"In its classical manifestation, occlusion of the arterial supply is caused by an embolus or a plug, resulting in ischemia and consequently a serious imbalance between the supply and metabolic demand, causing tissue hypoxia. During reperfusion, the restoration of blood flow is often associated with an exacerbation of tissue injury and an intense inflammatory response . Ischemia directly affects cells and triggers a series of events due to a lack of oxygen, resulting in different intensities of cellular damage and the consequent activation of cytotoxic enzymes, ultimately culminating in cell death. "
[Show abstract][Hide abstract] ABSTRACT: Ischemia-reperfusion (IR) injury is directly related to the formation of reactive oxygen species (ROS), endothelial cell injury, increased vascular permeability, and the activation of neutrophils and platelets, cytokines, and the complement system. Several studies have confirmed the destructiveness of the toxic oxygen metabolites produced and their role in the pathophysiology of different processes, such as oxygen poisoning, inflammation, and ischemic injury. Due to the different degrees of tissue damage resulting from the process of ischemia and subsequent reperfusion, several studies in animal models have focused on the prevention of IR injury and methods of lung protection. Lung IR injury has clinical relevance in the setting of lung transplantation and cardiopulmonary bypass, for which the consequences of IR injury may be devastating in critically ill patients.
Oxidative Medicine and Cellular Longevity 01/2015; 2015:590987. DOI:10.1155/2015/590987 · 3.36 Impact Factor
"Reperfusion injury defines the death of cardiomyocytes that were potentially viable at the termination of the ischemic insult . This is the main target of strategies aimed at reducing reperfusion injury, and as such the main target of ischemic conditioning techniques. "
[Show abstract][Hide abstract] ABSTRACT: Myocardial reperfusion injury has been identified as a key determinant of myocardial infarct size in patients undergoing percutaneous or surgical interventions. Although the molecular mechanisms underpinning reperfusion injury have been elucidated, attempts at translating this understanding into clinical benefit for patients undergoing cardiac interventions have produced mixed results. Ischemic conditioning has been applied before, during, or after an ischemic insult to the myocardium and has taken the form of local induction of ischemia or ischemia of distant tissues. Clinical studies have confirmed the safety of differing conditioning techniques, but the benefit of such techniques in reducing hard clinical event rates has produced mixed results. The aim of this article is to review the role of ischemic conditioning in patients undergoing percutaneous and surgical coronary revascularization.
Cardiovascular Revascularization Medicine 12/2014; 16(2). DOI:10.1016/j.carrev.2014.12.010
"Although LV remodeling in animal models is frequently generated by permanent coronary ligation without reperfusion, the ischemia–reperfusion (I/R) injury model is more clinically relevant, as the majority of patients with acute MI are treated with catheter-based or pharmacological reperfusion therapy (O'Gara et al. 2013). To date, pathological patterns of cardiac remodeling following I/R injury are not well characterized, except for the severity of injury (Yellon and Hausenloy 2007). "
[Show abstract][Hide abstract] ABSTRACT: Adverse left ventricular (LV) remodeling after acute myocardial infarction is characterized by LV dilatation and development of a fibrotic scar, and is a critical factor for the prognosis of subsequent development of heart failure. Although myofiber organization is recognized as being important for preserving physiological cardiac function and structure, the anatomical features of injured myofibers during LV remodeling have not been fully defined. In a mouse model of ischemia–reperfusion (I/R) injury induced by left anterior descending coronary artery ligation, our previous histological assays demonstrated that broad fibrotic scarring extended from the initial infarct zone to the remote zone, and was clearly demarcated along midcircumferential myofibers. Additionally, no fibrosis was observed in longitudinal myofibers in the subendocardium and subepicardium. However, a histological analysis of tissue sections does not adequately indicate myofiber injury distribution throughout the entire heart. To address this, we investigated patterns of scar formation along myofibers using three-dimensional (3D) images obtained from multiple tissue sections from mouse hearts subjected to I/R injury. The fibrotic scar area observed in the 3D images was consistent with the distribution of the midcircumferential myofibers. At the apex, the scar formation tracked along the myofibers in an incomplete C-shaped ring that converged to a triangular shape toward the end. Our findings suggest that myocyte injury after transient coronary ligation extends along myofibers, rather than following the path of coronary arteries penetrating the myocardium. The injury pattern observed along myofibers after I/R injury could be used to predict prognoses for patients with myocardial infarction.
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