To test whether dopexamine, a dopaminergic and β2-adrenergic receptor agonist, would: a) direct a greater share of cardiac output to gut than to muscle when used to increase systemic oxygen delivery (Do2) in endotoxic dogs; and b) enhance the ability of peripheral tissues to extract oxygen.
Two groups of eight dogs infused for 1 hr with 2 mg/kg Escherichia coli endotoxin. One group was continually infused with dopexamine (12 μg/min.kg) and the other group was not (control group). After 2 hrs, oxygen extracting ability was challenged by changing inspired gas to 12% oxygen for 30 mins.
Anesthetized, paralyzed, pumpventilated mongrel dogs.
Donor RBCs and dextran used during endotoxin infusion to maintain cardiac output while preserving hematocrit near 40%.
Measurements and Main Results
In the dopexamine-treated group, cardiac output, systemic Do2, and oxygen consumption (Vo2) were higher than in the control group during the first 90 mins, but were not thereafter. Gut and muscle blood flow did not differ between groups, but the fraction of cardiac output going to each region tended to be less in the dopexamine-treated dogs. Arterial lactate values increased to about 6 mmol/L in all dogs. In both groups, limb muscle first produced lactate but then took up lactate after the first hour. The gut in controls converted from lactate uptake in the first hour to producing about 20 μmol/min.100 g, whereas the gut never produced lactate in the dopexamine-treated group. During hypoxia, systemic Do2 and Vo2 decreased only in the dopexamine-treated group, even though oxygen extraction was only slightly above 40%. Oxygen extraction was not demonstrably improved by dopexamine treatment.
Dopexamine temporarily increased systemic Do2 and Vo2 in volume-expanded endotoxic dogs during normoxia and may have caused gut mucosa to be preferentially perfused and thus to be kept better oxygenated. (Crit Care Med 1991; 19:1552)