Basic Research On The Injury Of Heartsabout Paraquat Poisoning Rats And The Medication

BackgroundParaquat (paraquat, PQ) is a world wide application of herbicides.It is venomous toperson cultivate, but the mechanism is still not very clear. there is no specific antidotetherapy. Paraquat poisoning can cause acute lung injury (ALI), acute respiratory distresssyndrome (ARDS), multiple organ failure (MODS), eventually causing death of patients.But some patients in poisoning after a short period of time that the occurrence of death,considering the PQ poisoning in the early phase of cardiac injury in patients with acute PQpoisoning may be the cause of death. So to investigate the PQ heart injury induced bymechanism and effective treatment methods to decrease the mortality rate, improve theprognosis has important significance.ObjectiveThe main purpose is to investigate the pathogenic mechanism of paraquat and theoptimum therapeutic dose of ulinastatin in treating paraquat poisoning.MethodsAt the beginning of the experiment, we made the poisoning rats model, then extractedheart on the1st,3rd,7th,14th,respectively. With the methods of HE stain andimmunohistochemical, we observe the pulmonary tissue and assay the content of ICAM-A,NF-Kb, TNF-α in lung tissue. All of the60rats are provided by experimental animal centerof Jilin university. The body weight of the rats is (250+20) g, including male and femalehalf-and-half. The rats are divided into seven groups randomly. Group A is the normalcontrol group, using1ml physiological saline intragastric administration. Group B is PQpoisoning group, using PQ solution50mg/kg intragastric administration, and isodosephysiological saline intraperitoneal injection. Group C is ulinastatin therapeutic group, usingulinastatin one hundred and eighty thousand iu/kg intraperitoneal injection and then twice aday. We extracted the lung tissue on the1st,3rd,7th,14th day respectively after poisoning,then carried out the HE stain and immunohistochemical to observe the Cardiac tissue andassay the content of TNF-α in lung tissue, and then made statistic analysis to do groupcomparison. With the methods of HE stain, ICAM-A, NF-Kb, TNF-α immunohistochemicalstain and measuring the grey level, we investigate the pathogenesis about the heart injury caused PQ and the therapeutic efficacy about ulinastatin.ResultsThe results of HE stain suggest that, Paraquat poisoning in rats after myocardial bloodvessels to dilate, interstitial congestion, edema, or myocardial fiber fracture, the emergenceof the point sheet infarction gradually increased with time, resulting in14days began toease; ulinastatin treatment group myocardial injury is significantly reduced. Via NF-κB,ICAM-1, TNF-alpha immunohistochemical staining and measured TNF-alpha gray valueline statistical analysis found that rats can cause poisoning of NF-κB, ICAM-1and TNF-αexpression increased. Group C ulinastatin treatment group of NF-κB, ICAM-1and TNF-αexpression increased, weaker than the control group compared with group A group Bexposed groups.ConclusionParaquat poisoning of rat heart damage, NF-κB and ICAM-1, TNF-α expression inthe paraquat injury on the heart plays an important role. Ulinastatin injection couldsignificantly inhibit the inhibition of the expression of NF-κB and ICAM-1and TNF-α in asignificant therapeutic effect on the heart of paraquat poisoning.