{"title":"Changes of cardiac and skeletal muscle in pigs following transport stress","authors":"V. Bergmann","doi":"10.1016/S0014-4908(79)80038-1","DOIUrl":null,"url":null,"abstract":"<div><p>After lorry transport (60–120 min), fattening pigs (100–120 kg living weight) with clinical signs of exhaustion and acute circulation insufficiency showed acute ultrastructural damage to the myocard and the skeletal muscle. These represent the morphological equivalent of a stress induced cardiomyopathy and are to be counted among the stress myopathies of the pig. These changes may be caused particularly by the high lactate production of the predominantly glycolytically operating skeletal muscles and by the effects of cardial catecholamine release following transport stress. Attention is drawn to the model character of these changes for similar processes in humans.</p></div>","PeriodicalId":75841,"journal":{"name":"Experimentelle Pathologie","volume":"17 5","pages":"Pages 243-248"},"PeriodicalIF":0.0000,"publicationDate":"1979-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0014-4908(79)80038-1","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimentelle Pathologie","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0014490879800381","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9
Abstract
After lorry transport (60–120 min), fattening pigs (100–120 kg living weight) with clinical signs of exhaustion and acute circulation insufficiency showed acute ultrastructural damage to the myocard and the skeletal muscle. These represent the morphological equivalent of a stress induced cardiomyopathy and are to be counted among the stress myopathies of the pig. These changes may be caused particularly by the high lactate production of the predominantly glycolytically operating skeletal muscles and by the effects of cardial catecholamine release following transport stress. Attention is drawn to the model character of these changes for similar processes in humans.