TITLE

The impact of experimental hypoperfusion on subsequent kidney function

AUTHOR(S)
Saotome, Takao; Ishikawa, Ken; May, Clive N.; Birchall, Ian E.; Bellomo, Rinaldo
PUB. DATE
March 2010
SOURCE
Intensive Care Medicine;Mar2010, Vol. 36 Issue 3, p533
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
To investigate the short- and medium-term renal hemodynamic and functional responses to both short and sustained hypoperfusion. Eleven Merinos ewes. Animal laboratory of the University Physiology Institute. Prospective observational study. Studies were performed in conscious sheep after unilateral nephrectomy with a vascular occluder and flow probe implanted on the remaining renal artery. In five sheep, renal blood flow (RBF) was reduced by 25, 50 and 75%, respectively, by acute vascular occlusion for 30 min at weekly intervals. In another six sheep, RBF was reduced by 80% for 2 h. After 25, 50 or 75% renal hypoperfusion for 30 min, there was no associated extended loss of renal function. During 2 h of 80% hypoperfusion, urine output decreased from 80 to 17 ml, and creatinine clearance from 32 to 3 ml/min, whereas plasma creatinine increased from 103 to 132 μmol/l, and fractional excretion of sodium and urea increased. Release of occlusion induced brief hyperemia before all measured variables returned to normal within 8 h and remained normal for the following 72 h. At autopsy, the kidneys were histopathologically normal. Various degrees of renal hypoperfusion for 30 min did not induce prolonged changes in renal function or blood flow. Even with sustained severe hypoperfusion, there was rapid recovery to baseline function and flow. Unlike total ischemia, severe hypoperfusion alone is insufficient to induce subsequent persistent AKI.
ACCESSION #
48004565

 

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