Abstract
Numerous strategies have been designed to protect the myocardium against reactive oxygen species (ROS). The present study was designed to test wether LPBNAH, a new amphiphilic spin-trap derived from PBN is able to protect isolated perfused rat hearts against ROS injuries. Following total glola ischemia (30 min), hearts were reperfused in the presence or not of LPBNAH (10 micromol/l), and left ventricular function was continuously monitored. The addition of LPBNAH led to a significant recovery in left ventricular developped pressure (LVDevP, control: 16.5+/- 7.5, p < 0.05). To conclude, the present results strongly suggest that the modification of previous wellknown molecules in order to facilitate their access to intracellular site of ROS production might be of interest to limit oxidative stresses.
MeSH terms
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Animals
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Cyclic N-Oxides
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Disaccharides / chemistry
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Disaccharides / pharmacology*
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Disaccharides / therapeutic use
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Heart / drug effects*
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Heart / physiopathology
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Heart Rate / drug effects
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Imines / chemistry
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Imines / pharmacology*
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Imines / therapeutic use
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In Vitro Techniques
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Myocardium / metabolism*
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Neuroprotective Agents / chemistry
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Neuroprotective Agents / pharmacology*
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Nitrogen Oxides / chemistry
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Nitrogen Oxides / pharmacology*
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Oxidative Stress / drug effects
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Perfusion / methods
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Rats
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Rats, Wistar
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Reactive Oxygen Species / antagonists & inhibitors*
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Reactive Oxygen Species / metabolism
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Spin Labels
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Spin Trapping
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Time Factors
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Ventricular Function, Left / drug effects
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Ventricular Function, Left / physiology
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Ventricular Pressure / drug effects
Substances
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Cyclic N-Oxides
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Disaccharides
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Imines
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LPBNAH compound
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Neuroprotective Agents
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Nitrogen Oxides
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Reactive Oxygen Species
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Spin Labels
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phenyl-N-tert-butylnitrone