Splanchnic blood flow in man: evidence for mediation via a β-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⁻¹ kg⁻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⁻¹ kg⁻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)%; 10 ng of adrenaline min⁻¹kg⁻¹ and propranolol, 16.9 (10)%].

5. These data suggest that splanchnic vasodilatation is mediated via a β-adrenergic mechanism.