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No protection of the porcine kidney by ischaemic preconditioning

Published online by Cambridge University Press:  10 January 2001

Matthias Behrends
Affiliation:
Department of Pathophysiology and General Surgery, University of Essen, School of Medicine, Hufelandstrasse 55, 45122 Essen, Germany
Martin K. Walz
Affiliation:
Department of Pathophysiology and General Surgery, University of Essen, School of Medicine, Hufelandstrasse 55, 45122 Essen, Germany
Andreas Kribben
Affiliation:
Department of Nephrology, University of Essen, School of Medicine, Hufelandstrasse 55, 45122 Essen, Germany
Udo Helmchen
Affiliation:
and § Department of Pathology, University of Hamburg, 20246 Hamburg, Germany
Till Neumann
Affiliation:
Department of Pathophysiology and General Surgery, University of Essen, School of Medicine, Hufelandstrasse 55, 45122 Essen, Germany
Thomas Philipp
Affiliation:
Department of Nephrology, University of Essen, School of Medicine, Hufelandstrasse 55, 45122 Essen, Germany
Rainer Schulz
Affiliation:
Department of Pathophysiology and General Surgery, University of Essen, School of Medicine, Hufelandstrasse 55, 45122 Essen, Germany
Gerd Heusch
Affiliation:
Department of Pathophysiology and General Surgery, University of Essen, School of Medicine, Hufelandstrasse 55, 45122 Essen, Germany
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Abstract

One or more episodes of sublethal ischaemia and reperfusion delay infarct development during subsequent, sustained ischaemia in the heart and skeletal muscle. The present study tested whether or not such ischaemic preconditioning (IP) also protects the kidney. Enflurane-anaesthetized pigs underwent 60 min of right renal vessel occlusion (RVO), followed by 8 h of reperfusion without (placebo group, n = 8) or with three preceding cycles of 10 min RVO and 10 min reperfusion (IP group, n = 8). After 8 h of reperfusion, kidneys were oliguric in both groups (placebo group: 23 ± 21 ml h-1, IP group: 24 ± 27 ml h-1). A transient polyuric phase occurred in the IP group at 2 h reperfusion. The reperfused kidneys did not excrete inulin, creatinine or urea in both groups, although renal blood flow during reperfusion was similar to baseline. Morphological damage ranged in both groups from single cell necrosis to disseminated patchy necrosis; the number of pyknotic cells tended to be higher in the IP group than in the placebo group (27.0 ± 7.1 vs. 15.6 ± 5.6 %, n.s.). In anaesthetized pigs, IP did not therefore attenuate renal dysfunction and morphological damage resulting from 60 min of renal normothermic ischaemia followed by 8 h of reperfusion.

Type
Research Article
Copyright
© The Physiological Society 2000

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