Studies on the pathogenesis of ischemic cell injury. III. Morphological changes of the proximal pars recta tubules (P3) of the rat kidney made ischemic in vivo.

The pars recta of the proximal tubule of the rat kidney was examined by means of light and electron microscopy after 15, 30, 60 and 120 min of ischemia produced by clamping of the aorta. Also the effects of 24 hrs of blood reflow following the same ischemia periods were determined. The maximal changes occurring after ischemic periods of up to 60 min included: marked cell swelling, swelling of the inner compartments of the mitochondria, swelling of the endoplasmic reticulum and of microvilli, pronounced chromatin clumping in the nuclei and distortion of the Golgi apparatus. These cell changes were reported to be reversible in the previous paper of this series. After 24 hrs of blood reflow it was found that with increasing periods of primary ischemia, ranging from 15 to 120 min, an increasing number of pars recta tubules cells were undergoing necrosis. Theses findings indicate that some additional mechanism other than the initial ischemia per se must be responsible for the progressive cellular damage leading to the necrosis. This is in contrast to the pars convoluta of the proximal tubule, which does not undergo further degenerative changes after the primary ischemia has been ended. The "no reflow" phenomenon may satisfactorily explain the necrosis seen in the pars recta segments following various periods of ischemia after 24 hrs of arterial renal reflow.