Humans ; Myocardial Reperfusion Injury

Autophagy ; Humans ; Myocardial Reperfusion Injury

Humans ; Myocardial Infarction ; physiopathology ; Myocardial Reperfusion Injury

Humans ; Ischemic Postconditioning ; Myocardial Reperfusion Injury

BACKGROUND: This experiment was performed to determine the effect of polyphenolic (-)-epigallocatechin (EGCG), the most abundant catechin of green tea, given at reperfusion period. METHODS: Isolated rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Green tea extract (GT) was perfused with the following concentrations; 0, 0.5, and 1 micrometer (GT-O, GT-0.5, and GT-1, respectively). In a next experiment, hearts were assigned randomly to one of the following groups; Control, EGCG-1 (1 micrometer of EGCG), and EGCG-10 (10 micrometer of EGCG). GT and EGCG were perfused for a period of 5 min before and 30 min after reperfusion. For comparison of cardioprotection among groups, morphometric measurement was performed by 2,3,5-triphenyltetrazolium chloride staning. RESULTS: GT 1 micrometer (10.3 +/- 2.1%, P < 0.05) significantly reduced infarct volume as a percentage of ischemic volume compared to untreated hearts (27.4 +/- 1.1%). EGCG 10 micrometer (13.2 +/- 4.0%) significantly reduced myocardial infarction compared to control hearts (27.2 +/- 1.4%, P = 0.002). After 2 h of reperfusion, cardiodynamic variables, including left ventricular developed pressure, rate-pressure produce, +dP/dt(max), and -dP/dt(min) were significantly improved by 10 micrometer of EGCG compared to control hearts (P = 0.01, 0.016, 0.009, and 0.019, respectively). CONCLUSIONS: EGCG treatment at an early reperfusion period reduces myocardial infarction and improves cardiodynamics in isolated rat hearts.
Animals ; Catechin ; Heart ; Ischemia ; Myocardial Infarction ; Myocardial Reperfusion ; Myocardium ; Rats ; Reperfusion ; Reperfusion Injury ; Tea ; Tetrazolium Salts

BACKGROUND: This experiment was performed to determine the effect of polyphenolic (-)-epigallocatechin (EGCG), the most abundant catechin of green tea, given at reperfusion period. METHODS: Isolated rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Green tea extract (GT) was perfused with the following concentrations; 0, 0.5, and 1 micrometer (GT-O, GT-0.5, and GT-1, respectively). In a next experiment, hearts were assigned randomly to one of the following groups; Control, EGCG-1 (1 micrometer of EGCG), and EGCG-10 (10 micrometer of EGCG). GT and EGCG were perfused for a period of 5 min before and 30 min after reperfusion. For comparison of cardioprotection among groups, morphometric measurement was performed by 2,3,5-triphenyltetrazolium chloride staning. RESULTS: GT 1 micrometer (10.3 +/- 2.1%, P < 0.05) significantly reduced infarct volume as a percentage of ischemic volume compared to untreated hearts (27.4 +/- 1.1%). EGCG 10 micrometer (13.2 +/- 4.0%) significantly reduced myocardial infarction compared to control hearts (27.2 +/- 1.4%, P = 0.002). After 2 h of reperfusion, cardiodynamic variables, including left ventricular developed pressure, rate-pressure produce, +dP/dt(max), and -dP/dt(min) were significantly improved by 10 micrometer of EGCG compared to control hearts (P = 0.01, 0.016, 0.009, and 0.019, respectively). CONCLUSIONS: EGCG treatment at an early reperfusion period reduces myocardial infarction and improves cardiodynamics in isolated rat hearts.
Animals ; Catechin ; Heart ; Ischemia ; Myocardial Infarction ; Myocardial Reperfusion ; Myocardium ; Rats ; Reperfusion ; Reperfusion Injury ; Tea ; Tetrazolium Salts

OBJECTIVEA general review was made of studies involving: (1) The experimental evidence of remote ischemic preconditioning (RIPC) and relative clinical studies, (2) The experimental and clinical evidences of remote ischemic postconditioning (RIPOC), (3) The potential mechanistic pathways underlying their protective effects.

DATA SOURCESThe data used in this review were mainly from manuscripts listed in PubMed that were published in English from 1986 to 2010. The search terms were "myocardial ischemia reperfusion injury", "ischemia preconditioning", "ischemia postconditioning", "remote preconditioning" and "remote postconditioning".

STUDY SELECTION(1) Clinical and experimental evidence that both RIPC and RIPOC produce preservation of ischemia reperfusion injury (IRI) of myocardium and other organs, (2) Studies related to the potential mechanisms, by which remote ischemic conditioning protects myocardium against IRI.

RESULTSBoth RIPC and RIOPC have been shown to attenuate myocardial IRI in laboratory animals. Also, their cardioprotective effects have appeared in some clinical studies. Except the external, the detailed internal mechanisms of remote ischemic conditioning have been generally described. Through these descriptions better protocols can be developed to provide improved cardioprotective procedures.

CONCLUSIONSRemote ischemic conditioning is an endogenous cardioprotective mechanism from outside the heart that protects against myocardial IRI and represents a general form of inter-organ protection. Remote ischemic conditioning may have an immense impact on clinical practice in the near future.

Humans ; Myocardial Infarction ; complications ; therapy ; Myocardial Reperfusion Injury ; etiology ; therapy

Animals ; Autophagy ; Humans ; Myocardial Ischemia ; physiopathology ; Myocardial Reperfusion Injury ; physiopathology

Extracellular Traps ; Humans ; Ischemia ; Myocardial Ischemia ; Myocardial Reperfusion ; Myocardial Reperfusion Injury ; Neutrophils