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猪实验性应激时儿茶酚胺诱导的自由基与心肌细胞坏死

Catecholamine-induced free radicals in myocardial cell necrosis on experimental stress in pigs.

作者信息

Häggendal J, Jönsson L, Johansson G, Bjurström S, Carlsten J, Thorén-Tolling K

机构信息

Department of Pharmacology, University of Göteborg, Sweden.

出版信息

Acta Physiol Scand. 1987 Nov;131(3):447-52. doi: 10.1111/j.1748-1716.1987.tb08260.x.

DOI:10.1111/j.1748-1716.1987.tb08260.x
PMID:3425348
Abstract

Normal pigs, crossbreeds of Swedish Landrace and Yorkshire, about 6 months old, were subjected to experimental stress, induced by the myorelaxant succinylcholine, for 12 min. Besides one group of control pigs, one group of pigs were pretreated with alpha-tocopherol (vitamin E) combined with selenium (Tokosel Vet) injected i.m. every second day for 11 days, and another group was given zinc (ZnSO4.7H2O) in the fodder for 1 month plus one injection i.p. 2 days before the stress. The stress-induced heart lesions, morphologically graded according to evaluation scores, were significantly reduced in both the pretreated groups when compared with the control pigs. The blood levels of catecholamines (CA) were increased to about the same degree in the three groups during the stress. The protection observed is suggested to be due to the fact that vitamin E, selenium and zinc are involved in systems acting as scavengers of free radicals. The present results together with earlier ones are discussed to support the CA-hypothesis for stress-induced heart lesions: some types of stress can increase the sympathetic activity to such an extent that released CA, via beta-adrenoceptor mechanisms affects the cell metabolism to such a degree that cytotoxic free radicals are formed, producing myocardial cell necrosis.

摘要

选用约6月龄的瑞典长白猪与约克夏猪的杂交种正常猪,通过使用肌松剂琥珀酰胆碱诱导实验性应激,持续12分钟。除一组对照猪外,一组猪每隔一天肌肉注射α-生育酚(维生素E)与硒(托可硒兽药)进行预处理,共11天;另一组在应激前1个月在饲料中添加锌(ZnSO4·7H2O)并腹腔注射一次。与对照猪相比,两个预处理组中应激诱导的心脏病变(根据评估分数进行形态学分级)均显著减轻。应激期间,三组儿茶酚胺(CA)的血液水平升高程度大致相同。观察到的保护作用被认为是由于维生素E、硒和锌参与了作为自由基清除剂的系统。结合早期研究结果对目前的结果进行了讨论,以支持关于应激诱导心脏病变的CA假说:某些类型的应激可使交感神经活动增加到一定程度,以至于释放的CA通过β-肾上腺素能受体机制对细胞代谢产生影响,进而形成细胞毒性自由基,导致心肌细胞坏死。

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