Splanchnic blood flow in man: evidence for mediation via a beta-adrenergic mechanism

1. Superior mesenteric artery blood flow was examined by Doppler ultrasound in six male subjects aged 19-23 years during the infusion of saline (control), 10 and 40 ng of adrenaline min-1kg-1 for 30 min, or propranolol and 10 ng of adrenaline min-1kg-1 for 30 min, on four separate occasions. 2. Adrenaline infusion resulted in significant peak mean (SEM) rises in circulating adrenaline concentrations during the infusion period only [control, 0.20 (0.05) nmol/l; 10 ng of adrenaline min-1kg-1, 1.37 (0.29) nmol/l; 40 ng of adrenaline min-1kg-1, 3.73 (0.40) nmol/l; 10 ng of adrenaline min-1kg-1 and propranolol, 1.48 (0.16) nmol/l, P < 0.001 versus control]. These values are within the physiological range. 3. Superior mesenteric artery blood flow rose in a dose-dependent manner during the adrenaline infusions alone, but not during the infusion of adrenaline and propranolol [mean (95% confidence interval) area under the curve: control, -4.2 (-11 to +2.7)%; 10 ng of adrenaline min-1kg-1, +4 (-1 to 11.9)%; 40 ng of adrenaline min-1kg-1, +34 (+6.5 to +61.5)%; 10 ng of adrenaline min-1kg-1 and propranolol, -8.4 (-23 to +6)%]. 4. Superior mesenteric artery resistance fell during the adrenaline infusions alone and rose during the combined adrenaline and propranolol infusion [mean (SEM) area under the curve: control, 6.4 (2.7)%; 10 ng of adrenaline min-1kg-1, -2.9 (2.5)%; 40 ng of adrenaline min-1kg-1, -15 (1.4)%; 10ng of adrenaline min-1kg-1 and propranolol, 16.9 (10)%]. 5. These data suggest that splanchnic vasodilatation is mediated via a beta-adrenergic mechanism.