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Text
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Pages
773-779
Issue
3
Volume
151
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Title
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N-ACETYLCYSTEINE PRESERVES OXYGEN-CONSUMPTION AND GASTRIC-MUCOSAL PH DURING HYPEROXIC VENTILATION
Publisher
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American Journal of Respiratory and Critical Care Medicine
Date
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1995
1995-03
Subject
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cardiac-output; critically-ill patients; endotoxin; gas-exchange; General & Internal Medicine; l-arginine; nitric-oxide synthesis; relaxing factor; Respiratory System; septic patients; skeletal-muscle; superoxide
Creator
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Reinhart K; Spies C D; Meierhellmann A; Bredle D L; Hannemann L; Specht M; Schaffartzik W
Description
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Hyperoxic ventilation, used to prevent hypoxemia during potential periods of hypoventilation, has been reported to paradoxically decrease whole body oxygen consumption (Vo(2)). Reduction in nutritive blood flow due to oxygen radical production is one possible mechanism. We investigated whether pretreatment with the sulfhydryl group donor and O-2 radical scavenger N-acetylcysteine (NAG) would preserve whole body Vo(2) and prevent deterioration of oxygenation in gastric mucosal tissue during hyperoxia. Thirty-eight patients, requiring hemodynamic monitoring (radial and pulmonary artery catheters) due to sepsis syndrome, were included in this randomized experiment. All patients exhibited stable clinical conditions (hemodynamics, body temperature, hemoglobin, Flo(2) < 0.5). A gastric tonometer was placed to measure the gastric intramucosal pH (pH(i)), which indirectly assesses nutritive blood flow to the mucosa. Cardiac output was determined by thermodilution and Vo(2) by cardiovascular Fick. After baseline measurements, patients randomly received either 150 mg . kg(-1) NAC (n = 19) or placebo (n = 19) in 250 ml 5% dextrose intravenously over a period of 15 min. Measurements were repeated 30 min after starting NAC or placebo infusion, 30 min after starting hyperoxia (Flo(2) = 1.0), and 60 min after resetting the original Flo(2). There were no significant differences between groups in any of the measurements before treatment and after the return to baseline Flo(2) at the end of the study. NAG, but not placebo infusion, caused a slight but significant increase in cardiac output and decrease in systemic vascular resistance. Significant differences between groups during hyperoxia were: Vo(2) (NAG: 114 +/- 9 mi min(-1) m(-2) versus placebo: 81 +/- 31 ml . min(-1) m(-2); p = 0.008) and oxygen extraction ratio (NAG: 21 +/- 6% versus placebo: 14 +/- 5%; p = 0.003). The mean decrease of Vo(2) was 11% in the NAC group versus 34% in the placebo group. The mean decrease of the oxygen extraction ratio was 12% in the NAC group versus 34% in the placebo group. NAC prevented a decrease in pH(i) in hyperoxia (NAG: 7.28 +/- 0.10 versus placebo: 7.14 +/- 0.18; p = 0.012). NAC helped preserve whole body oxygen uptake, oxygen extraction ratio, and pH(i) during brief hyperoxia in these septic patients. This suggests that pretreatment with NAC can attenuate impaired tissue oxygenation during hyperoxia.
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Journal Article
1995
American journal of respiratory and critical care medicine
Bredle D L
cardiac-output
critically-ill patients
endotoxin
gas-exchange
General & Internal Medicine
Hannemann L
Journal Article
l-arginine
Meierhellmann A
nitric-oxide synthesis
Reinhart K
relaxing factor
Respiratory System
Schaffartzik W
septic patients
skeletal-muscle
Specht M
Spies C D
superoxide