TY - JOUR
T1 - Dopamine under α1-blockade, but not dopamine alone or fenoldopam, increases depressed gastric mucosal oxygenation
AU - Schwarte, Lothar A.
AU - Picker, Olaf
AU - Schindler, Achim W.
AU - Fournell, Artur
AU - Scheeren, Thomas W.L.
PY - 2004/1
Y1 - 2004/1
N2 - 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.
AB - 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.
KW - Animal study
KW - Catecholamines
KW - Compromised circulation
KW - Dopamine
KW - Fenoldopam
KW - Gastric mucosal oxygenation
KW - Mechanical ventilation
KW - Mechanism of action
KW - Monitoring
KW - Spectrophotometry
UR - http://www.scopus.com/inward/record.url?scp=1342309270&partnerID=8YFLogxK
U2 - https://doi.org/10.1097/01.CCM.0000099340.53754.5B
DO - https://doi.org/10.1097/01.CCM.0000099340.53754.5B
M3 - Article
C2 - 14707574
SN - 0090-3493
VL - 32
SP - 150
EP - 156
JO - Critical Care Medicine
JF - Critical Care Medicine
IS - 1
ER -