Ischemic preconditioning is not mediated by free radicals in the isolated rabbit heart.
Preconditioning has been implicated to involve a free radical mechanism in the in vivo infarct size model. We have demonstrated preconditioning in the isolated rabbit heart and studied the effect of Mn-superoxide dismutase (SOD) on preconditioning. Buffer perfused control hearts (C) were subjected to 1-h global ischemia followed by 1-h reperfusion, and the percent recovery of developed tension (%DT; relative to preischemic) was measured via a left ventricular balloon connected to a polygraph recorder. The coronary effluent was assayed for lactate dehydrogenase release (LDH; IU/kg BW). Preconditioned hearts (P) received a single episode of 5-min ischemia and 5-min reperfusion before 1 h of ischemia and reperfusion. SOD treated hearts received SOD at 5 mg/L in the buffers at all times. The results show that while SOD attenuated enzyme release and functional loss in control hearts, it had no effect on preconditioned hearts. Therefore, preconditioning is unlikely to be mediated by superoxide anion in the isolated rabbit heart.
Omar
B A
BA
Webb-Waring Lung Institute, University of Colorado, Denver 80262.
Hanson
A K
AK
Bose
S K
SK
McCord
J M
JM
D000818:Animals; D003327:Coronary Disease / Q000097:blood / Q000201:enzymology / Q000517:prevention & control*; D005609:Free Radicals; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000097:blood; D009200:Myocardial Contraction / Q000187:drug effects; D015425:Myocardial Reperfusion; D011817:Rabbits; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism*
D005609:Free Radicals; D013481:Superoxides; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase