| Objective To establish an animal model similar to the neonatal asphy- xia with injure of myocardium and to obsever CK-MB,cTnI in blood and apoptosis of myocardial cells.Methods Seven old SD ras(n=48) were radomly divided into Control group(n:8) and model group A,B,C,D,E 5groups(each group=8,after asphyxia6h,24h,48h,72h,7d).The model groups SD rats were put into separably 55ml contaner with CaO-NaOH0.005Kg,the mouth of bottl was sealed up a half of an hour,then being given oxygen 120 min and coming back with mother ras.After 6h,24h,48h,72h,7dWere deid.Blood CK-MB,cTnI was detected by ELISA Methods,apoptosis of myocardiumwas detected by TUNEL Methods and myocardium been made into pathological sections,pathological injure of myocardium tissue was observed through optical microscope and electron microscope.Result 1.The pathological injure of myocardium tissue was remarkable through optical microscope and electron microscope;2.Blood CK-MB,cTnI and apoptosis of myocardium the model groups was higher than control group(P＜0.05);3.Blood CK-MB was highest at 24h,than was lower gradually,Blood cTnI was highest at 72h,than was stable until 7d;the apoptosis of myocardium was more and more growed as time longer gradually.Conclusion1.Relatively convenient and easily got experimental normal pressure neonatal rat asphyxia modle which reproduced human neonatal asphyxia pathogenic mechanism and was successfully.2.Neonatal rat asphyxia modle had pathological injure of myocardium tissue and clinical fecture,apoptosis of myocardium cell was a styl of injure of myocardium after asphyxia.3.The pathological injure of myocardium tissue was remarkable through optical microscope and electron microscope,apoptosis of myocardium and Blood CK-MB,cTnI was higher remarkablein neonatal rat asphyxia modle.The modle was of long term stability and suitable for pathogenesy research of injure of myocardium produced by asphyxia and multiorgan damage which established a good foundation for observing After effect and reaseach of Relatively elements of asphyxia experim-ental. Objective:Myocardium damage was produced asphyxia which is important organof multiple organs disorder in asphyxia.Besides asphyxia,there were.other factors which take part in myocardium damage in asphyxia,it is unclear at present.Making neonatal rat asphyxia modle,revealing internal association between myocardium damage of asphyxia and oxyradical,antioxidase,expression of Heme oxygenase-1mRNA and heme oxygenase-1mRNA imhibition ZnPP.Observing affection of oxyradical,antioxidase,expression of heme oxygenase-1mRNA and heme oxygenase-1mRNA inhibition ZnPP to asphyxia myocardium damage.To illuminate intensive assocition factors with asphyxia myocardium damage.In order to provid reliable laboratory proof for prevention and treatment of asphyxia myocardium damage.Methods:88 after born 7d SD rats,male or female were randomly divided into control group(n=8),asphyxia group(n=40),and asphyxia +ZnPP group(n=40).The asphyxia group was further divided into 6h(n=8),24h(n=8);48h(n=8);72h(n=8); 7d(n=8);and asphyxia +ZnPP group further divied 6h(n=8);24h(n=8);48h(n=8); 72h(n=8);7d(n=8) too.Then,blood and myocardium tissue were took at 6h,24h,48h, 72h,7d.Myocardium tissue been made into pathological sections.1.Pathological injury of myocardium tissue was observed through optical microscope and eleotron microscope;2.Myocardial cell apoptosis was observed through TUNEL method;3. Expression of heme oxygenase-1mRNA was observed through in stitu hybridization histochemistry;4.CK-MB,cTnI level in blood was observed through ELISA method; 5.The activity of SOD was determinated by xanthine oxidase method;the activity of GSH-Px was determinated by the method of dithiobisnitrobenzoing acid;the activity of XOD was determinated by chemical colorimetry method;the content of MDA was determinated by thiobarbituric method in myocardium tissue.Result:1.Myocardium tissue's pathological changing;①asphyxia group:under optical microscop,myocardium cell swelling,there were a few inflammation cell and a little bleeding;under electon microscop,there were swelled mitochondrion, concentrated cell organs,condensed nucleu;②asphyxia+ZnPP:under optical microscop there was a lot of imflammation cell and bleed much,myocardial fibers arranged in disorder.Myocardial cell edema,becoming vacuole,under electron microscop,myocardial cell fusion,myocardial fibers melting,mitochondrion edema and pycnosis,mitochondrial crista melting,asphyxia+ZnPP group's pathogenesis injury was serious more than asphyxia group's.2.