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The role of nitric oxide and cell adhesion molecules on the microcirculation in ischaemia-reperfusion.
Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat.
Myocardial ischemia and reperfusion have been shown to impair coronary vasorelaxation to endothelium-dependent vasodilators. To examine the time course of this dysfunction, occlusion of the left…
Pharmacology of the endothelium in ischemia-reperfusion and circulatory shock.
Endothelial dysfunction is an important early-recurring phenomenon in virtually all forms of ischemia-reperfusion, including a variety of circulatory shock states and may be amplified by neutrophil-generated factors including oxygen-derived free radicals, cytokines, proteases, and lipid mediators.
Mediation of cardioprotection by transforming growth factor-beta.
When given before or immediately after ischemic injury, transforming growth factor-beta (TGF-beta) reduced the amount of superoxide anions in the coronary circulation, maintained endothelial-dependent coronary relaxation, and reduced injury mediated by exogenous TNF.
In vivo neutralization of P-selectin protects feline heart and endothelium in myocardial ischemia and reperfusion injury.
- A. Weyrich, X. Y. Ma, D. Lefer, K. Albertine, A. Lefer
- Biology, MedicineThe Journal of clinical investigation
- 1 June 1993
It is demonstrated that PMN adherence to endothelium by P-selectin is an important early consequence of reperfusion injury, and a specific monoclonal antibody to P- selectin exerts significant endothelial preservation and cardioprotection in myocardial ischemia and reperfusions.
Cardioprotective effect of insulin-like growth factor I in myocardial ischemia followed by reperfusion.
- M. Buerke, T. Murohara, C. Skurk, C. Nuss, K. Tomaselli, A. Lefer
- Biology, MedicineProceedings of the National Academy of Sciences…
- 15 August 1995
IGF-I appears to be an effective agent for preserving ischemic myocardium from reperfusion injury and protects via two different mechanisms--inhibition of polymorphonuclear leukocyte-induced cardiac necrosis and inhibition of reperfusions-induced apoptosis of cardiac myocytes.
Antibody to CD-18 exerts endothelial and cardiac protective effects in myocardial ischemia and reperfusion.
Inhibition of neutrophil adherence to the endothelium exerts significant protective effects in this model of reperfusion injury and induces significant myocardial injury and endothelial dysfunction in the cat involving a CD18-dependent neutrophIL adherence mechanism.
Vascular effects of HMG CoA-reductase inhibitors (statins) unrelated to cholesterol lowering: new concepts for cardiovascular disease.
Diminished basal nitric oxide release after myocardial ischemia and reperfusion promotes neutrophil adherence to coronary endothelium.
Results indicate that decreased basal release of endothelium-derived relaxing factor after myocardial ischemia/reperfusion precedes enhanced PMN adherence to the coronary endothelia, which may lead to PMN-induced myocardIAL injury.
Role of endothelial dysfunction in the pathogenesis of reperfusion injury after myocardial ischemia
- A. Lefer, P. Tsao, D. Lefer, Xinliang Ma
- Biology, MedicineFASEB journal : official publication of the…
- 1 April 1991
Endothelial dysfunction occurs after myocardial ischemia and reperfusion characterized by a marked reduction in endothelium‐dependent relaxation (EDR), which is then amplified by neutrophil adherence and diapedesis into the isChemic region enhancing post‐reperfusion ischemic injury.