Cytokine production and activation, a common phenomenon early after heart transplantation, is related at least in part to endothelial vasomotor dysfunction of the epicardial and microvascular compartment. These results support the hypothesis that coronary endothelial dysfunction after cardiac transplantation is an immunologic phenomenon. Since endothelial dysfunction seems to be a crucial step in the pathogenesis of cardiac allograft vasculopathy, coronary cytokine suppression should be a therapeutic target of improved future immunosuppressive regimens.
The present data indicate that induction of myocardial iNOS after 48 h I/R contributes to the development of reversible left-ventricular dysfunction, suggesting the involvement of iNOS in myocardial stunning. Whereas L-arginine is associated with further reduction of left-ventricular contractility, continuous inhibition of iNOS activation by AMG improves left-ventricular performance; this may be a novel and clinically important therapeutic modality in certain disease states associated with I/R, including cardiac operations using extracorporeal circulation and coronary angioplastic procedures.
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