ULTRASTRUCTURAL EVIDENCE OF MYOCARDIAL ALTERATIONS IN THE COURSE OF HETEROTOPIC HEART-TRANSPLANTATION

Citation
Li. Manneschi et al., ULTRASTRUCTURAL EVIDENCE OF MYOCARDIAL ALTERATIONS IN THE COURSE OF HETEROTOPIC HEART-TRANSPLANTATION, Journal of submicroscopic cytology and pathology, 28(3), 1996, pp. 401-408
Citations number
33
Categorie Soggetti
Cell Biology",Pathology
ISSN journal
11229497
Volume
28
Issue
3
Year of publication
1996
Pages
401 - 408
Database
ISI
SICI code
1122-9497(1996)28:3<401:UEOMAI>2.0.ZU;2-I
Abstract
Using a novel model of heterotopic rat heart transplantation, the pres ent study was undertaken to evaluate whether parenchymal and microvasc ular alterations of the ischemic and reperfused myocardium occurred an d could be related to local neutrophil infiltration. In such a model, hearts were rapidly excised from donor rats, maintained in a cold sali ne solution at 4 degrees C and then reimplanted in recipient animals. Muscle biopsies of the ischemic and reperfused myocardium were analyse d by ultrastructural and immunohistochemical techniques. Although the cold storage of the hearts provided a good protection against the isch emic insults, reperfusion with the recipient blood caused severe myoca rdial cell injury and microvascular damage. In particular, the microva scular 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 cel lular dysfunctions at reperfusion, in our samples the burst of these t oxic metabolites did not originate from such cells. In fact, no neutro phils were seen to accumulate within the ischemic as well as reperfuse d myocardium. Accordingly, the microvascular endothelium did not expre ss E-selectin, an adhesive molecule which is responsible for the incre ased adherence and emigration of neutrophils in the microvasculature.