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SUMMARY Serial studies have been carried out on bilaterally nephrectomized dogs bearing renal allografts or autografts. It has been shown that the renal cortical ischemia that develops with graft rejection is associated with a marked increase in vascular sensitivity to vasodilator drugs not found in the autografts; this suggests that increased vasomotor tone contributes to the cortical ischemia in early allograft rejection. In the late stage of rejection, the vessels still patent remain extremely sensitive to vasodilator action, but the peak flow that can be produced is considerably reduced. The latter suggests that a nonvasomotor component supersedes in the ischemia of late allografl rejection, when histological evidence of vascular destruction and obliteration becomes evident. The findings are consistent with the hypothesis that ischemia plays an important role in the pathogenesis of allograft rejection, and suggest that a reversible, functional component due to increased vascular tone occurs first.
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Hollenberg et al. (1968) studied this question.
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