Abstract
Renal ischemia in the rat caused a 50% decrease in the number of nuclear pores per μm 2 in freeze-fractured nuclei from the inner cortex after 20-, 60-, and 120-min ischemia and caused marked aggregation of membrane-intercalated particles in the concave fracture of the outer membrane. When 20-min ischemia, which causes reversible damage to the inner cortex of the rat kidney, was followed by 60- or 120-min reflow of blood, the pore count increased and particle aggregation in the outer membrane was partially reversed. After 240-min reflow the pore count returned to control numbers and the particles became disaggregated. When 60-min renal ischemia, which causes irreversible damage to the inner cortex, was followed by 60-, 120-, and 240-min reflow, the pore counts did not return to control numbers and the particles in the outer membrane only partially disaggregated. These changes in the nuclear envelope are postulated to be caused by functional changes in the ischemic kidney.
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