A Study Of Apoptosis On Asthma Rat's Myocardium

Background and purpose:The bronchus asthma is a familiar disease, its paroxysm characteristic is an inflammation to respiratory airway with airway high reaction and airway remodeling.In recent years, the reports of the outbreak rate and death rate about the bronchus asthma were on the increase year by year.In the forensic medicine, the reports of disputing case examples about sudden death caused by asthma also were increased gradually, there were still much difficulties on the analysis of cause of death now.Although there were many reports of damage for expressing, asthma sufferer in addition to lung a pathological changes as well having myocardium, these researching discovers about sudden death had been caused by asthma all did not had the particularity on the analysis of cause of death in forensic medicine, and the molcule pathology mechanism of myocardial damage had been caused by bronchus asthma was still not pure, the related cultural heritage reports were too more seldom seen.On the basis of successfully establishing the SD rat bronchus asthma animal model, this study has associatively adopted routine HE, myocardium organizes HSP70 immunohistochemistry,TUNEL and flow cytometry methods,and to study the myocardial damage that every kind of medicine interfere the expression regulation of the term bottom,and to inquiry into the pathologic mechanism in molcule that bronchus asthma myocardial cell has been injuried with period,to provide adequate morphologic grounds for the differential diagnosis of cause of sudden death caused by asthma in the forensic medicine.Methods:There were one hundred and twenty male Sparague-Dawely rates,they were one-month-year-old and 100±15 gram weight or so. On the basis of successfully establishing the SD rat bronchus asthma animal model, they were randomly divided into six groups: a group of adrenaline to deal with asthmatic syndrome, a group of amonophylline to deal with asthmatic syndrome, a group of adrenaline and amoniphylline to deal with asthmatic syndrome, a group of no drugs to deal with asthmatic syndrome, experimental control, normal control. Every group again was divided as four subgroups(2W,4W,6W,8W) according to death time by breaking off the cervical spine .Every subgroup had five rats .Each rat had been drawed its myocardium of cardiac ventricle after death.A slice of myocardium has been put into 10% Formalin solution to fixed, or conventional paraffin embedding and dicing,and has been taken routine HE with myocardium organizes HSP70 immunohistochemistry and TUNEL methods to examine their damage regulation.Another myocardium has been not taken fixing to keep fresh phase,and has been taken flow cytometry (FCM) to examine.All related experiment results has been studied by using microscope with IMAGE analytical system and homologous statisticses.Results:1 routine haematoxylin and eosin dyeingThe comparison groups and other experimental groups are not obviously distinctive.Myocardium cell dyeing and cell transverse striation are clear, and the cell nucleuses are compact, then have not seen any myocardium cell necrosis.Between the myocardium cell the nature has not seen the inflammation germ cell to infiltrate, the partial regions obviously myocardium fiber assumed the wave shape changing and myocardium fiber breaking off.2 myocardium organizes HSP70 immunohistochemistryIn the experimental control and normal control the positive test signal expressing of myocardium cytoplasm HSP70 of SD rat mostly were negative in each period of time.In the other experimental groups the positive test signal expressing of myocardium cytoplasm HSP70 of SD rat had begun to appear at experimental second week,and along with time lengthening,the myocardium cytoplasm HSP70 expression (PI-HSP70 value) had been strengthened gradually, to 8th week it was highest.According to different medicine intervention on the experimental groups, SD rat myocardium cytoplasm HSP70 positive signal expression intensity (PI - HSP70 value) had the remarkable difference in same period of time,were in turn: a group of adrenaline to deal with asthmatic syndrome > a group of adrenaline and amoniphylline to deal with asthmatic syndrome > a group of no drugs to deal with asthmatic syndrome >a group of amonophylline to deal with asthmatic syndrome.The experiment compares between the experimental control and normal control, there were not obvious difference on the PI -HSP70 value.3 TdT-mediated dUTP-biotin nick end labeling-TUNELIn each period of time, the majority of SD rat myocardium cell nucleus TUNEL positive signal expression intensity were negative in experimental control and normal control.In the other experimental groups the positive test signal expressing of myocardium cell nucleus TUNEL of SD rat had begun to appear at experimental second week,and along with time lengthening,the myocardium cell nucleus TUNEL expression (PI-TUNEL value) had been strengthened gradually, to 8th week it was highest.According to different medicine intervention on the experimental groups, SD rat myocardium cell nucleus TUNEL positive signal expression intensity (PI - TUNEL value) had the remarkable difference in same period of time,were in turn: a group of adrenaline to deal with asthmatic syndrome > a group of adrenaline and amoniphylline to deal with asthmatic syndrome > a group of no drugs to deal with asthmatic syndrome >a group of amonophylline to deal with asthmatic syndrome.The experiment compares between the experimental control and normal control, there were not obvious difference on the PI -TUNEL value.4 flow cytometer-FCMMyocardium cell apoptosis rates of all experimental groups obviously were higher than the controls.It had begun to increase gradually at experimental second week,and along with time lengthening, to 8th week it was highest.According to different medicine intervention on the experimental groups, SD rat myocardium cell apoptosis rate had the remarkable difference in same period of time,were in turn: a group of adrenaline to deal with asthmatic syndrome > a group of adrenaline and amoniphylline to deal with asthmatic syndrome > a group of no drugs to deal with asthmatic syndrome >a group of amonophylline to deal with asthmatic syndrome.The experiment compares between the experimental control and normal control, there were not obvious difference on the myocardium cell apoptosis rate. Conclusion:1 Myocardium cell of bronchia asthma SD rat has the certain degrees of damage,and it goes into action the extension of the time along with asthma but aggravation.2 The myocardium cell apoptosis caused by myocardium cell apoptosis mechanism activation promoted by the asthma that is an important of factor in the molecular pathology mechanism of asthma myocardium cell damage.The quantity and the expression of myocardium cell apoptosis goes into action the extension of the time along with asthma but aggravation.3 Some medicines about asthma may promote the myocardium cell apoptosis,such asβ2-acceptors excited medicinal preparations - adrenalin.4 In the forensic medicine about the antidiastole of cause of sudden death caused by asthma, the myocardium cell apoptosis caused by asthma has taken the heart function to suffer injury was a factor which was worth taking.In the forensic pathologic examination about the sudden death caused by asthma, as an assistant diagnosis basis of the myocardium cell damaging.,besides taking the routine HE examination method to examine the myocardium organization, and may consider taking the immunohistochemical method as well as TUNEL and the FCM method.