Abstract | OBJECTIVES: METHODS: Langendorff perfused C57/Bl6 mouse hearts were subjected to 20 min ischemia and 45 min reperfusion. Effects of adenosine-mediated preconditioning were assessed in the absence and presence of signaling inhibitors. RESULTS: CONCLUSIONS:
Adenosine-mediated preconditioning is dose-dependent with high level stimulation reducing contractile dysfunction in addition to necrosis. Preconditioning is triggered by a mito K( ATP) channel dependent process independently of PKC and NO. Subsequent protection against necrosis is also mediated by a mito K( ATP) channel dependent process independent of PKC and NO. In contrast, functional protection may be mediated by parallel mito K( ATP) and PKC dependent paths.
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Authors | Jason Peart, John P Headrick |
Journal | Cardiovascular research
(Cardiovasc Res)
Vol. 58
Issue 3
Pg. 589-601
(Jun 01 2003)
ISSN: 0008-6363 [Print] England |
PMID | 12798432
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Alkaloids
- Benzophenanthridines
- Calcium Channel Blockers
- Decanoic Acids
- Enzyme Inhibitors
- Hydroxy Acids
- Phenanthridines
- Phenethylamines
- Potassium Channels
- Receptors, Purinergic P2
- 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine
- Xanthine
- Hypoxanthine
- Nitric Oxide
- Inosine
- Adenosine Diphosphate
- 5-hydroxydecanoic acid
- chelerythrine
- L-Lactate Dehydrogenase
- Nitric Oxide Synthase
- Protein Kinase C
- Adenosine
- Diazoxide
- NG-Nitroarginine Methyl Ester
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Topics |
- Adenosine
(analogs & derivatives, pharmacology)
- Adenosine Diphosphate
(pharmacology)
- Alkaloids
- Animals
- Benzophenanthridines
- Calcium Channel Blockers
(pharmacology)
- Decanoic Acids
(pharmacology)
- Diazoxide
(pharmacology)
- Enzyme Inhibitors
(pharmacology)
- Hydroxy Acids
(pharmacology)
- Hypoxanthine
(pharmacology)
- Inosine
(pharmacology)
- Ischemic Preconditioning, Myocardial
(methods)
- L-Lactate Dehydrogenase
(metabolism)
- Male
- Mice
- Mice, Inbred C57BL
- Mitochondria, Heart
(metabolism)
- Myocardial Contraction
(drug effects)
- Myocardial Infarction
(metabolism, pathology, physiopathology)
- NG-Nitroarginine Methyl Ester
(pharmacology)
- Necrosis
- Nitric Oxide
(metabolism)
- Nitric Oxide Synthase
(antagonists & inhibitors)
- Perfusion
- Phenanthridines
(pharmacology)
- Phenethylamines
(pharmacology)
- Potassium Channels
(metabolism)
- Protein Kinase C
(metabolism)
- Receptors, Purinergic P2
(drug effects)
- Signal Transduction
(drug effects, physiology)
- Xanthine
(pharmacology)
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