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Objective:To explore whether barium chloride (BaCl 2) preconditioning has the protective effect on lipopolysaccharide (LPS)-induced acute respiratory distress syndrome (ARDS) model in mice and the possible mechanism. Methods:Sixty 8-12 week old healthy C57BL/6 male mice were randomly divided into control group, ARDS model group and BaCl 2 pretreatment group, with 20 mice in each group. The BaCl 2 pretreatment group was continuously injected with BaCl 2 (4 mg/kg through the tail vein) for 3 days before ARDS model establishment. ARDS model was established by intratracheally injecting (3 mg/kg) LPS. The control group was intratracheally given the same volume of 0.9% normal saline. On 24th hour after ARDS model establishment, some mice were sacrificed for obtaining fresh lung tissue. And the right lower lobe of the lung was separated for observing the pathological changes of lung tissue while the left lung tissue was used to measure the wet/dry weight ratio (W/D) of the lung. Some mice were sacrificed for observing pulmonary microvascular permeability at 2nd hours after injecting Evans blue (EB) through tail vein. The left mice were killed for alveolar lavage to measure the levels of tumor necrosis factor-α (TNF-α) via enzyme linked immunosorbent assay (ELISA). Results:Comparing with the control group, ARDS model group showed typical ARDS pathological changes, which included the increased W/D ratio (4.951±0.161 vs. 3.449±0.299, P < 0.01) and the content of EB in the lung tissue (μg/g: 0.130±0.027 vs. 0.085±0.011, P < 0.01), the damaged alveolar wall structure, lung congestion and exudates in the alveoli, as well as amounts of inflammatory cells. The pathological score of lung injury (10.33±1.15 vs. 1.67±0.58) and the level of TNF-α in BALF (ng/L: 900.85±247.80 vs. 68.21±5.79) were significantly increased in the ARDS model group (both P < 0.01). Comparing with the ARDS model group, the lung W/D ratio (4.620±0.125 vs. 4.951±0.161) and the EB content in the lung tissue (μg/g: 0.108±0.011 vs. 0.130±0.027) of BaCl 2 pretreatment group were significantly reduced (both P < 0.01). And the damaged pulmonary structural BaCl 2 pretreatment group were significantly alleviated. In addition, the pulmonary pathological score (5.00±1.00 vs. 10.33±1.15) and the level of TNF-α in BALF (ng/L: 169.16±73.33 vs. 900.85±247.80) were significantly decreased (both P < 0.01). Conclusion:Barium chloride pretreatment can improve the lung histopathological changes of ARDS model mice induced by LPS by reducing the permeability of pulmonary capillaries and local inflammatory reaction.Barium chloride has the protective effect against LPS attack in mice model of ARDS.
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10.3969/j.issn.2095-4344.2013.25.011
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Aim To observe the protective effects of choline and pilocarpine,the M3 receptor agonists,on the arrhythmias of Wistar rats induced by barium chloride.Methods Barium chloride was used to induce the experimental arrhythmias of Wistar rats.Choline,pilocarpine,and 4-diphenylacetoxy-N-methylpiperidine-methiodide (4-DAMP),the selective antagonist of M3 receptor,were used to explore the effects of M3 receptor on the arrhythmias induced by barium chloride.The occurence and the severity of arrhythmias were observed.Results Choline 10 mg?kg-1 and pilocarpine 0.2 mg?kg-1 inhibited the occurence of arrhythmias,shortened the duration of arrhythmias (P
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Aim To study the effect of [P-(1-Benzotriazole methl)-Benylacrylic acid sodium,abbreviated for BMBS] on experimental arrhythmias. Methods Arrhythmias models induced by drugs in animals were used to observe the effect of BMBS on experimental arrhythmias. Results BMBS 25,12.5 mg?kg -1 iv markedly increased the dose of aconitine for inducing Ventricular premature beats (VP), ventricular tachycardia (VT) and ventricular fibrillation (VF) in rats, as well as that of ouabain for inducing VP, VT, VF and cardiac arrest (CA) in guinea pigs. Also, it postponed the onset time and shortened the duration of arrhythmias induced by barium chloride in rats and decreased the number of animals showing biphasic arrhythmias. Conclusion BMBS has significant effect on experimental arrhythmias.
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Objective To study the safety of Plumula nelumbinis microcapsules and its anti-arrhythmic effect.Methods Acute toxicity test in mice,arrhythmia mice models induced by chloroform and arrhythmia rats models induced by barium chloride(BaCl2)were adopted.Results The maximum tolerance dose for mice was 16.0 g/kg body weight.The microcapsule decreased the incidence of chloroform-induced ventricular fibrillation in mice significantly(P 0.05,compared with the blank control group).Conclusion The preliminary results show that Plumula nelumbinis microcapsule is safe,and exerts anti-arrhythmic effect against experimental arrhythmia.