| Objective:1By observing the changes of skeletal muscle after theskeletal muscle ischemia reperfusion injury, to expore the mechanism of theskeletal muscle ischemia reperfusion and provide theoretical support for theclinical prevention and treatment of skeletal muscle ischemia reperfusioninjury.2By observing the expression of intercellular adhesion molecule-1which exist in the remote kidney damaged after rat’s skeletal muscle ischemiareperfusion injury, to explore the mechanism of the remote kidney damagecaused by the skeletal muscle ischemia-reperfusion injury and providetheoretical support for its prevention and treatment.Ischemia reperfusion is a common phenomenon frequently encountered inclinical work. Mccord put forward the definition of ischemia reperfusion in1985,which has been widely recognized. In clinical practice ischemiareperfusion injury occurred in the amputated limb, sports injuries, trauma,osteofascial compartment syndrome, artery embolization embolectomy, theapplication of a tourniquet for long time and so on. Ischemia reperfusioninjury means that the damage to structure and function of tissues and organswill not be restored with the restoration of blood flow after acute ischemia orlow blood perfusion for a certain time, but increase constantly and cause theirreversible pathological damage. Skeletal muscle is considered to be the mostsensitive tissue to ischemia in the limbs. And ischemia reperfusion injury canoccur in the tissues and organs that occur ischemia reperfusion but also canoccur in the remote organs because of the release of oxygen-derived freeradicals, the activation of neutrophil and the release of inflammatorycytokines.So serious skeletal muscle ischemia reperfusion injury can cause limb necrosis, amputation, and the other organs’ failure and even death.So thestudy on the mechanism, clinical prevention and treatment of skeletal muscleischemia reperfusion injury has far-reaching clinical significance.In recent years, much work has been done in order to explore themechanism of ischemia reperfusion injury. With the gradual deepening of thestudy, the role of oxygen-derived free radicals, calcium overload, no-reflowphenomenon and neutrophils has been gradually recognized. This experimentexpects that by observing the expression of ICAM-1in the remote kidneycaused by skeletal muscle ischemia reperfusion injury, to explore themechanism of the remote kidney damage caused by skeletal muscle ischemiareperfusion injury.Methods:27healthy and clean adult SD rats, body weight150-200g,were randomly divided into two groups:(1) control group (n=14), routineanesthetic only, do not block the hindlimb blood flow for7hours;(2)experimental group (n=13) completely blocked the right hindlimb blood flowfor3hours and reperfused for4hours after routine anesthetic with1ml/100gintraperitoneal injection of3%sodium pentobarbital. The skeletal muscletissue was collected for observing the morphologic change by HE stainingafter paraffin sections. The kidney tissue was collected for observing theexpression of ICAM-1in the kidney tissue by immunohistochemical stainingafter paraffin sections. The professional image analysis software Image-ProPlus6.0was used to analyse the mean optical density value of the positivecells. The data analysis was applied with the statistical software SPSS13.0byindependent-samples T test (size of test α=0.05).Results:1The result of skeletal muscle tissue by HE staining: In the control group,the skeletal muscle tissue was morphologically normal. In the experimentalgroup, the arrangement of the muscle fibers was disordered, the muscle cellwas obviously swollen, cell gap significantly was widened, interstitial edema,interstitial capillary was dilatate and filled with blood cells, inflammatory cellinfiltration, part of the muscle cells were dissolved and necrotic. 2The results of kidney tissue by immunohistochemical staining: In thecontrol group, the kidney muscle tissue was morphologically normal. ICAM-1was weakly positive in the renal glomerulus cells and positive in the renaltubular epithelial cells. In the experimental group, the renal glomerulus cellsand renal tubular epithelial cells were obviously swollen, interstitial edema,inflammatory cell infiltration and part of the renal tubular epithelial cells weredenaturalized and necrotic and ICAM-1was strongly positive.The averageoptical density value of the experimental group was (0.02520.0016),andthat of the control group was (0.015810.0013). Compared to the controlgroup, the mean optical density value of the experimental group wassignificantly greater than the control group. The results shew significantdifference, which had statistical significance (P <0.05).Conclusions:1Under the conditions set in this experiment, the skeletal muscle tissuedid occur ischemia, hypoxia and other pathological changes.2The skeletalmuscle ischemia reperfusion injury did cause kidney damage.3The skeletalmuscle ischemia reperfusion renal tissue ICAM-1expression The increase ofICAM-1in the kidney tissue caused by the skeletal muscle ischemiareperfusion injury hint that ICAM-1participated in the kidney damage afterthe skeletal muscle ischemia reperfusion injury.4This experiment did not findapparent presence of renal casts, which could not exclude the possibility thatthe skeletal muscle ischemia or reperfusion time was too short.5Inflammatory cell infiltration and part of the cells were necrotic were found inthis experiment, which hint that neutrophil and cell apoptosis participatedin the skeletal muscle ischemia reperfusion injury.6The exact mechanism of kidney damage after the skeletal muscle ischemiareperfusion injury need further study. |
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