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Objective To observe the effects of mild hypothermia on the myocardial mitochondrial injury induced by oxidative stress after restoration of spontaneous circulation (ROSC) in rat of cardiac arrest model.Methods Eighteen male Wistar rats were randomly (raudom number) divided into normal temperature group and mild hypothermia group after ROSC.Ultrasound was used to measure the left ventricular ejection fraction (EF),shortening fraction (FS) and stroke volume (SV).The levels of glutathione (GSH),malondialdehyde (MDA) and adenosine triphosphate (ATP) in myocardium were detected.The ultramicroscopic structure of myocardial mitochondria was observed under transmission electron microscope at 4 h after ROSC.Results There were no significant differences in basic life support (BLS) time,dosage of epinephrine and number of defibrillation attempt between two groups (P ＞ 0.05).The concentrations of GSH and ATP in myocardium of rats in hypothermia group were significantly higher than those in normal temperature group,while the level of MDA was significantly lower in hypothermia group than that in normal temperature group.Echocardiographic findings showed that hypothermia could significantly improve the EF,FS and SV after ROSC.The hypothermia decreased the myocardial mitochondria injury rather than normothermia [mitochondrial injury score:(0.21-±0.04) vs.(0.42 ±0.08),P ＜ 0.05].Conclusions In this model,mild hypothermia can decrease myocardial oxidative stress injury,improving the cardiac function after ROSC.
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Objective To explore the effects of estrogen on oxidative stress of the lung tissue induced by acute paraquat (PQ) poisoning. Methods Thirty-two male adult New Zealand rabbits were randomly divided into model group and estrogen intervention group, 16 rabbits in each group. The model of lung injury induced by PQ poisoning was reproduced by feeding 16 mg/kg of 20% PQ through gastric tube. The rabbits in estrogen intervention group received intravenous infusion of 5 mg/kg estrogen after PQ challenge for 7 days, and the rabbits in model group received an equal volume of normal saline. Three rabbits in each group were sacrificed at 1, 2 and 3 days respectively after exposure. The lung tissue was harvested, the levels of reactive oxygen species (ROS) was determined by 2',7'-dichlorofluorescin diacetate (DCFH-DA), malondialdehyde (MDA) was determined by thiobarbituric acid (TBA), the mRNA expression of manganese-containing superoxide dismutase (MnSOD) was determined by reverse transcription-polymerase chain reaction (RT-PCR), and adenosine triphosphatase (ATP) content in mitochondrion was determined by enzyme linked immunosorbent assay (ELISA). The pathological changes in lung were observed under light microscopy using hematoxylin and eosin (HE) staining, and the lung injury was evaluated with lung injury score. Results The contents of ROS and MDA in lung within 3 days after PQ poisoning were gradually increased, and MnSOD mRNA expression and ATP content were gradually decreased. Estrogen intervention could significantly reduce the production of ROS and MDA after PQ poisoning [3-day ROS (fluorescence intensity): 161.05±30.04 vs. 188.30±31.80, 3-day MDA (mmol/L): 98.71±0.92 vs. 122.12±1.24], up-regulate MnSOD mRNA expression (integral A value: 3.05±0.90 vs. 1.22±0.24), and increase ATP content in mitochondrion (ng/L: 3.75±0.92 vs. 2.28±0.29) with statistically significant differences (all P < 0.01). In lung tissue after PQ poisoning, congestion, edema, focal pulmonary consolidation, pulmonary interstitial and alveolar space were infiltrated by a large number of neutrophil, alveolar interval were thickened obviously and the above phenomenon were most serious at 3 days after poisoning as shown under optical microscope. Estrogen intervention could significantly improve lung injury as compared with that of model group, and the lung injury score at 3 days was significantly lower than that of model group (11.8±0.7 vs. 13.5±1.0, P < 0.01). Conclusions The oxidative stress indicators in the lung tissue after PQ poisoning were obviously abnormal, the pathological damage was serious with time dependence. The administration of estrogen can reduce acute lung injury after PQ poisoning by reducing the oxidative stress.
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AIM: To probe into the anti-epilepsy action of artificial Calculus Bovis,by observing its effect on the behavioral of the experimental epileptic rats,neuron loss in the hippocampus and hilus,and GAD positive cell alteration in the hippocampus.METHODS: SD rats were divided into three groups: group A(artificial Calculus Bovis treatment group);group B(acute epilepsy group) and group C(control group).A model of acute epilepsy rats was established by PTZ.The rat's behavioral alteration was observed by the Racine' scale.The neurons in the hippocampus and hilus were calculated by Nissl staining.The GAD positive cells were observed by immunohistochemical staining.RESULTS: The latency of the first seizure in group A was longer than that in group B,while the seizure times in group A was less than that in group B.Besides,in group A,both the neuron loss amount in the hippocampus and hilus and the GAD positive cell loss amount in the hippocampus were less than those in group B.CONCLUSION: The artificial Calculus Bovis prolonged the latency of the first seizure time,decreased the frequency of seizure,and prevented the neuron loss and protected the GAD positive cells.