ARE THE EFFECTS OF NORADRENALINE, ADRENALINE AND DOPAMINE INFUSIONS ON VO2 AND METABOLISM TRANSIENT

Objective: To determine whether noradrenaline, adrenaline and dopamine have persistent actions on VO2 and metabolism. Design: Descriptive la boratory investigation. Setting: Laboratory of the Department of Anaes thesiology at a University Hospital. Subjects: 9 volunteers. Intervent ion: VO2 and the plasma concontration of glucose and free fatty acids were measured prior to and during a 4 h infusion of saline (control), noradrenaline (0.14 mug/kg min) adrenaline (0.08 mug/kg min) or dopami ne (7 mug/kg min), n = 9 each. VO2 was measured using an open circuit gas exchange system. Measurements and main results: VO2 increased from 250 +/- 22 ml/min to 280 +/- 38 ml/min during noradrenaline, to 298 /- 30 ml/min during adrenaline and to 292 +/- 39 ml/min during dopamin e infusion. The plasma glucose concentration increased from 6.2 +/- 0. 6 mmol/l to 8.8 +/- 0.8 mmol/l, 13.2 +/- 1.4 and 7.3 +/- 0.4 mmol/l du ring infusion of noradrenaline, adrenaline or dopamine, respectively. The plasma free fatty acid concentration increased from 0.28 +/- 0.10 mmol/l to 0.79 +/- 0.21 mmol/l during noradrenaline and to 0.52 +/- 0. 09 mmol/l during dopamine. In contrast, free fatty acid values average d baseline values at the end of the adrenaline infusion after an initi al increase to 0.72 +/- 0.31 mmol/l. Conclusions: Administration of no radrenaline, adrenaline or dopamine resulted in persistent increases i n VO2 in volunteers. With the exception of the transient adrenaline ef fect on fatty acids the metabolic actions were steady during 4 h of ad renergic stimulation. Since the adrenergic effect on VO2 is persistent over time a similar action in patients (e.g. septic shock) during tre atment with adrenoceptor agonists may be important. Thus, an increase in VO2 during therapy may not only reflect an oxygen debt but also a p harmacodynamic action of adrenoceptor mediated calorigenic and metabol ic induction.