PATHOGENESIS OF VASCULAR INJURY IN REJECTING RAT RENAL-ALLOGRAFTS

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  • 1 January 1977
    • journal article
    • research article
    • Vol. 141  (3) , 135-147
Abstract
Unmodified rejection of rat renal allografts was characterized by the early onset and rapid progression of endothelial damage in venules and capillaries which culminated in ischemic cortical necrosis. This pattern of endothelial injury correlated with lymphocyte accumulation in vascular lumens and was not duplicated by renal perfusion with alloantibodies or prevented by C''3 [activated third complement component] depletion. Endothelial integrity and normal graft function were maintained over study intervals extending to 200 days when Brown Norway (BN) rat kidneys were transplanted into Lewis (Le) rat kidney recipients subjected to neonatal thymectomy or lymph drainage. Vascular lesions occurred when syngeneic thoracic duct lymphocytes were transfused into these recipients, but irreversible endothelial injury could be prevented by simultaneous injections of immune plasma. The destruction of donor endothelium may be mediated by thymus-dependent immune mechanisms which can be altered by thoracic duct drainage to promote indefinite survival of renal allografts across major histocompatibility loci.