Suprarenal Aortic Clamping and Reperfusion Above the Superior Mesenteric Artery (SMA-SRACR) and Not Below the SMA (Renal-SRACR) Induces Early Renal Apoptosis

BACKGROUND:
We have previously shown the SMA-SRACR in the rat causes a more severe down-regulation of renal function and blood flow compared to the renal SRACR model. The role of apoptosis in contributing to the down-regulation of renal function following suprarenal aortic clamping and reperfusion is unknown. This study examines the hypothesis that early cell death (apoptosis) is one of the mechanism(s) that contributes to renal injury following SMA-SRACR.
METHODS:
Anesthetized male Sprague Dawley rats (300g) were subjected to SMA-SRACR, Renal-SRACR (or Sham) for 30 minutes followed by 60 minutes of reperfusion. Creatinine clearance (CrCl) was calculated and all kidneys were removed and separated into renal cortex (Co) and medulla (Me). The proteins were separated by Western Blot for Caspace 8 at 42/44 kilodaltons (C8-42) or 14 Kd (C8-14) and P38-MAP-kinase (P38) content by Western Blot Analysis. The blots were objectively analyzed by Densitometry and reported as Mean. ± SEM (N≥5, p< 0.05 by ANOVA when compared to the Sham group (a), Renal-SRACR (b).
RESULTS: See Table.
CONCLUSIONS: Our results showed that SMA-SRACR induced a marked increase in Caspace 8 14 Kd in the cortex and medulla when compared to the Sham and Renal-SRACR. The increased content of C8-14 Kd in the cortex and medulla following SMA-SRACR was associated with a profound decrease in CrCl compared to the Sham and renal-SRACR. These data suggest that SMA-SRACR induced marked decrease in renal function may be due in part to early apoptotic changes in the cortex and medulla.