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METHODSSixty Sprague-Dawley rats were randomly divided into five groups: negative control, positive control, low-dose DCE (1 472 mg/m(3)), middle-dose DCE (2 550 mg/m(3)), and high-dose DCE (4 418 mg/m(3)). The three DCE groups received static inhalation of DCE 6 hours a day for 6 consecutive days. The positive control group received intraperitoneal injection of lipopolysaccharide (5 mg/kg) and were sacrificed 8 hours after injection. Blood and brain tissue were collected, followed by determination of brain water content and HE staining for pathological examination of brain tissue.

RESULTSThe rats in DCE groups suffered decreased body weight with increasing DCE dose (P < 0.01), and brain water content rose with increasing DCEdose. The brain water content of middle-dose DCE group (80.09 ± 0.14%) and high-dose DCE group (80.28±0.10%) increased significantly as compared with that of the negative control group (79.46±0.23%) (P < 0.001). Optical microscopy discovered loose structure and vasodilation in the brain tissue of middle-dose DCE group, indicating obvious brain edema; the high-dose DCE group and positive control group had spongiform and vacuolated brain tissues with severe vascular dilation, indicating severe brain edema.

CONCLUSIONA rat model of subacute toxic encephalopathy induced by 1, 2-dichloroethane has been successfully established.

Animals ; Disease Models, Animal ; Ethylene Dichlorides ; toxicity ; Male ; Neurotoxicity Syndromes ; Rats ; Rats, Sprague-Dawley

1.One Death Case Caused by Subacute Poisoning of 1,2-Dichloroethane.

2.Successful rescue of a case with 1, 2-dichlorethane and cyclohexanone intoxication.

3.Two cases of occupational acute severe 1, 2-dichloroethane poisoning.

4.Investigation on subacute poisoning accident in dichlorethane construction site.

5.One case of ethylene dichloride poisoning with wrong diagnosis as epilepsy.

6.Clinical manifestation and head MRI of severe dichloroethane poisoning induced toxic encephalopathy.

7.Experience of treatment of subacute encephalopathy induced by 1, 2-dichloroethane poisoning.

8.Therapy of encephalopathy induced by severe dichloroethane poisoning.

9.Discussion on the treatment of increased intracranial pressure caused by the occupational acute 1,2-dichloroethane poisoning.

10.Establishment of a rat model of subacute toxic encephalopathy induced by 1, 2-dichloroethane.

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