|
Objective: This study through the establishment of acute organophosphate poisoning (AOPP) rat model, the application of different doses of atropine and pralidoxime chloride its treatment. By observing the rat clinical manifestations, neurological changes in cell morphology and the determination of rat brain acetylcholinesterase (AChE)-positive cells in the area ratio of acute organophosphate poisoning mechanism of nerve injury, while understanding the different doses of atropine and pralidoxime chloride due to its nervous system injury, and further guide clinical treatment. Methods: 2LD50 omethoate gavage model of acute organophosphate poisoning, and 70 rats were randomly divided into 7 groups grouping principles, each 10. Group A (control group): the experimental group to the same volume of saline intragastric infusion; while the remaining six groups intragastric perfusion 2LD50 (100mg/kg) omethoate; B group (untreated group): Not after exposure any treatment; C group (small amount of atropine dose pralidoxime chloride); D group (moderate amount of atropine, pralidoxime chloride); E group (surprise given the amount of phosphorus chloride amount atropine); F group (small dose of atropine moderate amount of phosphorus chloride set); G group (large doses of atropine moderate pralidoxime chloride). 24h after the animals anesthetized by intraperitoneal injection of chloral hydrate in vivo after brain tissue were excised cerebral cortex, hippocampus brain tissue specimens were quickly placed in 4% paraformaldehyde solution, fixed, do hematoxylin - eosin (hematoxylin -eosin, HE) staining morphology, electron microscopy and acetylcholinesterase (AChE) immunohistochemical staining. By observing the clinical manifestations of rat nerve cells and determination of morphological changes in rat brain AChE positive cell area ratio of indirect to understand nerve damage, through statistical methods whether the differences between groups. Results: The clinical manifestations of a poisoned rat in group A (control group) rats did not have any toxic manifestations; B group (untreated) rats exposed to approximately 20min after apparent poisoning, including muscarinic manifestations (nausea, vomiting, sweating, lacrimation, salivation, miosis, and shortness of breath, which has three significant difficulty in breathing), nicotinic manifestations (limb muscle fibrillation occurs), the performance of the central nervous system (ataxia, coma and convulsions); C group were mild muscle fibrillation, dry mouth and ataxia, no muscarinic manifestations; D group were mild ataxia; E poisoning rats without clinical manifestations, only light degree of dry mouth; F rats were mild nausea, vomiting, salivation, miosis, and spiritual malaise; G rats atropine poisoning, such as the previous expansion of the pupil, dry mouth, skin and mucous membranes dry, while extreme irritability, irritability. 2 HE staining rats in group A (control group) did not have any rat nervous system lesions; B group (untreated) rat nerve cells appear edema, degeneration and necrosis; C rats also appeared obvious nerve cells edema, but no nerve cell necrosis; D group, F, and G group of nerve cells in rats with mild edema; E rat nerve cells occasionally edema, no obvious lesions. 3 rat cortical neurons performance electron microscopy: A group (control group) did not have any lesions in rats; E rats showed normal neurons; D group, F, and G of neurons in rats did not occur edema, But performance gap widened blood vessels, swelling of mitochondria; C neurons of rats with mild edema, some vascular gap widened, mitochondrial swelling; B group (untreated) neurons showed edema, accompanied by vascular gap widened, mitochondrial swelling. Hippocampal neurons: A group (control group) did not have any lesions in rats; E rats showed normal neurons, glial cell edema; D group, F, and G of neurons in rats did not occur edema, But the performance of neuronal shrinkage, increased electron density neuropil and glial cell edema; C group were mild neuronal and glial edema; B group (untreated) neurons showed edema, organelles basic normal. 4 Immunohistochemical staining rat AChE in Group A (control group) in rat brain tissues expressed significantly, while in group B (untreated) rat brain tissues rarely by image analysis, and A group was statistically significant (P lt; 0.05), poisoning group compared with control group AChE positive cells decreased, organic phosphorus on AChE inhibition. AChE in different brain tissue of rats treated with different expression by image analysis, with the A group and B group were statistically significant (P lt; 0.05), can be considered organic phosphorus compounds inhibit AChE, treatment group AChE with resurrection; E and group C and D group, there was statistically significant (P lt; 0.05), can be considered assault group of smaller amount of phosphorus chloride dose and moderate-dose pralidoxime chloride group resurrection of AChE role better; F, and G and D group, no statistical significance (P gt; 0.05), still can not think of atropine on AChE affected. Conclusion: Acute organophosphate poisoning can lead to cerebral cortex, hippocampus injury; different doses of pralidoxime chloride group on rat cerebral cortex, hippocampus AChE were with resurrection, to surprise the amount of phosphorus chloride group resurrection best, moderate amount of chlorine Phosphorus given group, followed by a small dose pralidoxime chloride worst group, suggesting different doses of pralidoxime chloride are to relieve cerebral cortex, hippocampus damage effect, and the amount of phosphorus chloride to assault the best; different doses of atropine brain cortex, hippocampus AChE positive cell area than group comparison meaningless, and the cerebral cortex, hippocampus and electron microscopy HE undifferentiated nerve cell morphology, still can not think of atropine on the cerebral cortex, hippocampus AChE influential, suggesting that different doses of atropine to alleviate rat cerebral cortex, hippocampus injury had no effect, but will relieve M-like symptoms through mechanisms such as central nervous system damage mitigation remains to be further studied.
|