Korean J Anesthesiol Lee, et al. fore, we report the data for 90 successfully completed infarct infarct-sparing effect by EGCG. The infarct reducing effect experiments (each group n = 9). There were no significant group differences in body weight, heart weight, heart to body weight ratio, LV volume, AR volume and AR to LV ratio (Table 1). Ten μM of EGCG targeting reperfusion significantly reduced infarct size over risk area from 33.5 ± 4.1 % to 14.4 ± 1.1% (P < 0.001 vs. CON) (Fig. 3). Ten μM of the nonspecific OPR antagonist naloxone (14.3 ± 1.3%, P < 0.001 vs. CON) could not block the infarct-limitation effect by of EGCG was significantly reversed by 200 nM of the A1 ADR antagonist DPCPX (25.9 ± 1.9%, P < 0.01) and 15 nM of the A2B ADR antagonist MRS1706 (29.3 ± 1.7%, P < 0.01) but not by 10 μM of the A2A ADR antagonist ZM241385 (23.9 ± 1.9%) and 100 nM of the A3 ADR antagonist MRS1334 (24.1 ± 1.8%) (Fig. 4). Discussion EGCG. However, 1 μM of the nonspecific ADR antagonist 8-SPT In the present study, EGCG targeting reperfusion effectively (27.1 ± 1.9%, P > 0.05 vs. CON) blocked the anti-infarct effect by reduced infarct size after myocardial ischemia and reperfusion. EGCG. Naloxone and 8-SPT itself did not alter infarct size (30.9 Interestingly, the infarct reducing effect by EGCG was totally ± 4.5% for NAL and 29.6 ± 3.2% for 8-SPT, P > 0.05 vs. CON). All four ADR antagonists had a tendency to attenuate the Fig. 3. (A) Representative sequential left ventricle (LV) slices from each group showing area of necrosis (pale area) with TTC staining. (B) % of infarct area (AN) over area at risk (AR). All data are expressed as means ± SEM. CON: untreated control hearts, EGCG: polyphenol (-)-epigallocatechin gallate, NAL : nonspecific opioid receptor antagonist naloxone, SPT: nonspecific adenosine receptor antagonist 8-(p-sulfophenyl)theophylline hydrate. *P < 0.05 vs. CON, †P < 0.05 vs. EGCG. www.ekja.org Fig. 4. (A) Representative sequential left ventricle (LV) slices from each group showing area of necrosis (pale area) with TTC staining after adenosine receptor (ADR) antagonist pretreatment in EGCG treat hearts. (B) % of infarct area (AN) over area at risk (AR). All data are expressed as means ± SEM. CON: untreated control hearts, EGCG: polyphenol (-)-epigallocatechin gallate, DPCPX: A1 ADR antagonist, ZM241385: A2a ADR antagonist, MRS1706: A2b ADR antagonist, MRS1334: A3 ADR antagonist. *P < 0.05 vs. CON, †P < 0.05 vs. EGCG. 343