Dopamine under α1-blockade, but not dopamine alone or fenoldopam, increases depressed gastric mucosal oxygenation*

Abstract

To compare the effects of dopamine, both in the presence and absence of α1-blockade, and fenoldopam on microvascular gastric mucosal oxygenation and systemic oxygen transport under compromised circulatory conditions, both without and with fluid resuscitation.

Randomized controlled animal study.

University department of anesthesiology.

Eight anesthetized dogs with chronically implanted ultrasound flow probes around the pulmonary artery for continuous measurement of cardiac output.

On different days, the dogs received in random order either dopamine (2.5 and 5.0 μg·kg−1·min−1, with or without α1-blocker pretreatment), the selective DA1-agonist fenoldopam (0.1 and 1.0 μg·kg−1·min−1, with and without DA1-blocker pretreatment), or saline (control). These interventions were performed under compromised cardiocirculatory conditions (induced by ventilation with positive end-expiratory pressure [PEEP] of 10 cm H2O), both without and with fluid resuscitation.

We continuously measured regional microvascular hemoglobin saturation (μHbO2) in gastric mucosa by reflectance spectrophotometry and systemic oxygen transport (ḊO2). Ventilation with PEEP significantly decreased ḊO2 (from 19 ± 2 to 9 ± 1 mL·kg−1·min−1, mean ± sem) and gastric mucosal μHbO2 (from 57 ± 2% to 37 ± 3%). Fluid resuscitation restored ḊO2 back to baseline (from 9 ± 1 to 19 ± 2 mL·kg−1·min−1) but only partially restored μHbO2 (from 37 ± 3% to 50 ± 4%). Under both conditions, dopamine with and without α1-blockade significantly increased ḊO2 (by about 5 mL·kg−1·min−1 in the nonresuscitated state and 10 mL·kg−1·min−1 in the fluid resuscitated state, respectively), but only dopamine in the presence of α1-blockade also significantly increased gastric mucosal μHbO2 (by 5 ± 1% and 7 ± 2% in the nonresuscitated and fluid resuscitated states, respectively). Fenoldopam under all study conditions did not significantly affect ḊO2 or μHbO2, either in the presence or absence of DA1-blockade.

During compromised cardiocirculatory conditions, α1-receptor activation during dopamine infusion prevented an increase in gastric mucosal oxygenation. Furthermore, selective DA1-stimulation (by fenoldopam) was insufficient to overcome the PEEP-induced depression of μHbO2. The responses of gastric mucosal oxygenation did not parallel changes in systemic oxygen transport. These findings were independent of fluid resuscitation.