Ultrastructural evidence of myocardial alterations in the course of heterotopic heart transplantation.

Using a novel model of heterotopic rat heart transplantation, the present study was undertaken to evaluate whether parenchymal and microvascular alterations of the ischemic and reperfused myocardium occurred and could be related to local neutrophil infiltration. In such a model, hearts were rapidly excised from donor rats, maintained in a cold saline solution at 4 degrees C and then reimplanted in recipient animals. Muscle biopsies of the ischemic and reperfused myocardium were analysed by ultrastructural and immunohistochemical techniques. Although the cold storage of the hearts provided a good protection against the ischemic insults, reperfusion with the recipient blood caused severe myocardial cell injury and microvascular damage. In particular, the microvascular endothelium showed numerous discontinuities due to the partial destruction of endothelial cell. The altered endothelial integrity was associated with aggregation and adhesion of platelets to the luminal surface. Contrary to other models of ischemia and reperfusion, where neutrophils are considered the major source of oxygen radicals and cellular dysfunctions at reperfusion, in our samples the burst of these toxic metabolites did not originate from such cells. In fact, no neutrophils were seen to accumulate within the ischemic as well as reperfused myocardium. Accordingly, the microvascular endothelium did not express E-selectin, an adhesive molecule which is responsible for the increased adherence and emigration of neutrophils in the microvasculature.