Myocardial infarct extension during reperfusion after coronary artery occlusion: Pathologic evidence

Decreased defence against free radicals in rat heart during normal reperfusion after hypoxic, ischemic and calcium-free perfusion

Pathologic assessment of myocardial cell necrosis and apoptosis after ischemia and reperfusion with molecular and morphological markers.

In order to define the serial morphologic correlates of unmodified first-set cardiac allograft rejection in an inbred rat strain combination, a series of Wistar-Furth cardiac allografts transplanted to normal nonsensitized Lewis recipients were studied as a function of time with the use of well-documented ultrastructural tracer techniques. Colloidial carbon was employed as a vascular label for detection of microvascular endothelial structural alterations, and horseradish peroxidase was used as a tracer probe for localization of cell-membrane permeability dysfunction of allograft endothelium and cardiocytes as well as of elements of the cellular infiltrate. Wistar-Furth to Wistar-Furth syngeneic heart grafts and Wistar-Furth recipients' own hearts provided appropriate control data. This study was demonstrated that severe diffuse loss of functional and structural integrity of the microvascular endothelium precedes the development of extensive damage to cardiac muscle cells and thus provides strong evidence that the allograft microcirculation is the primary target of immunologic injury. In addition, the sequential pattern of injurious changes present in the rejecting allografts was similar to that observed in certain models of delayed-type hypersensitivity and of skin graft rejection, raising the possibility that lymphokine-mediated mechanisms may be of major pathogenetic significance in this setting.

A controlled serial ultrastructural tracer study of first-set cardiac allograft rejection in the rat. Evidence that the microvascular endothelium is the primary target of graft destruction.

Rejection of whole organ allografts must be viewed as an extraordinarily complex phenomenon which involves specific and non-specific cellular and humoral mediators. Previous studies using a rat cardiac atlograft model have demonstrated the importance of the genetic component of rejection, i.e., the effect upon the rate of rejection of particular donor-recipient strain combinations as wel! as the state of recipient sensitization as determinants of specific humoral and cellular reactions (Guttmann 1974, 1976a, 1976b). Both recipient immune responsiveness as well as donor immunogenicity may be variables in determining the rate of rejection, which is clearly reflected in the morphologic manifestations of ongoing graft destruction. In addition, there is an instance whereby an immune response gene for allograft rejection has been mapped to the RTl B region, and has been shown to operate in a particular strain combination (Butcher 1982).

Pathogenetic Studies of Cardiac Allograft Rejection Using Inbred Rat Models

Reperfusion effect upon ischemic myocardial injury.

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Reperfusion effect upon ischemic myocardial injury.