TY - JOUR
T1 - Nonresuscitated endotoxemia induces microcirculatory hypoxic areas in the renal cortex in the rat
AU - Johannes, Tanja
AU - Mik, Egbert G.
AU - Ince, Can
PY - 2009
Y1 - 2009
N2 - The pathophysiology of acute renal failure (ARF) in sepsis is only partly understood. In several animal models of septic ARF, no profound tissue hypoxia or decrease in microcirculatory Po2 (muPo2) can be seen. We hypothesized that heterogeneity of microcirculatory oxygen supply to demand in the kidney is obscured when looking at the average muPo2 during endotoxemia. In 20 anesthetized and ventilated rats, MAP, renal blood flow (RBF), and creatinine clearance (CLcrea) were recorded. Renal muPo2 was measured by phosphorescence quenching, allowing measurement of muPo2 distributions. Five animals received a 1-h LPS infusion (10 mg kg h). In 5 rats, RBF was mechanically reduced to 2.1 +/- 0.2 mL min. Five animals served as time control. LPS infusion significantly reduced RBF to 2.1 +/- 0.2 mL min and induced anuria. Average cortical muPo2 decreased from 68 +/- 4 to 52 +/- 6 mmHg, with a significant left shift in the cortical oxygen histogram toward hypoxia. This shift could not be observed in animals receiving mechanical RBF reduction. In these animals, CLcrea was reduced to 50%. An additional group of rats (n = 5) received fluid resuscitation. In these animals, RBF was restored to baseline, CLcrea increased approximately 50%, and the cortical microcirculatory hypoxic areas disappeared after resuscitation. In conclusion, endotoxemia was associated with the occurrence of cortical microcirculatory hypoxic areas that are not detected in the average Po2 measurement, proving the hypothesis of our study. These observations suggest the involvement of hypoxia in the pathogenesis of endotoxemia-induced ARF
AB - The pathophysiology of acute renal failure (ARF) in sepsis is only partly understood. In several animal models of septic ARF, no profound tissue hypoxia or decrease in microcirculatory Po2 (muPo2) can be seen. We hypothesized that heterogeneity of microcirculatory oxygen supply to demand in the kidney is obscured when looking at the average muPo2 during endotoxemia. In 20 anesthetized and ventilated rats, MAP, renal blood flow (RBF), and creatinine clearance (CLcrea) were recorded. Renal muPo2 was measured by phosphorescence quenching, allowing measurement of muPo2 distributions. Five animals received a 1-h LPS infusion (10 mg kg h). In 5 rats, RBF was mechanically reduced to 2.1 +/- 0.2 mL min. Five animals served as time control. LPS infusion significantly reduced RBF to 2.1 +/- 0.2 mL min and induced anuria. Average cortical muPo2 decreased from 68 +/- 4 to 52 +/- 6 mmHg, with a significant left shift in the cortical oxygen histogram toward hypoxia. This shift could not be observed in animals receiving mechanical RBF reduction. In these animals, CLcrea was reduced to 50%. An additional group of rats (n = 5) received fluid resuscitation. In these animals, RBF was restored to baseline, CLcrea increased approximately 50%, and the cortical microcirculatory hypoxic areas disappeared after resuscitation. In conclusion, endotoxemia was associated with the occurrence of cortical microcirculatory hypoxic areas that are not detected in the average Po2 measurement, proving the hypothesis of our study. These observations suggest the involvement of hypoxia in the pathogenesis of endotoxemia-induced ARF
U2 - https://doi.org/10.1097/SHK.0b013e31817c02a5
DO - https://doi.org/10.1097/SHK.0b013e31817c02a5
M3 - Article
C2 - 18497704
SN - 1073-2322
VL - 31
SP - 97
EP - 103
JO - Shock (Augusta, Ga.)
JF - Shock (Augusta, Ga.)
IS - 1
ER -