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

Lothar A. Schwarte, Olaf Picker, Achim W. Schindler, Artur Fournell, Thomas W.L. Scheeren

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

Objective: 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. Design: Randomized controlled animal study. Setting: University department of anesthesiology. Subjects: Eight anesthetized dogs with chronically implanted ultrasound flow probes around the pulmonary artery for continuous measurement of cardiac output. Interventions: 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 DA 1-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 H 2O), both without and with fluid resuscitation. Measurements and Main Results: 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 ḊO 2 (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. Conclusions: During compromised cardiocirculatory conditions, α1-receptor activation during dopamine infusion prevented an increase in gastric mucosal oxygenation. Furthermore, selective DA 1-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.

Original languageEnglish
Pages (from-to)150-156
Number of pages7
JournalCritical Care Medicine
Volume32
Issue number1
DOIs
Publication statusPublished - Jan 2004

Keywords

  • Animal study
  • Catecholamines
  • Compromised circulation
  • Dopamine
  • Fenoldopam
  • Gastric mucosal oxygenation
  • Mechanical ventilation
  • Mechanism of action
  • Monitoring
  • Spectrophotometry

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