| Background：Fluoroacetamide is an efficient, highly toxic,strongly absorbent organic fluoriderodenticide,long residual period,no corrosive effect.Fluoroacetamide poisoning has anacute onset and rapid progression.It often causes the heart, brain, lung, liver, kidneyand other organs damaged.Bcause it can cause the second time poisoning in humanand animals, the country has banned its production and use for the moment. Butbecause of its obvious effect, many vendors are still producting and selling itillegally,which makes fluoroacetamide poisoning incidents often occurred,indeedthere is an upward trend in recent years. Fluoroacetamide has obvious damage to theheart,which reflected in the myocardial cell and conduction systemdamaged,myocardial damage rate is above80%.Fluoroacetamide poisoning can causeall kinds of arrhythmia, heart failure,drop of blood pressure, even ventricularfibrillation;abnormal cardiac function is the second cause of death. At present themechanism of poisoning recognized as is that fluoroacetamide make three carboxylicacid cycle interrupt, which lead to the different organ injured,but the degree of injuryand treatment of myocardial after poisoning is lack of further research. Investigationof myocardial injury degree caused by fluoroacetamide poisoning and the effectivemethod of treatment has an important clinical implication to improve the prognosisand reduce the mortality rate.Objective：The main purpose is to investigate the myocardial damage degree of rat offluoroacetamide poisoning,and the relationship with oxidative damage;whetheracetamide combined with alprostadil injection has protective effects on myocardialinjury in poisoning rats.Methods：Making fluoroacetamide poisoning rat model through gavage method, the amount of rats was eighty, half was male and half was female.The rats were randomlydivided into4groups. Group A was normal control group, this group was given1mlof normal saline by gavage and then given the same dose of normal saline daily byintraperitoneal injection.Group B was fluoroacetamide poisoning group,this groupgiven fluoroacetamide solution with the dose of6mg/kg by gavage to makefluoroacetamide poisoning model,then given the same dose of normal saline daily byintraperitoneal injection.Group C was the acetamide treatment group,this group givenfluoroacetamide solution with the dose of6mg/kg by gavage to make fluoroacetamidepoisoning model,then given acetamide with the dose of2.8g/kg after contamination anhour by intraperitoneal injection(Q12H).Group D was the acetamide+alprostadilinjection treatment group, this group given fluoroacetamide solution with the dose of6mg/kg by gavage to make fluoroacetamide poisoning model,then given acetamidewith the dose of2.8g/kg after contamination an hour by intraperitonealinjection(Q12H),at the same time given alprostadil with the dose of10ug/kg byintraperitoneal injection once a day additionally.Group E was the alprostadil injectiontreatment group, this group given alprostadil with the dose of10ug/kg byintraperitoneal injection once a day.After contamination of the healthy rats,themyocardial tissue were collected to stained with HE to observe the myocardialmorphological changes at different time points(4h,1d,3d,7d);The level of creatinekinase(CK),creatine isoenzyme(CK-MB),aspartate aminotransferase(AST) in theblood and the level of myocardial superoxide dismutase (SOD), malondialdehyde(MDA) in the myocardial tissue were tested, then statistical analysis was carried outto discuss its significance.Results：HE staining showed that the myocardial injury of fluoroacetamide poisoning ratsappeared in1d.The myocardial injury appeared spotty or focal degeneration andnecrosis, surrounding cytoplasm’s eosinophils staining increased, with the infiltrationof inflammatory cells; myocardial injury in3d is the most severe, myocardial cellsappeared necrosis, dissolved and disappeared largely, with the infiltration of a largenumber of inflammatory cells; myocardial injury started to appear the granulation organization in group D and C in7d.When group D was compared with group C andE, the myocardial injury extent is smaller and lesser. Myocardial enzyme start to risein4h, reach the peak at1d, decrease in3d, return to normal standard in7d. Whengroup D was compared with group B and E, the value of CK-MB and AST had astatistical significance(P <0.01) in1d,but when compared with group C and E in theother time point, it had no statistical significance(P>0.05).After fluoroacetamidepoisoning, the content of SOD decreased while the content of MDA increased inmyocardial tissue,when compared with the control group,it was significantly different(P <0.01); The content of MDA in group D was obviously lower than this in group Cand E(P <0.01); the content of SOD in three groups had no statistical significance(P>0.05).Conclusion：(1) Fluoroacetamide poisoning can lead to myocardial injury, which mainlyappeared focal or large-scale necrosis, with the infiltration of inflammatory cells. Themost severe injury after poisoning appeared in3d.Myocardial enzymes reached thepeak in1d,returned to normal standard basically in7d.(2)After fluoroacetamide poisoning,the content of SOD decreased while thecontent of MDA increased in myocardial tissue in healthy rats.So we concluded thatthe myocardial injury associated with oxidative damage.(3) Acetamide combined with Alprostadil Injection have a protective effect tomyocardial injury of the rats of fluoroacetamide poisoning, it can reduce the contentof myocardial injury;shorten the time of myocardial tissue repaired;it has the effect ofanti-oxidative damage which reflected by cleaning up oxygen free radicals andreducing the content of SOD in myocardial tissue effectively. |
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