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Myocardial ischemia and reperfusion injury

Cardiovascular Pathology, 2005
Myocardial ischemic injury results from severe impairment of coronary blood supply and produces a spectrum of clinical syndromes. As a result of intensive investigation over decades, a detailed understanding is now available of the complexity of the response of the myocardium to an ischemic insult.
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Pharmacological therapy for myocardial reperfusion injury

Current Opinion in Pharmacology, 2004
In the ischemic myocardium, reperfusion is necessary for the salvage of cells and cardiac function. However, reperfusion itself causes 'reperfusion injury', leading to the damage of myocardial cells. This is reduced by several interventions, as measured by the limitation of infarct size or reduction of arrhythmias.
George V, Moukarbel   +2 more
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Myocardial reperfusion injury

1999
Abstract Early in the history of cardiac surgery, it was recognized that some patients who underwent technically successful operations suffered from a syndrome of low cardiac output in the early postoperative period. It was also apparent that the perioperative mortality was increased in these patients. Autopsy and clinical studies in the
Robert C Gorman, Timothy J Gardner
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Myocardial postconditioning: reperfusion injury revisited

American Journal of Physiology-Heart and Circulatory Physiology, 2005
coronary heart disease is the leading cause of death in the Western world and represents one of the major burdens on healthcare systems today. Targeting those strategies that limit the damage sustained as a result of a lethal ischemic insult has been a major goal for many years.
Andrew, Tsang   +2 more
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Connexin43 and Myocardial Ischemia-Reperfusion Injury

Cardiovascular & Hematological Disorders-Drug Targets, 2018
Recently, the treatment and prevention of ischemic cardiomyopathy is one of the emerging research topics in the cardiovascular field. Gap junction is the basic structure of cardiac electrophysiology. Connexin is the basic unit of gap junctions. Connexin43(CX43) is the most abundant member of Cx family in the heart, the normal expression of Cx43 is ...
Lingyun, Zu   +4 more
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Timing of Treatment for Myocardial Reperfusion Injury

Journal of Cardiovascular Pharmacology, 1999
Early reperfusion of acute myocardial infarctions halts cell death due to ischemia but causes further injury, probably by oxidant mechanisms. We identified the window of opportunity during which antioxidants must be present in therapeutic concentrations to prevent reperfusion injury during 90 min of ischemia and 48 h of reperfusion in 57 dogs.
L D, Horwitz, Y, Kong, A D, Robertson
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Zinc and myocardial ischemia/reperfusion injury

BioMetals, 2013
As an important trace element, zinc is required for the normal cellular structure and function, and impairment of zinc homeostasis is associated with a variety of health problems including cardiovascular disease. Zinc homeostasis is regulated through zinc transporters, zinc binding molecules, and zinc sensors.
Zhelong, Xu, Juan, Zhou
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Unresolved issues in myocardial reperfusion injury

Cardiovascular Pathology, 2010
While the basic pathobiology of myocardial ischemic injury and reperfusion has been determined over the last 50 years, there are important, unresolved, or at least not completely elucidated, issues in the field. These include the relative contributions of different modes of cell injury and death to evolving myocardial infarcts; interactions of ...
Louis Maximilian, Buja   +1 more
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Myocardial Reperfusion Injury: The Critical Challenge

Critical Care Nursing Clinics of North America, 1992
Oxygen-free radical production and reperfusion injury are complex mechanisms. New and improved methods for maximizing the benefits of reperfusion while minimizing reperfusion injury are on the horizon in the 1990s. Critical care nurses play a crucial role in the assessment, planning, and intervention of patients experiencing the deleterious effects of ...
V J, Coombs, L, Black, S N, Townsend
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Cellular recruitment in myocardial ischaemia/reperfusion injury

European Journal of Clinical Investigation, 2016
AbstractBackgroundMyocardial infarction (MI) is strictly linked to atherosclerosis. Beyond the mechanical narrowing of coronary vessels lumen, during MI a great burden of inflammation is carried out. One of the crucial events is represented by the ischaemia/reperfusion injury, a complex event involving inflammatory cells (such as neutrophils, platelets,
BONAVENTURA, ALDO   +2 more
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