We are analyzing https://link.springer.com/article/10.1007/s00395-009-0032-4.

Title:
Intracoronary acid infusion as an alternative to ischemic postconditioning in pigs | Basic Research in Cardiology
Description:
Previous studies suggested that prolongation of acidosis during reperfusion is protective and may be an important mechanism of postconditioning protection. The aim of this study was to analyze the therapeutic value of this intervention during in vivo coronary reperfusion, and to compare it with ischemic postconditioning. Pigs were submitted to 48 or 60 min of ischemia and 2 h of reperfusion. Animals were allocated to either intracoronary infusion of Krebs solution at dose and duration previously described as optimal in rat hears (pH 6.4 for the first 3 min of reperfusion), ischemic postconditioning (8 cycles of 30 s ischemia/reperfusion) or their respective control groups (n = 9–11 per group). Neither prolongation of acidosis nor postconditioning modified infarct size after 48 min of ischemia as compared to pooled controls. In contrast, in animals submitted to 60 min of coronary occlusion, infarct size was reduced both by infusion of acid Krebs and ischemic postconditioning (57.92 ± 18.15% and 56.91 ± 7.50 vs. 75.37 ± 9.29% in controls, P < 0.01), despite having similar areas at risk. However, an increased incidence of ventricular fibrillation was observed in pigs reperfused with acid Krebs as compared to ischemic postconditioning (11 out of 20 vs. 3 out of 19 pigs, P < 0.05). In conclusion, in pigs submitted to coronary occlusion, intracoronary acid infusion and postconditioning offered protection against cell death only after prolonged coronary occlusion. Both interventions were equally effective, but intracoronary acid infusion was associated with high risk of ventricular fibrillation. These results are strongly against translation of acidic reperfusion to patients with acute myocardial infarction.
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article, pubmed, google, scholar, reperfusion, cas, postconditioning, res, myocardial, ischemic, basic, cardiol, physiol, heart, cardiovasc, coronary, garciadorado, injury, pigs, acidosis, infarct, size, cardioprotection, protection, ischemia, infarction, circ, acid, rat, circulation, infusion, inserte, occlusion, ventricular, acute, myocardium, privacy, cookies, content, research, intracoronary, garcía, min, access, hearts, april, ruizmeana, piper, cohen, yang,

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month download article/chapter david garcía-dorado phosphatidylinositol 3-kinase-akt pathway article basic research post-ischemic systolic dysfunction related subjects article rodríguez-sinovas garcía del blanco full article pdf antonio rodríguez-sinovas glycine protects cardiomyocytes post-conditioning depends servicio de cardiología privacy choices/manage cookies acute myocardial infarction generalitat de catalunya departament de salut hospital universitari vall hospital universitario vall myocardial infarct size lethal reoxygenation injury myocardial segment shrinkage short ischemic insults european economic area respective control groups st-segment elevation translating animal experiments collateral blood flow reperfusion activates akt �modified reperfusion” protects anoxia/reoxygenation injury ischemic pig heart te lintel hm intracoronary acid infusion conditions privacy policy prolonged coronary occlusion coronary artery occlusion vivo coronary reperfusion post-conditioning acutely ischemic myocardium acute coronary occlusion multiple balloon inflations 1007/s00395-008-0762-8 piot pig heart model perpetuates myocardial acidosis percutaneous coronary intervention hausenloy dj accepting optional cookies myocardial infarction article log

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Heusch G (2004) Postconditioning: old wine in a new bottle?

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         description:Previous studies suggested that prolongation of acidosis during reperfusion is protective and may be an important mechanism of postconditioning protection. The aim of this study was to analyze the therapeutic value of this intervention during in vivo coronary reperfusion, and to compare it with ischemic postconditioning. Pigs were submitted to 48 or 60 min of ischemia and 2 h of reperfusion. Animals were allocated to either intracoronary infusion of Krebs solution at dose and duration previously described as optimal in rat hears (pH 6.4 for the first 3 min of reperfusion), ischemic postconditioning (8 cycles of 30 s ischemia/reperfusion) or their respective control groups (n = 9–11 per group). Neither prolongation of acidosis nor postconditioning modified infarct size after 48 min of ischemia as compared to pooled controls. In contrast, in animals submitted to 60 min of coronary occlusion, infarct size was reduced both by infusion of acid Krebs and ischemic postconditioning (57.92 ± 18.15% and 56.91 ± 7.50 vs. 75.37 ± 9.29% in controls, P < 0.01), despite having similar areas at risk. However, an increased incidence of ventricular fibrillation was observed in pigs reperfused with acid Krebs as compared to ischemic postconditioning (11 out of 20 vs. 3 out of 19 pigs, P < 0.05). In conclusion, in pigs submitted to coronary occlusion, intracoronary acid infusion and postconditioning offered protection against cell death only after prolonged coronary occlusion. Both interventions were equally effective, but intracoronary acid infusion was associated with high risk of ventricular fibrillation. These results are strongly against translation of acidic reperfusion to patients with acute myocardial infarction.
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      description:Previous studies suggested that prolongation of acidosis during reperfusion is protective and may be an important mechanism of postconditioning protection. The aim of this study was to analyze the therapeutic value of this intervention during in vivo coronary reperfusion, and to compare it with ischemic postconditioning. Pigs were submitted to 48 or 60 min of ischemia and 2 h of reperfusion. Animals were allocated to either intracoronary infusion of Krebs solution at dose and duration previously described as optimal in rat hears (pH 6.4 for the first 3 min of reperfusion), ischemic postconditioning (8 cycles of 30 s ischemia/reperfusion) or their respective control groups (n = 9–11 per group). Neither prolongation of acidosis nor postconditioning modified infarct size after 48 min of ischemia as compared to pooled controls. In contrast, in animals submitted to 60 min of coronary occlusion, infarct size was reduced both by infusion of acid Krebs and ischemic postconditioning (57.92 ± 18.15% and 56.91 ± 7.50 vs. 75.37 ± 9.29% in controls, P < 0.01), despite having similar areas at risk. However, an increased incidence of ventricular fibrillation was observed in pigs reperfused with acid Krebs as compared to ischemic postconditioning (11 out of 20 vs. 3 out of 19 pigs, P < 0.05). In conclusion, in pigs submitted to coronary occlusion, intracoronary acid infusion and postconditioning offered protection against cell death only after prolonged coronary occlusion. Both interventions were equally effective, but intracoronary acid infusion was associated with high risk of ventricular fibrillation. These results are strongly against translation of acidic reperfusion to patients with acute myocardial infarction.
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