Hydrogen peroxide mediates reperfusion injury in the isolated rat heart.
In an isolated, normothermic rat heart model (Langendorff, 37 degrees C), dimethylthiourea (DMTU) infusion only during reperfusion reduced both injury and measurable hydrogen peroxide (H2O2) concentrations after global ischemia. Cardiac function was assessed by measurement of ventricular developed pressure (DP). H2O2 was assessed using H2O2 dependent aminotriazole inactivation of myocardial catalase. Depletion of xanthine oxidase by two methods (tungsten or allopurinol inhibition) also improved recovery of function and H2O2 production. The results indicate that XO derived H2O2 contributes to myocardial reperfusion injury.
Brown
J M
JM
Department of Surgery, University of Colorado Health Sciences Center, Denver.
Terada
L S
LS
Grosso
M A
MA
Whitman
G J
GJ
Velasco
S E
SE
Patt
A
A
Harken
A H
AH
Repine
J E
JE
D000640:Amitrole; D000818:Animals; D002374:Catalase / Q000032:analysis; D003326:Coronary Circulation; D006321:Heart / Q000503:physiopathology*; D006861:Hydrogen Peroxide / Q000378:metabolism*; D066298:In Vitro Techniques; D009206:Myocardium / Q000201:enzymology; D051381:Rats; D015427:Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control; D013890:Thiourea / Q000031:analogs & derivatives / Q000494:pharmacology; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors
C038983:1,3-dimethylthiourea; D006861:Hydrogen Peroxide; D002374:Catalase; D014969:Xanthine Oxidase; D013890:Thiourea; D000640:Amitrole