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Reestablishment of blood supply to ischemic myocardium leads to biochemical and cellular changes which are believed to reduce the amount of potentially salvageable myocardium (reperfusion injury). In this situation, adenosine is known to have myocardial protective properties. Activation of adenosine A2-receptors may account for most of the beneficial effects of adenosine in reperfusion injury because A2-receptor activation mediates vasodilation, inhibits neutrophil adhesion to vascular endothelium and diminishes generation of free radicals by neutrophils, thus acting on some of the key mechanisms of reperfusion injury such as postischemic vascular dysfunction and neutrophil-mediated damage. Therefore, we investigated the effect of an intracoronary A2-agonist, CGS 21680, on regional postischemic myocardial function (measured as wall thickening) and infarct size determined by triphenyltetrazolium chloride (TTC) staining. Fourteen anesthetized open-chest dogs underwent 1-h left anterior descending artery (LAD) occlusion and 6-h reperfusion and were randomly assigned to receive intracoronary CGS 21680 or to serve as control. The drug was infused for 60 min starting 5 min before reperfusion with a concentration of 10 -7M at a rate of 10 ml/min under anoxic conditions. The infusion was then continued for the first 55 min of reperfusion with 10 -6M at a rate of 1 ml/min. Intracoronary infusion of CGS 21680 led to significant improvement in regional wall function in postischemic myocardium (p < 0.05 vs. control). Thickening fraction (percentage of baseline) increased from −13.1 ± 13.7% (mean ± SD) during occlusion to 15.3 ± 29.8% at 30 min of reperfusion in the CGS 21680 treatment group and remained at this level throughout the reperfusion period. In the control group, thickening fraction was - 23.7 ± 16.2% during occlusion and did not recover during reperfusion. A significant reduction in infarct size was noted in the treatment group (11.5 ± 7.9% of area at risk) as compared with the control group (28.6 ± 11.4%, p < 0.05). These findings support the hypothesis that the protective effect of adenosine on reperfusion injury is not due to replenishment of the nucleoside pool but rather is induced by stimulation of the adenosine A2-receptor.
Schlack et al. (Thu,) studied this question.