PMID- 18497704
OWN - NLM
STAT- MEDLINE
DCOM- 20090330
LR  - 20161124
IS  - 1540-0514 (Electronic)
IS  - 1073-2322 (Linking)
VI  - 31
IP  - 1
DP  - 2009 Jan
TI  - Nonresuscitated endotoxemia induces microcirculatory hypoxic areas in the renal 
      cortex in the rat.
PG  - 97-103
LID - 10.1097/SHK.0b013e31817c02a5 [doi]
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 (microPO2) can be seen. We hypothesized that 
      heterogeneity of microcirculatory oxygen supply to demand in the kidney is 
      obscured when looking at the average microPO2 during endotoxemia. In 20 
      anesthetized and ventilated rats, MAP, renal blood flow (RBF), and creatinine 
      clearance (CLcrea) were recorded. Renal microPO2 was measured by phosphorescence 
      quenching, allowing measurement of microPO2 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 microPO2 
      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.
FAU - Johannes, Tanja
AU  - Johannes T
AD  - Department of Physiology, Academic Medical Center, University of Amsterdam, The 
      Netherlands.
FAU - Mik, Egbert G
AU  - Mik EG
FAU - Ince, Can
AU  - Ince C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Lipopolysaccharides)
RN  - AYI8EX34EU (Creatinine)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Acute Kidney Injury/chemically induced/metabolism/*physiopathology
MH  - Animals
MH  - Blood Flow Velocity/drug effects
MH  - Creatinine/metabolism
MH  - Disease Models, Animal
MH  - Endotoxemia/chemically induced/metabolism/*physiopathology
MH  - Hypoxia/chemically induced/metabolism/*physiopathology
MH  - Kidney Cortex/*blood supply/metabolism/*physiopathology
MH  - Lipopolysaccharides/*toxicity
MH  - Male
MH  - Microcirculation/drug effects
MH  - Oxygen/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Resuscitation
EDAT- 2008/05/24 09:00
MHDA- 2009/03/31 09:00
CRDT- 2008/05/24 09:00
PHST- 2008/05/24 09:00 [entrez]
PHST- 2008/05/24 09:00 [pubmed]
PHST- 2009/03/31 09:00 [medline]
AID - 10.1097/SHK.0b013e31817c02a5 [doi]
PST - ppublish
SO  - Shock. 2009 Jan;31(1):97-103. doi: 10.1097/SHK.0b013e31817c02a5.