Intracellular electrolyte composition following renal ischemia. The technique of electron microprobe analysis was used to determine the intracellular electrolyte concentrations in proximal or distal tubular cells of the rat kidney during ischemia. When the exposed kidney was maintained in air during ischemia, the composition of the surface cells differed little from control, and the electrolyte disturbances were confined to the deeper lying cells. When maintained in nitrogen, all cells underwent changes in cellular electrolyte concentrations that were uniform, indicating that the surface cells can preserve their composition during ischemia by utilizing oxygen from the air. In the proximal tubular cells, after 20 or 60 min of ischemia in nitrogen, sodium increased from 20 to 93 or 112, chloride rose from 21 to 53 or 66, potassium fell from 141 to 65 or 42, phosphate decreased from 145 to 110 or 95 mmoles·kg^-1 of wet wt, and the dry wt dropped from 22.6 to 20.3 or 17.5% of wet wt, respectively. In the distal tubular cells, 20 min of ischemia in nitrogen produced little effect on cellular comoosition, but after 60 min, sodium increased from 11 to 77, chloride rose from 15 to 48, potassium fell from 134 to 89, phosphate decreased from 168 to 145 mmoles·kg^-1 of wet wt, and the dry wt dropped from 20.8 to 18.4% of wet wt. The disturbances in sodium and potassium are caused primarily by an inhibition of the sodium/potassium pump, whereas the changes in chloride, phosphate, and dry weight content result mainly from an influx of extracellular fluid. When blood flow was reintroducing, the electrolyte disturbances were rapidly reversed in all cells, restoration being virtually complete within 60 min, but returned in some proximail cells by 18 hr of reperfusion. Thus, the disturbance in electrolyte composition increases with the duration of ischemia, is less pronounced in the distal than proximal cells and, although initially completely reversible when blood flow is restored, reappears in the proximal cells 1 day after the initial injury.