BACKGROUND: The synthetic beta(2)-adrenergic and dopaminergic agonist dopexamine is supposed to prevent splanchnic hypoperfusion in critically ill patients, thus potentially interacting with haemodynamic effects of early enteral nutrition. However, precise mechanism of action and interaction with postprandial splanchnic hyperaemia of the drug are largely unknown, even in healthy subjects. MATERIALS AND METHODS:Twelve healthy volunteers received dopexamine 1 microg x kg(-1) min(-1) and dopexamine and placebo (NaCl 0.9%) 3 microg x kg(-1) min(-1) in a randomized, double-blinded order (crossover-design). Splanchnic (Doppler ultrasound) and systemic (noninvasive cardiac monitoring) haemodynamic parameters were assessed at baseline and during infusion (fasted as well as 15, 30, 45 and 60 min after a standard liquid meal). RESULTS: In fasted humans, dopexamine enhanced time-averaged maximum velocity (TAMX) in the superior mesenteric artery (1 microg + 40%; 3 microg + 82%, P < 0.05), portal vein (+ 63%; + 121%, P < 0.05) and femoral artery (+ 66%; + 87%, P < 0.05), in proportion to the increase of cardiac index (+ 33%; + 77%, both P < 0.05). In the postprandial state, TAMX rose significantly in the superior mesenteric artery (+ 139%) and portal vein (+ 68%) in the placebo group, showing the same absolute extent as dopexamine. The physiological postprandial buffer response of hepatic artery was conserved under all conditions. CONCLUSIONS: Continuous infusion of dopexamine enhances mesenterial and portal perfusion in a dose-dependent manner without affecting the extent of physiological postprandial hyperaemia. Thus, dopexamine and enteral nutrition may interact with splanchnic haemodynamics by different pathways.
RCT Entities:
BACKGROUND: The synthetic beta(2)-adrenergic and dopaminergic agonist dopexamine is supposed to prevent splanchnic hypoperfusion in critically illpatients, thus potentially interacting with haemodynamic effects of early enteral nutrition. However, precise mechanism of action and interaction with postprandial splanchnic hyperaemia of the drug are largely unknown, even in healthy subjects. MATERIALS AND METHODS: Twelve healthy volunteers received dopexamine 1 microg x kg(-1) min(-1) and dopexamine and placebo (NaCl 0.9%) 3 microg x kg(-1) min(-1) in a randomized, double-blinded order (crossover-design). Splanchnic (Doppler ultrasound) and systemic (noninvasive cardiac monitoring) haemodynamic parameters were assessed at baseline and during infusion (fasted as well as 15, 30, 45 and 60 min after a standard liquid meal). RESULTS: In fasted humans, dopexamine enhanced time-averaged maximum velocity (TAMX) in the superior mesenteric artery (1 microg + 40%; 3 microg + 82%, P < 0.05), portal vein (+ 63%; + 121%, P < 0.05) and femoral artery (+ 66%; + 87%, P < 0.05), in proportion to the increase of cardiac index (+ 33%; + 77%, both P < 0.05). In the postprandial state, TAMX rose significantly in the superior mesenteric artery (+ 139%) and portal vein (+ 68%) in the placebo group, showing the same absolute extent as dopexamine. The physiological postprandial buffer response of hepatic artery was conserved under all conditions. CONCLUSIONS: Continuous infusion of dopexamine enhances mesenterial and portal perfusion in a dose-dependent manner without affecting the extent of physiological postprandial hyperaemia. Thus, dopexamine and enteral nutrition may interact with splanchnic haemodynamics by different pathways.