Myocardial ischemia is a condition in which lack of blood flow to the cardiac muscle occurs resulting in deficient oxygen and nutrient supply to the heart. The restoration of blood flow to an organ or tissue is termed reperfusion. Brief episodes of ischemia and reperfusion given after prolonged ischemia and at the onset of reperfusion denotes postconditioning. Myocardial postconditioning is a phenomenon in which myocardium from lethal ischemia-reperfusion injury is protected. However, numerous experimental studies reveal that the cardioprotective effects of postconditioning are suppressed in various pathological states. This review critically discusses the mechanisms involved in the cardioprotective effects of postconditioning and factors affecting the cardioprotective potential of myocardial postconditioning.
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http://dx.doi.org/10.1007/s12272-011-0901-x | DOI Listing |
Front Pharmacol
December 2024
Department of Anesthesiology, The Affiliated Baiyun Hospital of Guizhou Medical University, Guiyang, Guizhou Province, China.
Background: Acid-sensing ion channels are activated during myocardial ischemia and are implicated in the mechanism of myocardial ischemia-reperfusion injury (MIRI). Acid-sensing ion channel 3 (ASIC3), the most pH-sensitive member of the ASIC family, is highly expressed in myocardial tissues. However, the role of ASIC3 in MIRI and its precise effects on the myocardial metabolome remain unclear.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
November 2024
Department of General and Molecular Pathophysiology, Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine.
The surgical intervention during myocardial infarction (MI) is associated with the risk of reperfusion injury, infiltration of tissues with polymorphonuclear neutrophils, and neutrophil extracellular trap (NET) formation. We hypothesized that inhibition of NETs with the use of quercetin might be a promising cardioprotective strategy. Wistar rats underwent LAD occlusion (MI) for 40 min followed by 90 min of reperfusion.
View Article and Find Full Text PDFHeliyon
November 2024
Department of Anesthesiology, Qingdao Women and Children's Hospital, School of Medicine, Shandong University, Jinan, China.
Objective: Dexmedetomidine (Dex) is a potent agonist of the α2 adrenergic receptor that has been shown to possess sedative and hypnotic properties. Dex can protect against myocardial ischemia-reperfusion injury (MIRI) by inhibiting ferroptosis. However, these studies were based on Dex post-conditioning, and the role of α2 adrenergic receptors in this process is unclear.
View Article and Find Full Text PDFInt J Mol Sci
October 2024
Department of Anesthesiology, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Endothelial dysfunction (ED) is closely associated with most cardiovascular diseases. Experimental models are needed to analyze the potential impact of ED on cardioprotection in constant pressure Langendorff systems (CPLS). One cardioprotective strategy against ischemia/reperfusion injury (I/RI) is conditioning with the lipid emulsion Intralipid (IL).
View Article and Find Full Text PDFBr J Pharmacol
January 2025
Cardiometabolic and HUN-REN-SU System Pharmacology Research Group, Center for Pharmacology and Drug Research & Development, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
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