The Changes Of Biochemical Indexes In Myasthenia Induced By Omethoate Poisoning In Mice

Acute organophosphrus poisoning can result in three syndromesof the central neural system of human being: acute cholinergic crisi(ACC), termediate myasthemia syndrome (IMS) and organophosphateinduced delayed polyneuropathy OPIDP). The relationship ofcholinesterase, myocardium zymogram and the change ofintramuscular power is nearly known,although there are case reportsof OP-induced myopathy.The present study was designed to establisha myasthenia mouse experimental model to observe the change ofzymogram in IMS. Eight-week-old male mice, healthy and smooth coat, weight 20±g,were divided into 4 groups at random.Group A (n=8) is normal,given no poison and no medicine cure.Group B (n=18) is brine group,muscle injecting brine with the same dose as omethoate. Group C isthe 24hr group.there are 10 mice per cage which is assigned by 4time-point (30min, 2h, 4h, 12h). Group D is 1~7 days group.there are15 mice per cage as the same assignment (24h, 48h, 72h, 96h and5~7d). Group C and D are celiac injected with omethoate (50mg/kg)and atropine (10mg/kg) at the same time. The toxic mice survive theurgent period treated with atropine only. Clinical signs, such as posture, activity, foraging, weight areobserved on time. The intramuscular power is evaluated by Lennon'smeasure in group D, declining board and traction test are also used forthe evaluation. The animals are taken blood 1ml through the heart atthe time of 30 min, 2h, 4h, 12h, 24h and 1~7d. Centhifug-alizing theblood and the serum are taken,examined CHE, CK, AST and LDH.The result shows that CHE activity is persistent inhibition. The levelsof AST, CK and LDH are higher, especially CK. It is significantlydifferent in comparison with the level of group A and B (p<0.05).Thisis also significantly different between two point in group C. So isthat in group D except CHE and LDH (p<0.05). The percentage ofmyasthenia mice is significantly higher after poisoning 1-4d than thatafter poisoning 5~7d (p<0.05). Furthermore it is the highest afterpoisoning 48h.The zymogram level of muscle weakness mice atrandom is significantly higher in comparison with that of normalmuscle mice (p<0.05).Acetylcholine is the chemical conductive medium of centralneural system and cholinogenic nerve. The toxicity oforganophosphorus pesticide is that it combines with cholinesterase toform phosphatidyl cholinestsrase, the latter is steady and can'tdecompose acetylcholine , makes acetylcholine accumulate in effectorand results in the clinical syndrome. We can have CHE activity as thestandard of poisoning grade judgement and distinguishable diagnose.In the experiment, CHE activity is persistently inhibited afterpoisoning 1~7d. And it can be inhibited whether the mouse ismyasthenia or not. So the CHE activity inhibition may be the start-upfactor, not the efficient-amse about IMS. The higher level of CK isoften observed in RM, respiratory muscle weakness and cardialdamage after poisoning. So we study the change of enzymology inIMS after eliminating the forenamed syndromes. In our experiment itis difficult to eliminate the disadvantageous factors resulted from thecardial damage of mice. So pathological examination is necessary tothe patients of organophosphorus pesticide poisoning except the usingof deficient dose of atropine and oximes.IMS is characterized by cranial and respiratory muscle weaknesswhich occurs 1~4d after poisioning,following the cholinergic phase.All of them have got out of acute cholinergic crisis, and they haveregained consciousness, no rale in the lung with cranial, respiratoryand neck muscle weakness or two of them have done. Half of themmake tendon reflex weaken. Persistent inhibition of CHE activity issuggested to underlie IMS. Oximes and atropine treatment can'tcontrol the muscle injure. It can recovery by itself except death inpatients with respiratory muscle weakness.The occurrence of IMS is related with:① the category of poison:DDV, dimethoate, 1605, monocrotophos, omethoate, methamidophosand so on. Most of them are high and poignant toxicants. They may bechange into new nerval toxicant after liver metabolize. ②organophosphate consumption. ③ prior oximes and atropinetreatment. ④ the inhibition of CHE. ⑤ the drop level of blood K+.In our experiment we build up the animal model with mouse,which has muscle weakness or not after poisoning. The diverse andsensitivity of enzymology is different. We would continue to studyother enztmology referred to IMS in future.The findings in this study is that the percentage of muscleweakness is higher after poinsoning 1~4d, especially 48h. Theinhibition of CHE is persistent and it is lower within 24h. It causes15% inhibition of CHE activity at most. And the CHE activity beginsto recovery after poisoning 1 days but still under the normal, whichcauses 70%~90% inhibition and is nothing with muscle power. Thelevel of myocardium zymogram is higher, especially CK. So it can beone of the standards of enzymology following poisoning earlier.There are many other factors that can result in the high level of CK, itcan not be regarded as the independent factor for IMS.