Nephrology Dialysis Transplantation, Vol 12, Issue 8 1586-1594, Copyright © 1997 by Oxford University Press
A Hemmskerk, E Huisman, A van Lambalgen, G van den Bos, M Hennekes, L Thisjs and G Tangelder
Background: The hypothesis that renal failure during
septic shock may occur as a result of hypoxia-related cell dysfunction was
investigated in two rat models of distributive shock.
Method: Pentobarbitone-anaesthetized rats received
either a bolus (1 ml) of living Escherichia coli
bacteria (hospital-acquired strain, 1 x 10x9 CFU/ml;
BA-group, n=7), or a 1-h infusion of endotoxin (E.coli
O127.B8: 8 mg/kg; ET-group, n=7). Results: Urine flow
in the BA- and ET-group reached a nadir at 1 h but thereafter increased and
reached values higher than control at 3 h. At this time point, renal oxygen
delivery had decreased, in the BA-group mainly due to a fall in arterial
oxygen content and in the ET-group to a fall in renal plasma flow
(clearance of 131I-hippurate). However, renal oxygen
extraction had significantly increased, by 31% in the BA and by 59% in the
ET group, while renal oxygen consumption remained the same. Net tubular
sodium reabsorption had decreased by 55% in the BA and by 25% in the ET
group, due to a fall in glomerular filtration rate (clearance of
creatinine). Hence an excess oxygen consumption was found which was caused
neither by an increased renal glucose release nor by the presence of an
increased number of leukocytes stuck in the glomeruli. Renal tubular cells
showed normal morphology. An indication that proximal tubular function in
the BA and ET group remained largely intact were normal ATP levels, absence
of urinary glucose, and a normal fractional excretion of sodium. However,
since urine flow had increased in shocked rats at 3h, water appeared
selectively lost. Conclusion: Our data indicate that
in rat models of septic shock renal failure is not caused by cortical
hypoxia or a shortage of cellular energy supply.
Keywords: E. coli bacteria;
E. coli endotoxin; oxygen consumption; renal blood
flow; sodium reabsorption; urine flow
ORIGINAL ARTICLES
Renal function and oxygen consumption during bacteraemia and endotoxaemia in rats
Laboratory for Physiology, Department of Clinical Chemistry and Medical Intensive Care Unit, Research School Vrije Universiteit (ICaR-VU), van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands
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