Effects of N-(2-mercaptopropionyl)-glycine on postischemic contractile function in ischemic/reperfused hearts. Dissociation of thiobarbiturate-reacting substance formation and contractile dysfunction.
The present study was undertaken to determine whether N-(2-mercaptopropionyl)-glycine, a membrane-permeable antioxidant agent, improves the ischemia/reperfusion-induced cardiac contractile dysfunction. Rat isolated hearts were subjected to a 35 min global ischemia, followed by a 60 min reperfusion. Ischemia/reperfusion did not result in the recovery of postischemic left ventricular developed pressure. Reperfusion markedly increased the content of the thiobarbiturate-reacting substance in the myocardium. Treatment of the perfused heart with 1 mM of N-(2-mercaptopropionyl)-glycine, either during a 30 min pre-ischemia or during a 30 min pre-ischemia and the first 10 min of reperfusion, resulted in an appreciable recovery of the postischemic left ventricular developed pressure and an attenuation of the increase in thiobarbiturate-reacting substance content. When hearts were treated with the same concentration of the agent only during the first 10 min of reperfusion, the cardiac contractile function was not improved during reperfusion despite the increase in thiobarbiturate-reacting substance content of the reperfused myocardium. These results suggest that the increase in thiobarbiturate-reacting substance content during reperfusion is independent of the postischemic contractile failure.
Tanonaka
K
K
Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Japan.
Yoneda
M
M
Kamiyama
T
T
Liu
J
J
Takeo
S
S
D000818:Animals; D003402:Creatine Kinase / Q000187:drug effects; D004195:Disease Models, Animal; D005998:Glycine / Q000502:physiology*; D006321:Heart / Q000187:drug effects*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects* / Q000502:physiology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar
D003402:Creatine Kinase; D005998:Glycine