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BACKGROUND: The pathways induced/activated by mercury poisoning that lead to muscle pain remain unclear. The present study addressed the structural changes observed in the peripheral nerve following mercury poisoning. OBJECTIVE: To establish the mercury poison rat model, rats were intragastrically administered mercury. The correlation between post-mercury poison-induced muscular pain and tibial nerve morphological changes were observed. DESIGN: Observational contrast animal study.SETTING: Shangdong Academy of Occupational Health and Occupational Medicine.MATERIALS: Thirty adult Sprague Dawley rats of equal gender. Mercury chloride (HgCl2, analytical grade: 99.99%; batch number: 990402) was provided by Shanghai Chemical Reagent Factory, and sodium dimercaptopropanesulfonate (DMPS) injection by Shanghai Harvest Pharmaceutical Co., Ltd. (batch number: 0309011).METHODS: This study was performed at the Animal Experimental Center of Shangdong Academy of Occupational Health and Occupational Medicine from December 2005 to January 2006. Rats were randomly divided into high-dose mercury, low-dose mercury, and control groups, with 10 rats in each group. Rats in the two mercury groups were intragastrically administered 17 mg/kg and 8.5 mg/kg HgCl2 solution, respectively, once a day to establish a rat model of subacute mercury poisoning. Rats in the control group were intragastrically administered 2 mL saline, once a day. Intragastric administration in the three groups lasted for (20 ± 2) days. After model establishment, rats in the two mercury groups were injected DMPS once a day to remove mercury. The injection lasted for 3 days after every 4-day interval. Seven days was regarded as one treatment cycle, and there were two treatment cycles in total.MAIN OUTCOME MEASURES: Mercury-induced muscular pain status; ultrastructural changes of the right tibial nerve following model establishment and mercury removal under transmission electron microscope.RESULTS: Thirty rats were included in the final analysis. Muscular pain status: one rat exhibited mercury-induced muscular pain. Red swelling of the skin was observed on the posterior claws, lower limbs, and tail. The rat incessantly licked and scratched the red swelling of the skin, ted over, and occasionally hissed. The axon myelin sheath of the tibial nerve was intact, clear, and dense. The mitochondrial membrane was intact and smooth, and the cristallin was clear. Microfilaments and microtubules were tightly arranged. Axon pathological changes and demyelination lesion occurred in the right tibial nerve in the two mercury groups. However, mercury removal with DMPS for two treatment cycles did not inhibit the peripheral nerve lesion. In the pain model rats, the myelin sheath of the tibial nerve was mottled. Mitochondria in the axoplasm were swollen, the structure was unclear, numbers were decreased, and cristallin disappeared. The mitochondrial membrane was broken, and the microfilament was reduced and unorganized. After two treatment cycles of mercury removal with DMPS, nerve demyelination lesion was aggravated, and the myelin sheath was increasingly mottled. Both rarefaction degeneration and vacuolar transformation were observed in most of the axon myelin sheath. The axonal membrane was damaged to a certain degree.CONCLUSION: Subacute HgCl2 poisoning might result in tibial nerve injury. The myelin sheath of the tibial nerve was mottled in mercury poisoned rats without muscular pain. Nevertheless, the correlation between mercury poisoning and pain remains unclear. The injured tibial nerve of the rats was not repaired after dimercaptopropanesulfonate treatment.