Contribution of the renal medulla to enhanced ketogenesis with Ringer's acetate administration during hepatic inflow occlusion.

Abstract

We have reported that the administration of Ringer's acetate solution (AR) maintains plasma ketone body concentrations even during hepatic ischemia due to enhanced ketogenesis in the kidney. In this study we tried to clarify which part of the kidney, cortex or medulla, contributes to the enhanced ketogenesis. During 20 minutes of hepatic inflow occlusion, AR or Ringer's lactate solution (LR) was administered. Ketone body concentrations in arterial and renal venous blood and renal cortical and medullary tissue were measured enzymatically. Results are expressed as means +/- SEM. At 20 minutes of hepatic inflow occlusion, arterial ketone body concentrations decreased to 38% of preischemic values with the LR infusion but increased under AR administration and were four times higher than that with LR. The renal arteriovenous difference in ketone body concentration was 16 +/- 14 micromol/ml before hepatic inflow occlusion and -52 +/- 14 with AR administration, indicating that renal ketogenesis occurred during hepatic ischemia. Total ketone body concentrations in the renal cortex and medulla were 56 +/- 6 and 61 +/- 5 micromol/g, respectively with LR, but increased to 186 +/- 29 and 248 +/- 25 micromol/g, respectively during AR administration. The concentration in the medulla was higher (p = 0. 12) than that in the cortex but did not reach statistical difference. Renal ketogenesis increases during hepatic inflow occlusion with AR administration. It is likely that the enhancement of ketogenesis takes place predominantly in the medulla of the kidney.