chloramphenicol-succinate has been researched along with Myocardial-Infarction* in 2 studies
2 other study(ies) available for chloramphenicol-succinate and Myocardial-Infarction
Article | Year |
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Cardioprotection through autophagy: ready for clinical trial?
Interventions that reduce infarct size in animal models have largely failed to improve outcome in patients suffering acute myocardial infarction (MI), or 'heart attack'. Our group recently reported a reduction of infarct size by chloramphenicol treatment in a porcine in vivo model of acute MI, through a mechanism involving the induction of autophagy. Since 2005 several studies have implicated autophagy as a target for cardioprotection. Topics: Animals; Anti-Infective Agents; Autophagy; Chloramphenicol; Clinical Trials as Topic; Comorbidity; Coronary Vessels; Humans; Myocardial Infarction; Myocardium; Placebos; Swine; Time Factors; Treatment Outcome | 2011 |
Profound cardioprotection with chloramphenicol succinate in the swine model of myocardial ischemia-reperfusion injury.
Emerging evidence suggests that "adaptive" induction of autophagy (the cellular process responsible for the degradation and recycling of proteins and organelles) may confer a cardioprotective phenotype and represent a novel strategy to limit ischemia-reperfusion injury. Our aim was to test this paradigm in a clinically relevant, large animal model of acute myocardial infarction.. Anesthetized pigs underwent 45 minutes of coronary artery occlusion and 3 hours of reperfusion. In the first component of the study, pigs received chloramphenicol succinate (CAPS) (an agent that purportedly upregulates autophagy; 20 mg/kg) or saline at 10 minutes before ischemia. Infarct size was delineated by tetrazolium staining and expressed as a % of the at-risk myocardium. In separate animals, myocardial samples were harvested at baseline and 10 minutes following CAPS treatment and assayed (by immunoblotting) for 2 proteins involved in autophagosome formation: Beclin-1 and microtubule-associated protein light chain 3-II. To investigate whether the efficacy of CAPS was maintained with "delayed" treatment, additional pigs received CAPS (20 mg/kg) at 30 minutes after occlusion. Expression of Beclin-1 and microtubule-associated protein light chain 3-II, as well as infarct size, were assessed at end-reperfusion. CAPS was cardioprotective: infarct size was 25±5 and 41±4%, respectively, in the CAPS-pretreated and CAPS-delayed treatment groups versus 56±5% in saline controls (P<0.01 and P<0.05 versus control). Moreover, administration of CAPS was associated with increased expression of both proteins.. Our results demonstrate attenuation of ischemia-reperfusion injury with CAPS and are consistent with the concept that induction of autophagy may provide a novel strategy to confer cardioprotection. Topics: Animals; Anti-Bacterial Agents; Apoptosis Regulatory Proteins; Autophagy; Cardiotonic Agents; Chloramphenicol; Disease Management; Female; Gene Expression Regulation; Humans; Male; Microtubule-Associated Proteins; Myocardial Infarction; Myocardial Reperfusion Injury; Myocardium; Swine | 2010 |