The Study On The Mechanisms Of Ischemia-Reperfusion Injury And Its Influence On The Expression Of Adhesion Molecules(ICAM-1)Apart Between Organizations In Lung Tissue Of Rats

Objective: By observing the expression of intercellular adhesionmolecule-1in lung tissue of rat skeletal muscle ischemia-reperfusion injury,toexplore Ischemia-reperfusion injury to the mechanism of action of visceradamage apart, and in order to provide a theoretical basis for the prevention ofclinical therapy equipment.The theory ischemia reperfusion injury was proposed by McCord in1985.That means tissue and organs damaged aggravated after ischemia injury whenthe blood supply retunes to the tissue following a period of ischemia or lack ofoxygen. IR injury is induced by long duration of ischemia associated withseveral clinical conditions such as limb replantation, sport injury, trauma,artery embolism and tourniquet injury after limbs surgery. Usually，doctorsalways focus on recovering blood supply as quickly as possible and ignore thefact that the tissue damage continued following the blood supply returned. IRinjury is a common and important clinical problem in skeletal muscle injurywhich affects many different organ systems including muscle necrosis, limbdysfunction, physical disability even life-threatening. IR injury not onlyaffects local tissue suffer from secondary damage, but also affects the remoteorgans (such as lung, liver, kidney and so on) suffer from secondary injuryby the affect of oxygen free radical and inflammatory factors. So the mortalityand disability of ischemia reperfusion injury are very high. IR injury hasbecome a very important problem for vascular, orthopedic, trauma andemergency surgeon to solve.Recently, a lots of research works had been performed to explore themechanism of IR injury. With the develop of the research work undergoing,the theories about IR injury mechanism such as oxygen free radical, calcium overload, no reflow and neutrophil hypothesis were acceptable by scientists.At the same time, more and more research reveal that apoptosis andinflammatory factors also play a very important role on IR injury. Theresearch work get into the cell organelle.IR injury make local as well as system organs ischemic damage byinflammatory mediators. The ischemic damage of remote organs induced byinflammatory factors. Neutrophil play an important role on inflammatoryresponse. During the inflammatory response neutrophil accumulated,activated and release inflammatory mediators. The most important step in thisprocedure is intracellular adhesion molecular-1(ICAM-1) mediatedneutrophil-endothelial cell adhesion. In this experiment we detect theexpression of ICAM-1in lung tissue following skeletal muscleischemia/reperfusion injury, to explore the role of ICAM-1plays in remoteorgan injuries induced by skeletal muscle IR injury.Methods: Choose27adult SD rats being healthy and clean, body weight150-200g, which were randomly divided into two groups:①The control group(n=14):routine anesthetic only, do not block the hind-limb blood flow for7h,then sacrificed②Experimental group (n=13):routine anesthetic with1ml/100g intraperitoneal injection of3%sodium pentobarbital, blocked withblocking the right hind limb blood flow completely for4h and reperfused for3h, then sacrificed. The skeletal muscle tissue and lung tissue were collectedfor observing the morphologic change by HE staining, observing theexpression of ICAM-1in the lower lobe right lung tissue byimmunohistochemical staining after paraffin sections,used the professionalimage analysis software Image-Pro Plus6.0to analysis the determination ofthe mean optical density value of the positive cells. The data analysis ofvariance was applied with the software SPSS13.0by Independent-Samples TTest, with P <0.05as significant differences.Results:1HE staining of skeletal muscle tissue under light microscopeThe morphology of skeletal muscle tissue in control group is normal,while in experimental group, the muscle cells markedly swollen,the intercellular space widened significantly,and the interstitial blood vesselexpansion of congestion, part of the muscle fiber dissolving andnecrosis,inflammatory cells infiltration apparent.2The observation of immunohistochemistry resultsThe expression of ICAM-1in the epithelial membrane of the lung tissueand the vascular endothelial cells is tawny particles. The average opticaldensity value of the positive cells in the experimental group is (0.11600.022).The average optical density value of the positive cells in the control group is(0.01170.0038). Compared with the control group and the experimentalgroup was significantly greater than the mean optical density value of thecontrol group, the results showed a significant difference (P <0.05).Conclusion:1In ischemia-reperfusion injury, some pathological changessuch as ischemia, hypoxia happened in the Situ skeletal muscle tissue；2. Inanimal models of ischemia-reperfusion injury, the skeletal muscleischemia-reperfusion injury caused by distant lung injury;3.In the skeletalmuscle ischemia-reperfusion injury, ICAM-1participated in the process ofcouse lung injury;4. The exact mechanism of ICAM-1in distant organ injuryneeds further study.