①The level of CK-MB,cTnI in blood in asphyxia group was higher much than that in control group(P＜0.01);②the level of CK-MB,cTnI in blood in asphyxia+ZnPP group was higher much than control group(P＜0.01);③the level of CK-MB,cTnI in blood in asphyxia+ZnPP group was higher than that in asphyxia group(P＜0.05).3.①Myocardial cell apoptosis in asphyxia group was higher much than that in control group(P＜0.01);②Myocardial cell apoptosis in asphyxia+ZnPPgroup was higher much than that in control group(P＜0.01);③the myocardial cell apoptosis in asphyxia+ZnPP group was higher than that in asphyxia group(P＜0.05).4.①Activity of SOD,GSH-PxXin myocardium tissue in asphyxia group was lower much than that in control group,activity of XOD,MDA content in myocardium tissue in asphyxia group was highermuch than that in control group(P＜0.01);②Activity of SOD,GSH-Px in myocardium tissue in asphyxia+ZnPP group was lower much than that in control group,activity of XOD,content of MDA in myocardium tissum in asphyxia+ZnPP was higher much than incontrol grou(P＜0.01);③Activity of SOD, GSH-PX in myocardium tissue in asphyxia+ZnPP was lower much than that in asphyxia group,activity of XOD,content of MDA in myocardium tissue in asphyxia+ZnPP group was higher much than in asphyxia group(P＜0.01).5.①Expression of HO-1mRNA in myocardial cell in asphyxia group was highermuch than that in control group(P＜0.01;②expression of HO-1 mRNA in myocardial cell in asphyxia+ZnPP group was higher a little than that in control (P＜0.05);③expression of HO-1mRNA in myocardial cell in asphyxia group was higher much than that in asphyxia+ZnPP group(P＜0.01).6.Myocardium tissue pathological damage and apoptosis of myocardial cell contint until 7d after asphyxia.Conclusion:1.After asphyxia,myocardium tissue damage after asphyxia was obvious,apoptosis of myocardial cell was higher much,there was bleed,a few inflammation cells and CK-MB,cTnI level in blood is higher much.2.After asphyxia,CK-MB,cTnI level in blood is higher much.apoptosis of myocardial cell was higher much than that in control group,which indicated apparent apoptosis of myocardial cell was a style of myocardium tissue damage.3.After asphyxia,oxidative stress increased strong in myocardium,the lower activity of SOD,GSH-PX,the higher activity of XODand MDA content,the more serious in myocardium tissue was,which indicated apparent:Oxidative stress is a important factor in myocardium tissue after asphyxia.4.Expression of HO-1mRNA in myocardial cell in asphyxia group was higher much than that in control group and asphyxia+ZnPP group,expression of HO-1mRNA in myocardial cell in asphyxia group was higher little than that in control group,which means hypoxia inducted high expression of HO-1mRNA of myocardial cell.ZnPP can inhibition expression of HO-1mRNA under hypoxia.5.When hypoxia,there was colse relationship between myocardium tissue damage and expression of HO-1mRNA.The higher expression of HO-1mRNA in myocardial cell was,the more little damage of myocardium tissue was.6.Expression of HO-1mRNA was closed relationship with oxidative stress,the higher expression of HO-1mRNA was,the more activity of SOD,GSH-PX was,the lower activity of XOD and content of MDA was.So maybe using HO-1 induction to protect and treat damage of myocardium tissue after asphyxia is necessary.7.Oxidative stress plays a important role in myocardium tissue damage in asphyxia stress.Increasing expression of HO-1mRNA can inhibiton strong oxidative stress, which indicated apprent;HO-1mRNA and HO-1 can decreased damage of myocardium tisssue when hypoxia.So maybe using antioxidative stress drug to be important treating method to damage of myocardium tissue after asphyxia. |
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