Skeletal Muscle Ischaemia-reperfusion Injury: Further Characterisation of a Rodent Model

Background: postischaemic damage in skeletal muscle may be reflected in changes to microvascular blood flow, vascular permeability, and subsequent tissue viability. Previous preclinical studies have not addressed all these parameters, and have not used periods of ischaemia and reperfusion relevant t...

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Bibliographic Details
Published in:European journal of vascular and endovascular surgery 2001-12, Vol.22 (6), p.523-527
Main Authors: Homer-Vanniasinkam, S, Rowlands, T.E, Hardy, S.C, Gough, M.J
Format: Article
Language:English
Subjects:
Animal model
Animals
Blood Flow Velocity
Disease Models, Animal
Edema - etiology
Edema - pathology
Hindlimb - blood supply
Ischaemia
Ischemia - diagnostic imaging
Ischemia - pathology
Ischemia - physiopathology
Male
Microspheres
Muscle
Muscle, Skeletal - blood supply
Muscle, Skeletal - pathology
Necrosis
Radioisotopes
Radionuclide Imaging
Rats
Rats, Sprague-Dawley
Regional Blood Flow
Reperfusion injury
Reperfusion Injury - diagnostic imaging
Reperfusion Injury - pathology
Reperfusion Injury - physiopathology
Rodent
Tissue Survival
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Summary:Background: postischaemic damage in skeletal muscle may be reflected in changes to microvascular blood flow, vascular permeability, and subsequent tissue viability. Previous preclinical studies have not addressed all these parameters, and have not used periods of ischaemia and reperfusion relevant to the clinical setting. This study aimed to develop an animal model hindlimb ischaemia-reperfusion to simulate acute lower limb ischaemia. Methods: a rodent model of hindlimb tourniquet-induced ischaemia-reperfusion was employed. Gastrocnemius muscle blood flow (GMBF; radio-labelled microspheres), oedema (GMO; using a wet:dry ratio method) and viability (GMV; histochemistry and computerised planimetry) were quantified. Results: 6 h ischaemia per seresulted in neither muscle oedema nor loss of viability, but these changes were apparent following 4 h reperfusion. Early reperfusion at 10 min demonstrated low reflow, with GMBF improving at 120 min before declining sharply at 240 min. Conclusion: prolonged hindlimb ischaemia followed by reperfusion in this rodent model caused significant reductions in gastrocnemius muscle blood flow, associated with muscle oedema and necrosis. These three parameters have not been previously reported together in the same model. This reproducible model could be used in the evaluation of potential therapeutic intervention strategies aimed at ameliorating skeletal muscle reperfusion injury.
ISSN:1078-5884
1532-2165
DOI:10.1053/ejvs.2001.1467