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The role of nitric oxide and cell adhesion molecules on the microcirculation in ischaemia-reperfusion.
Cardiac necrosis can be significantly attenuated by treatment with NO, an organic NO donor, L-arginine, or specific blockers of CAMs given just prior to reperfusion, and this approach is a promising one for a variety of types of reperfusions injury. Expand
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 leftExpand
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. Expand
Pharmacology of the endothelium in ischemia-reperfusion and circulatory shock.
  • A. Lefer, D. Lefer
  • Chemistry, Medicine
  • Annual review of pharmacology and toxicology
  • 1993
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. Expand
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. Expand
Cardioprotective effect of insulin-like growth factor I in myocardial ischemia followed by reperfusion.
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. Expand
Vascular effects of HMG CoA-reductase inhibitors (statins) unrelated to cholesterol lowering: new concepts for cardiovascular disease.
The statins were found to exert direct cardiovascular effects which clearly are independent of their cholesterol lowering effects, and are not directly attributable to a reduction in serum cholesterol levels. Expand
The Role of L‐Arginine in Ameliorating Reperfusion Injury After Myocardial Ischemia in the Cat
The ability of L-arginine to reduce necrotic injury in a cat model of myocardial ischemia plus reperfusion is demonstrated, and this reduction in infarct size is associated with the preservation of endothelial function and attenuation of neutrophil accumulation in ischemic cardiac tissue. Expand
Time course of coronary vascular endothelial adhesion molecule expression during reperfusion of the ischemic feline myocardium
The timing of endothelial cell expressed P‐selectin and ICAM‐1 could coordinate neutrophil trafficking during the early stages of reperfusion and demonstrate sequential expression of three major endothelialcell adherence molecules in situ following myocardial ischemia and reperfusions. Expand
In vivo neutralization of P-selectin protects feline heart and endothelium in myocardial ischemia and reperfusion injury.
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. Expand