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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