BACKGROUND: Adenosine is a potent vasoactive substance that may be responsible for mediating the altered haemodynamics found in patients with cirrhosis. AIM: The administration of oral theophylline was used to investigate the effect of adenosine receptor antagonism upon the circulation of patients with cirrhosis. METHODS: Twenty eight patients were given oral theophylline and intravascular haemodynamic measurements obtained over approximately one hour. RESULTS: After 240 mg of oral theophylline elixir the hepatic venous pressure gradient mean fell from 21.8 (2.1) to 19.9 (2.4) mm Hg (p < 0.01), and azygos blood flow fell from 481 (94) to 375 (83) ml/min (p < 0.05). There were no changes in cardiac output or systemic vascular resistance despite a fall in mean arterial pressure (92.2 (2.0) to 89.2 (1.8) mm Hg; p < 0.05) and a rise in heart rate (78.3 (3.0) to 82.4 (3.2); p < 0.001). Left renal vein flow measured by a reverse thermodilution catheter rose from 387 (91) to 601 (119) ml/ min (p < 0.05). The proportion of cardiac output perfusing the left kidney rose from 5.0 (1.3) to 9.7 (2.8)%. CONCLUSIONS: These changes indicate a significant role for adenosine in the renal vasoconstriction and a more minor role in the maintenance of portal hypertension.
BACKGROUND:Adenosine is a potent vasoactive substance that may be responsible for mediating the altered haemodynamics found in patients with cirrhosis. AIM: The administration of oral theophylline was used to investigate the effect of adenosine receptor antagonism upon the circulation of patients with cirrhosis. METHODS: Twenty eight patients were given oral theophylline and intravascular haemodynamic measurements obtained over approximately one hour. RESULTS: After 240 mg of oral theophylline elixir the hepatic venous pressure gradient mean fell from 21.8 (2.1) to 19.9 (2.4) mm Hg (p < 0.01), and azygos blood flow fell from 481 (94) to 375 (83) ml/min (p < 0.05). There were no changes in cardiac output or systemic vascular resistance despite a fall in mean arterial pressure (92.2 (2.0) to 89.2 (1.8) mm Hg; p < 0.05) and a rise in heart rate (78.3 (3.0) to 82.4 (3.2); p < 0.001). Left renal vein flow measured by a reverse thermodilution catheter rose from 387 (91) to 601 (119) ml/ min (p < 0.05). The proportion of cardiac output perfusing the left kidney rose from 5.0 (1.3) to 9.7 (2.8)%. CONCLUSIONS: These changes indicate a significant role for adenosine in the renal vasoconstriction and a more minor role in the maintenance of portal hypertension.
Authors: J Llach; P Ginès; V Arroyo; J M Salmerón; A Ginès; W Jiménez; J Gaya; F Rivera; J Rodés Journal: Hepatology Date: 1993-01 Impact factor: 17.425