Reperfusion injury: a review of the pathophysiology, clinical manifestations and therapeutic options

Maxwell, Simon; Lip, Gregory Y.H.

doi:10.1016/s0167-5273(96)02854-9

Cited by 333 publications

(227 citation statements)

References 198 publications

Supporting

Mentioning

198

Contrasting

Unclassified

Order By: Relevance

“…Therapeutic strategies targeting free radical generation have not been successful in clinical practice: two small clinical studies using recombinant human SOD in patients with acute myocardial infarction undergoing thrombolysis [67] or balloon angioplasty [68] demonstrated no significant improvement in left ventricular function. Unfortunately, prolonged coronary occlusion (more than 2h) is usually present in the clinical setting of reperfused myocardial infarction and may cause extensive irreversible myocardial damage, leaving fewer myocytes to be affected by free radical mediated injury [69], [70]. Furthermore, ROS-mediated actions are not always harmful.…”

Section: Generation Of Reactive Oxygen Species (Ros) and The Post-infmentioning

confidence: 99%

The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

572

499

View full text Add to dashboard Cite

Myocardial infarction is the most common cause of cardiac injury and results in acute loss of a large number of myocardial cells. Because the heart has negligible regenerative capacity, cardiomyocyte death triggers a reparative response that ultimately results in formation of a scar and is associated with dilative remodeling of the ventricle. Cardiac injury activates innate immune mechanisms initiating an inflammatory reaction. Toll Like Receptor-mediated pathways, the complement cascade and reactive oxygen generation induce Nuclear Factor (NF)-κB activation and upregulate chemokine and cytokine synthesis in the infarcted heart. Chemokines stimulate the chemotactic recruitment of inflammatory leukocytes into the infarct, while cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. Monocyte subsets play distinct roles in phagocytosis of dead cardiomyocytes and in granulation tissue formation through the release of growth factors. Clearance of dead cells and matrix debris may be essential for resolution of inflammation and transition into the reparative phase. Transforming Growth Factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation while promoting myofibroblast phenotypic modulation and extracellular matrix deposition. Myofibroblast proliferation and angiogenesis result in formation of highly vascularized granulation tissue. As the healing infarct matures, fibroblasts become apoptotic and a collagen-based matrix is formed, while many infarct neovessels acquire a muscular coat and uncoated vessels regress. Timely resolution of the inflammatory infiltrate and spatial containment of the inflammatory and reparative response into the infarcted area are essential for optimal infarct healing. Targeting inflammatory pathways following infarction may reduce cardiomyocyte injury and attenuate adverse remodeling. In addition, understanding the role of the immune system in cardiac repair is necessary in order to design optimal strategies for cardiac regeneration.

show abstract

Section: Generation Of Reactive Oxygen Species (Ros) and The Post-infmentioning

confidence: 99%

The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

572

499

View full text Add to dashboard Cite

show abstract

“…Therefore it is thought that inhibition of apoptosis can attenuate the MI/R injury [8]. There are some hypotheses and findings used to explain the pathogenesis of MI/R such as oxidative stress, Ca +2 overloading, loss of membrane phospholipids, neutrophil mediated endothelial dysfunction, progressive decrease in microvascular flow and depletion of the high energy phosphate store [9]. Oxidative stress is mostly related to the increased formation of reactive oxygen and nitrogen species (ROS and RNS), which transmogrify the phospholipids and proteins leading to lipid peroxidation.…”

Section: Overview Of the Myocardial Ischemia Reperfusion Injurymentioning

confidence: 99%

Pathophysiology of Myocardial Ischemia Reperfusion Injury: A Review

Parlakpınar

Orum²,

Sağır³

2013

Med-Science

View full text Add to dashboard Cite

show abstract

“…Energy stores are depleted and certain active processes, such as the maintenance of ion concentration differences, shut down. This may be particularly important for the calcium balance, as internal calcium pumps such as those on the mitochondria or sacroplasmic reticulum may work against the increasing calcium concentration arriving from the extracellular space, speeding the depletion of energy in the cell [Maxwell and Lip, 1997].…”

Section: Ischemia-reperfusion Injurymentioning

confidence: 99%

The influence of extremely low frequency magnetic fields on cytoprotection and repair

Robertson

Thomas

Bureau

et al. 2006

Bioelectromagnetics

View full text Add to dashboard Cite

Ischemia-reperfusion injuries, such as those suffered from various types of cardiovascular disease, are major causes of death and disability. For relatively short periods of ischemia, much of the damage is potentially reversible and in fact, does not occur until the influx of oxygen during the reperfusion stage. Because of this, there is a window of opportunity to protect the ischemic tissue. Here, we review several mechanisms of protection, such as heat shock proteins, opioids, collateral blood flow, and nitric oxide induction, and the evidence indicating that magnetic fields may be used as a means of providing protection via each of these mechanisms. While there are few studies demonstrating direct protection with magnetic field therapies, there are a number of published reports indicating that electromagnetic fields may be able to influence some of the biochemical systems with protective applications.

show abstract

Reperfusion injury: a review of the pathophysiology, clinical manifestations and therapeutic options

Cited by 333 publications

References 198 publications

The immune system and cardiac repair

The immune system and cardiac repair

Pathophysiology of Myocardial Ischemia Reperfusion Injury: A Review

The influence of extremely low frequency magnetic fields on cytoprotection and repair

Contact Info

Product

Resources

About