Results 351 to 360 of about 282,175 (385)
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Bucillamine Prevents Myocardial Reperfusion Injury

Journal of Cardiovascular Pharmacology, 2001
Injury during reperfusion can partially offset the benefit of relief of ischemia in myocardial infarctions rapidly treated with thrombolytic drugs or angioplasty. We assessed whether bucillamine (N-[2-mercapto-2-methylpropionyl]-L-cysteine) is potentially useful to treat myocardial reperfusion injury.
Nancy A. Sherman, Lawrence D. Horwitz
openaire   +2 more sources

Neutrophils and myocardial reperfusion injury

Pharmacology & Therapeutics, 1996
Ischaemia induces an acute inflammatory response in myocardial tissue with an early phase of neutrophil accumulation, which is accelerated by reperfusion. In experimental models, interventions that deplete neutrophils or inhibit their function cause a significant reduction in myocardial infarct size. These cells, therefore, may exacerbate tissue injury
openaire   +3 more sources

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.
openaire   +3 more sources

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.
Chakib M. Ayoub   +2 more
openaire   +3 more sources

Melatonin attenuates diabetic cardiomyopathy and reduces myocardial vulnerability to ischemia‐reperfusion injury by improving mitochondrial quality control: Role of SIRT6

Journal of Pineal Research, 2020
Targeting mitochondrial quality control with melatonin has been found promising for attenuating diabetic cardiomyopathy (DCM), although the underlying mechanisms remain largely undefined.
Liming Yu   +11 more
semanticscholar   +1 more source

Reperfusion injury, stunning and myocardial viability

Australian and New Zealand Journal of Medicine, 1993
Abstract:Recent experimental data suggest that current thrombolytic strategies may not yet have achieved their full potential for myocardial salvage. In fact, reperfusion may result in microvascular and myocardial cellular injuries. These may translate into transient loss of contractile function (‘myocardial stunning’), and possibly contribute to the ...
Andrew Tonkin, Robert K Chan
openaire   +3 more sources

Lethal Myocardial "Reperfusion Injury"

Journal of thrombosis and thrombolysis, 1997
Peer Reviewed ; http://deepblue.lib.umich.edu/bitstream/2027.42/48021/1/11239_2004_Article_255436 ...
openaire   +4 more sources

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.
Derek J. Hausenloy   +2 more
openaire   +3 more sources

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.
Juan Zhou, Zhelong Xu
openaire   +3 more sources

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.
Alastair D. Robertson   +2 more
openaire   +2 more sources

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