| IntroductionAcute organophosphorus pesticide poisoning has been a global problem that is threatening the health of human. How to take effective measures, reverse conditions of AOPP and decrease case fatality rate is still one of the important subjects in emergency and first aid fields. Severe AOPP patients usually die from MODS or MOF, and people have paid close attention to the function of cytokines for the recent years.As an blood purification method, peritoneal dialysis has been applied widely in acute poisoning and made great effects in clinic, but we still have to inquire into the fuction it acts on cytokines.Objective Through observing the levels of TNF-α,TGF-β1 in serums and TGF-β1/ TNF-αratio and comparing the differences of control and PD group, exploring the effects of TNF-αand TGF-β1 on MODS induced by AOPP, and influencing PD towards them, then supply science proofs for application of PD in clinic and new approach for the treatment of AOPP. Methods Model of rabbits with acute organophosphorus pesticide poisoning was made, by intragastric administration of 25 mg/kg(0.5LD50)40% omethoate. Rabbits of control group were given Pralidoxime Chloride and Atropine for intramuscular injection. Besides these, animals of PD group were inserted in by peritoneal dialysis tube and given peritoneal dialysis for ten times. We observed the levels of TNF-α,TGF-β1 in serums and TGF-β1/ TNF-αratio Results After intoxication, the levels of TNF-αof both groups increased obviously ,achieved peak at 24 hours and the PD group returned the pre-intoxication level, while the control group didn't. The levels of TGF-β1 aslo increased obviously, come to the climax at 48 hours and still at a high level at 72 hours.TGF-β1/ TNF-αratio grow up gradually after 24 hours; the levels of TNF-α,TGF-β1 in PD group were lower than that of control group.DiscussionOrganophosphorus pesticide is one of high efficiency insecticides which has been widely used nowadays, and AOPP takes the first place of acute pesticides poisoning. After poisoning,AOPP patients have hydroxycholine- like,nicotine–like and central nervous system syndrome, acute pulmonary edema,intermediate syndrome,brain edema and organs injuries can also occur in severe cases, some may even die from MODS or MOF induced by SIRS. The mechanisms of MODS induced by AOPP are complex and extensive, including cholinenergy and non cholinenergy mechanisms.In recent years ,the effects of SIRS on MODS induced by AOPP have been paid close attention to.As a fierce stressor , Organophosphorus pesticides lead to a series of emergency reactions, stimulate autonomic nerve,endocrine and immune systems to release pro-inflammatory (IL-1,IL-6,TNF and so on)and anti-inflammatory mediators (TGF-β1,IL-4,IL-10),make immune function in lower,confused and paralysis state,the anomaly systemic immunne state cause SIRS and then bring out MODS.Furthermore,at the early stage of AOPP,the organs and cells got ischemia and anoxia because of respiratory failure,pulmonary edema,shock,lead to ischemia-reperfusion injury,and cause SIRS and then bring out MODS. and lead to extensive injuries of tissues and organs and MODS. So the fuction of the cytokine in the process of MODS induced by AOPP is important to identify and pathogenesy of MODS after AOPP.As a primary cell factor to activate cascade reaction of cytokine in SIRS, TNF-αplays an important part in the process of SIRS/CARS. The mechanisms of tissue injury of TNF in inflammatory reaction are the following :to activate complement system,promote adherecne of leukocyte,activate release reactions of neutrophile granulocytes and mononuclear macrophages,advance blood clotting and induce release of other inflammatory cytokine, through which TNF makes great effects on MODS. Our study proved that the level of TNF-αof both groups increased after intoxication, reached the peaks at 24 hours and didn't return to the pre-poisoning level at 72 hours, which induced that TNF-αis an earlier released pro-inflammatory factor, and SIRS participated the process of MODS induced by AOPP.TGF-β1 is one kind of earlier anti-inflammatory cytokine in inflammatory reaction, it can exercise its restraints upon the proliferation and dissociation of immunocytes,and on the decrease of cytokines prodiction,through which TGF-β1 reduces the fuction of immunity of the organism.This study showed that the levels of TGF-β1 of both groups increased after intoxication , the levels of TGF-β1 of the control group increased gradually and reached peaks at 48 hours ,then decreased gradually ,and had not return to the pre-poisoning level at 72 hours, which proved that there is anti-inflammatory reaction in AOPP and TGF-β1 was the earlier released anti-inflammatory factor.The dynamic change of TGF-β1/TNF-αratio was also observed in this study, and the results showed that after intoxication ,the ratio of the control group had not obviously increased until 24 hours(P>0.05),and then increased obviously after 24 hours(P<0.01), and still at a high level at 72 hours(P<0.01); the TGF-β1/TNF-αratio of the PD group had slightly increased at 12 hours, then decreased gradually at 24 hours, but didn't have statistics discrepancy, then increased obviously after 48 hours,and more obviously increased at 72 hours.This study proved that after intoxication, pro-inflammatory factor(TNF-α) and anti- inflammatory factor(TGF-β1) both complement system,promote adherecne of leukocyte,activate release reactions of neutrophile granulocytes and mononuclear macrophages,advance blood clotting and induce release of other inflammatory cytokine, through which TNF makes great effects on MODS. Our study proved that the level of TNF-αof both groups increased after intoxication, reached the peaks at 24 hours and didn't return to the pre-poisoning level at 72 hours, which induced that TNF-αis an earlier released pro-inflammatory factor, and SIRS participated the process of MODS induced by AOPP.TGF-β1 is one kind of earlier anti-inflammatory cytokine in inflammatory reaction, it can exercise its restraints upon the proliferation and dissociation of immunocytes,and on the decrease of cytokines prodiction,through which TGF-β1 reduces the fuction of immunity of the organism.This study showed that the levels of TGF-β1 of both groups increased after intoxication , the levels of TGF-β1 of the control group increased gradually and reached peaks at 48 hours ,then decreased gradually ,and had not return to the pre-poisoning level at 72 hours, which proved that there is anti-inflammatory reaction in AOPP and TGF-β1 was the earlier released anti-inflammatory factor.The dynamic change of TGF-β1/TNF-αratio was also observed in this study, and the results showed that after intoxication ,the ratio of the control group had not obviously increased until 24 hours(P>0.05),and then increased obviously after 24 hours(P<0.01), and still at a high level at 72 hours(P<0.01); the TGF-β1/TNF-αratio of the PD group had slightly increased at 12 hours, then decreased gradually at 24 hours, but didn't have statistics discrepancy, then increased obviously after 48 hours,and more obviously increased at 72 hours.This study proved that after intoxication, pro-inflammatory factor(TNF-α) and anti- inflammatory factor(TGF-β1) both On the whole, there are pro-inflammatory reaction and anti-inflammatory reaction exist in AOPP, and excessively release of pre-inflammatory mediators and anti-inflammatory mediators and the disorder of this balance are the important mechanisms of MODS induced by AOPP. PD can lower pre-inflammatory mediator(TNF-α) and anti-inflammatory mediator (TGF-β1), which supply new target and way for PD to treat AOPP in clinic.Conclusion SIRS/CARS play an important role in the process of MODS induced by AOPP; TGF-β1/TNF-αratio can reflect the immunne state of the organism and can be an reference index of balance of SIRS/CARS; PD can lower pre-inflammatory mediator(TNF-α) and anti- inflammatory mediator (TGF-β1), prevent excessive pro-inflammatory reaction and anti-inflammatory reation, and have great effects to block up the process of SIRS to MODS in AOPP.
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