzodiazepine receptor ligand activity was greater in animals with acute liver failure than in controls (223 +/- 65 vs. 103 +/- 23 ng diazepam equivalents/gm; p < 0.002) 1 to 3 hr after the last diazepam dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased levels of natural benzodiazepine receptor agonists, produced in the body (endogenous) or ingested with food (exogenous) have been proposed as one of the factors causing hepatic encephalopathy in both experimental animals and human subjects. However, the divergent response of hepatic encephalopathy to benzodiazepine antagonists sheds doubt on this attractive hypothesis. Acute liver failure was induced in male Sprague-Dawley rats (n = 17) with intraperitoneal thioacetamide (600 mg/kg/day for 3 days) while 14 control rats received vehicle only. Acute liver failure developed in all treated rats (AST: 1,898 +/- 1,359 IU/L vs. controls, 45 +/- 5 IU/L, p < 0.005; bilirubin: 36 +/- 27 mumol/L vs. controls, 1.5 +/- 0.5 mumol/L, p < 0.005; centrizonal necrosis) and grade 3 or 4 hepatic encephalopathy (neurologic assessment and activity monitoring). However, benzodiazepine receptor ligand activity, measured in the supernatant of whole-brain homogenates with a [3H]flumazenil binding competition assay, was clearly increased in only 1 of 17 rats with acute liver failure compared with controls (52.7 +/- 34.1 vs. 44.3 +/- 18.9 ng diazepam equivalents/gm; NS). To evaluate whether the reported increase in benzodiazepine receptor ligand activity could be due to prolonged residence of exogenous benzodiazepine-like substances, additional rats with acute liver failure and controls were treated with diazepam (five doses of 0.5 mg/kg at 12-hr intervals by gavage). Benzodiazepine receptor ligand activity was greater in animals with acute liver failure than in controls (223 +/- 65 vs. 103 +/- 23 ng diazepam equivalents/gm; p < 0.002) 1 to 3 hr after the last diazepam dose.(ABSTRACT TRUNCATED AT 250 WORDS)

CORRESPONDENCE 541 RI, demonstrated by Mostbeck et al. (13) in normal subjects, is related to the higher end-diastolic frequency shift with the reduction of cardiac cycle. In our cirrhotic patients, resistance indexes directly correlated with heart rate. As Colli et al. suggest, renal vasoconstriction evaluated by resistance indexes could be partly hidden by the simultaneous increase of heart rate. Thus, the correlation would be underestimated. We calculated RI corrected for heart rate according to Mostbeck [corrected RI = observed RI-0.0026 * (80-observed heart rate)], and the r value of the correlation between corrected RI and heart rate was 0.66, whereas that between RI and heart rate was 0.33 ( Fig. 1). Thus, the observation of Colli et al. only further emphasizes our hypothesis.We hope we have been able to clarify all the points raised. REFERENCES 1. Sacerdoti D, Bolognesi M, Merkel C, Angeli P, Gatta A. Renal vasoconstriction in cirrhosis evaluated by duplex Doppler ultrasonography. HEPATOLOGY 1993;17:219-224. 2. Platt JF, Marn CS, Baliga PK, Ellis JH, Rubin JM, Merion RM.Renal dysfunction in hepatic disease: early identification with 3. 4. 5. 6. 7.8. 9. 10. 11.duplex Doppler US in patients who undergo liver transplantation. Radiology 1992; 1835301-805. Colli A, Cocciolo M, Riva C, Martinez E. Abnormal renovascular impedence in patients with hepatic cirrhosis: detection with duplex US. Radiology 1993;187:561-563. Maroto A, Gines A, Salo J, Gines P, Jiminez W, Arroyo V. Diagnosis of renal failure of cirrhosis by Doppler sonography: prognostic value of resistive index. J Hepatol 1993; 18(suppl 1):S145. JH. Distinction between obstructive and non-obstructive pyelocaliectasis with duplex Doppler sonography . AJR Am J Roentgenol 1989;153:997-1000. Rodgers PM, Bates JA, Irving HC. Intrarenal Doppler ultrasound studies in normal and acutely obstructed kidneys. Br J Radio1 Sabba C, Merkel C, Zoli M, Ferraioli G, Gaiani S, Sacerdoti D, Bolondi L. Operators, machines, and a time interval variability of echo-Doppler flowmetry for portal hemodynamics. J Hepatol 1993; 18(suppl 1):S166. Arroyo V, Gines P, Planas R, Panes J, Rodes J . Management of patients with cirrhosis and ascites. Semin Liver Dis 1986;6: