Int J Angiol 1996; 5(1): 59-63
DOI: 10.1007/BF02043467
Original Articles

© Georg Thieme Verlag KG Stuttgart · New York

Influence of a short-term acute ischemia and reperfusion on skeletal muscle metabolism and morphology in rabbits

Igor Huk1 , Joseph Nanobashvili1 , Andreas Punz2 , Herwig Lassner2 , Markus Mueller3 , Helga Siegl4 , Christoph Neumayer5 , Martina Mittlboeck6 , Erich Roth2
  • 1Department of Vascular Surgery, University of Vienna, Vienna, Austria
  • 2Department of Metabolic Research, University of Vienna, Vienna, Austria
  • 3Department of Clinical Pharmacology, University of Vienna, Vienna, Austria
  • 4Department of Anatomy, University of Vienna, Vienna, Austria
  • 5Department of Medical Computer Sciences, University of Vienna, Vienna, Austria
  • 6Center for Biomedical Research, University of Vienna, Vienna, Austria
Presented at the 36th Annual World Congress International College of Angiology, New York, New York, July 1994
Further Information

Publication History

Publication Date:
23 April 2011 (online)

Abstract

The duration of the ischemia and reperfusion of the limbs determines the extent of tissue damage. The purpose of this study was to validate an in vivo model of ischemia-reperfusion injury with a short-term ischemic period of 1 hour which is comparable to several clinical situations. Thirteen New Zealand rabbits were randomly assigned to either (1) the sham operation (control), or (2) ischemiareperfusion group response to 1 hour of ischemia followed by 2 hours of reperfusion. Ischemia was created by clamping bilateral common femoral arteries and tourniquet occlusion of collateral circulation. Alterations of plasma potassium, malondialdehyde (MDA), muscle tissue intercellular thromboxane B2 (TxB2) concentrations, and morphometric determinations of skeletal muscle were parameters used to quantify reperfusion injury. Interstitial edema (median fraction of muscle interfiber area was 16.57% vs 13.39% in control,p=0.02), muscle cell shrinkage (median muscle fiber area was 3.70×103 μm2 vs 4.55×103 in control,p= 0.04), increased plasma potassium (median 4.7 mmol/L vs 3.6,p=0.02) in 2 hours and increased interstitial TxB2 in 1 hour were manifestation of reperfusion injury. We conclude that expansion of the extracellular space not accompanied by changes of plasma MDA may indicate that lipidperoxidation in reperfused muscle was negligible and interstitial edema was related to thromboxane A2 synthesis.

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