Dextrose administration exacerbates acute renal ischemic damage in anesthetized dogs
M. Moursi, C. L. Rising, G. B. Zelenock and L. G. D'Alecy
To determine if moderate hyperglycemia produced by dextrose administration
was detrimental in normothermic renal ischemia, 15 halothane-anesthetized
mongrel dogs underwent right nephrectomy and 60 minutes of left renal
artery and vein occlusion. Six dogs received 1 L of lactated Ringer's
solution (LR) and six others received 1 L of 5% dextrose in lactated
Ringer's solution (D5LR). Three sham-operated dogs received 1 L of D5LR and
underwent right nephrectomy but no occlusions. All dogs received 500 mL of
fluid before occlusion and 500 mL after occlusion. The blood glucose
concentration for the LR group was 7.6 mmol/L (137 mg/dL) after 500 mL and
7.2 mmol/L (130 mg/dL) after 1000 mL. In the D5LR group, the blood glucose
concentration was 21.5 mmol/L (387 mg/dL) after 500 mL and 20.2 mmol/L (363
mg/dL) after 1000 mL. In the sham-operated group, the blood glucose
concentration was 22.8 mmol/L (410 mg/dL) after 500 mL and 20.7 mmol/L (373
mg/dL) after 1000 mL. At 30 hours, the plasma creatinine concentration rose
from 70 to 300 mumol/L (0.8 to 3.4 mg/dL) in the LR group and from 90 to
500 mumol/L (1.0 to 5.8 mg/dL) in the D5LR group; the increase for the D5LR
group was significantly greater than that for the LR group. In the
sham-operated group, the plasma creatinine concentration was stable
throughout the 30-hour period. This study demonstrates a significant
detrimental effect of dextrose administration on renal function during
normothermic ischemia.