Abstract | BACKGROUND: METHODS: Langendorff perfused rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Hearts were treated with 10 µM of EGCG, with or without the ADR or OPR antagonist at early reperfusion. Infarct size measured with 2,3,5-triphenyltetrazolium chloride staining was chosen as end-point. RESULTS: EGCG significantly reduced infarct volume as a percentage of ischemic volume (33.5 ± 4.1%) compared to control hearts (14.4 ± 1.1%, P < 0.001). A nonspecific ADR antagonist 8-(p-sulfophenyl) theophylline hydrate (27.1 ± 1.9%, P < 0.05 vs. EGCG) but not a nonspecific OPR antagonist naloxone (14.3 ± 1.3%, P > 0.05 vs. EGCG) blocked the anti- infarct effect by EGCG. The infarct reducing effect of EGCG was significantly reversed by 200 nM of the A(1) ADR antagonist DPCPX (25.9 ± 1.1%, P < 0.05) and 15 nM of the A(2B) ADR antagonist MRS1706 (29.3 ± 1.7%, P < 0.01) but not by 10 µM of the A(2A) ADR antagonist ZM241385 (23.9 ± 1.9%. P > 0.05 vs. EGCG) and 100 nM of the A(3) ADR antagonist MRS1334 (24.1 ± 1.8%, P > 0.05). CONCLUSIONS: The infarct reducing effect of EGCG appears to involve activation of ADR, especially A(1) and A(2B) ADR, but not OPR.
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Authors | Sang Kwon Lee, June Hong Kim, Jeong Su Kim, Youngho Jang, Jun Kim, Yong Hyun Park, Kook Jin Chun, Mi Young Lee |
Journal | Korean journal of anesthesiology
(Korean J Anesthesiol)
Vol. 63
Issue 4
Pg. 340-5
(Oct 2012)
ISSN: 2005-7563 [Electronic] Korea (South) |
PMID | 23115687
(Publication Type: Journal Article)
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