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Articles in PresS, published online ahead of print October 10, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00563.2002
Submitted on July 8, 2002
Accepted on October 4, 2002
1 University of Southern California, The Heart Institute, Good Samaritan Hospital, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: ThorstenReffelmann{at}web.de.
Two independent cardioprotective interventions, Na+/H+-exchange inhibition and ischemic preconditioning (PC), were investigated with respect to differential effects on microvascular and myocardial salvage in anesthetized rabbits (30 minutes ischemia, 180 minutes reperfusion). 300 µg/kg cariporide before occlusion and PC reduced infarct size (IS, triphenyltetrazolium) (control: 46.0±4.2% of RA (risk area), cariporide: 17.6±3.7% (p<0.01), PC: 27.5±4.1% (p<0.01)), and concomitantly anatomic no-reflow (ANR, thioflavin S) (control: 40.4±3.7%, cariporide: 19.0±2.9% (p<0.01), PC: 26.9±3.4% (p<0.05)). Regional myocardial blood flow (RMBF, radioactive microspheres) in the RA, deteriorating between 30 and 180 minutes of reperfusion (control: 79±6% to 26±2% of non-ischemic flow), was shifted to higher values with both treatments (Cariporide: 110±12% to 49±7%, p<0.05, PC: 109±8% to 38±6%, p<0.05). However, neither intervention uncoupled the close relationship between IS and ANR (r=0.92-0.95) or RMBF. Cariporide given at reperfusion, did not alter IS, ANR, RMBF, or their close interrelationships. Since size and spatial distribution of no-reflow and myocardial necrosis remained closely coupled with independent cardioprotective interventions, a potential causal connection between microvascular and myocardial salvage is discussed.
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