نتایج جستجو برای: myocardial ischemic reperfusion injury
تعداد نتایج: 520115 فیلتر نتایج به سال:
BACKGROUND Reperfusion injury of ischemic myocardium has been attributed to neutrophil infiltration, inflammatory activation and cardiac necrosis/apoptosis. Serine protease inhibition with aprotinin is cardioprotective, but the mechanism is unknown. METHODS AND RESULTS We studied aprotinin in a rat model of myocardial ischemia for 20 minutes and reperfusion for 20 minutes, 8 hours or 24 hours...
The heart is an organ that requires an important energy input to ensure its contractile function. Myocardial ischemia happens when there is a deficiency of blood flow that is responsible for the passage from an aerobic to anaerobic metabolism. Myocardial ischemia results from an imbalance between inputs and the needs of nutrient and oxygen to the myocardium. The restoration of myocardial perfus...
Inhibition of angiotensin II type 1 receptor (AT1R) is an important therapy in the management of hypertension, particularly in the immediate post-myocardial infarction period. Yet, the role of AT1R in the acute onset of myocardial ischemia and reperfusion injury still remains controversial. Thus, the present study determined the effects of chronic losartan treatment on heart ischemia and reperf...
OBJECTIVE Neutrophils (PMNs) contribute importantly to the tissue injury associated with ischemia and subsequent reperfusion of a vascular bed. The effects of a recombinant soluble human form of P-selectin glycoprotein ligand-1 (rsPSGL.Ig) on PMN-endothelial cell interactions were investigated in a well established model of feline myocardial-ischemia reperfusion injury. METHODS Cats were subj...
The discovery of ischemic postconditioning (IPost) has rejuvenated the field of cardioprotection. As an interventional strategy to be applied at the onset of myocardial reperfusion, the transition of IPost from a bench-side curiosity to potential clinical therapy has been impressively rapid. Its existence also confirms the existence of lethal myocardial reperfusion injury in man, suggesting tha...
Diabetes is an independent risk factor for myocardial ischemia, and many epidemiological data and laboratory studies have revealed that diabetes significantly exacerbated myocardial ischemia/reperfusion injury and ameliorated protective effects. The present study aimed to determine whether pharmacological postconditioning with atorvastatin calcium lessened diabetic myocardial ischemia/reperfusi...
BACKGROUND AND PURPOSE Galanin is a multifunctional neuropeptide with pleiotropic roles. The present study was designed to evaluate the potential effects of galanin (2-11) (G1) on functional and metabolic abnormalities in response to myocardial ischemia-reperfusion (I/R) injury. EXPERIMENTAL APPROACH Peptide G1 was synthesized by the 9-fluorenylmethoxycarbonyl (Fmoc)-based solid-phase method....
The study was to evaluate the roles of Adiponectin (ADP) in alleviating myocardial ischemia-reperfusion injury in rats with Remote Ischemic Postconditioning (RIP). A total of 57 healthy male SD rats were randomly divided into 3 groups (the sham operation group (S), the myocardial ischemia-reperfusion group (I/R), and the RIP group (R). The myocardial ischemia-reperfusion injury model was establ...
Reperfusion is needed to initiate reflow of blood in cardiac arrest triggered by surgical intervention or pathologically-induced cardiac ischemia. However, subsequent reperfusion may lead not only to the recovery of ischemic cardiac tissue, but also to the paradoxical phenomenon of myocardial ischemia/reperfusion (IR) injury, including protracted organ recovery, myocardial stunning, and acute m...
BACKGROUND The heart is a tumor necrosis factor-alpha (TNF-alpha)-producing organ. Recent basic experimental and clinical evidence suggests that TNF-alpha is an important mediator of myocardial injury during acute myocardial infarction, chronic heart failure, cardiac allograft rejection, and cardiopulmonary bypass operations. Although it is known that the myocardium itself is capable of produci...
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