{"title":"氧自由基与心肌肥厚的组织损伤。","authors":"C Guarnieri, C Muscari, C M Caldarera","doi":"10.1007/978-1-4757-1287-2_15","DOIUrl":null,"url":null,"abstract":"<p><p>Cyanide-resistant respiration in heart homogenates supplemented with 1 mM NADH was greater in hypertrophied homogenates (60 days banding) with respect to control homogenates, particularly when the homogenates were incubated in 100% oxygen. The intermyofibrillar mitochondria from hypertrophied hearts produced more superoxide radicals than sub-sarcolemmal mitochondria, and both values were greater than in the unbanded group. H2O2 formation was more evident in the intact mitochondria prepared from hypertrophied hearts than in those of the control hearts. Moreover, the perfusion of isolated hearts in anoxic and reoxygenated conditions caused a greater lipoperoxidative and functional damage at the mitochondrial level in hypertrophied hearts than in the control hearts. These results, correlate with the reduction in mitochondrial function found in the overloaded hearts, suggest an involvement of the reactive species of oxygen in the formation of cardiac damage induced by prolonged aortic banding.</p>","PeriodicalId":77831,"journal":{"name":"Advances in myocardiology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"19","resultStr":"{\"title\":\"Oxygen radicals and tissue damage in heart hypertrophy.\",\"authors\":\"C Guarnieri, C Muscari, C M Caldarera\",\"doi\":\"10.1007/978-1-4757-1287-2_15\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Cyanide-resistant respiration in heart homogenates supplemented with 1 mM NADH was greater in hypertrophied homogenates (60 days banding) with respect to control homogenates, particularly when the homogenates were incubated in 100% oxygen. The intermyofibrillar mitochondria from hypertrophied hearts produced more superoxide radicals than sub-sarcolemmal mitochondria, and both values were greater than in the unbanded group. H2O2 formation was more evident in the intact mitochondria prepared from hypertrophied hearts than in those of the control hearts. Moreover, the perfusion of isolated hearts in anoxic and reoxygenated conditions caused a greater lipoperoxidative and functional damage at the mitochondrial level in hypertrophied hearts than in the control hearts. These results, correlate with the reduction in mitochondrial function found in the overloaded hearts, suggest an involvement of the reactive species of oxygen in the formation of cardiac damage induced by prolonged aortic banding.</p>\",\"PeriodicalId\":77831,\"journal\":{\"name\":\"Advances in myocardiology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1985-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"19\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advances in myocardiology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1007/978-1-4757-1287-2_15\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in myocardiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-1-4757-1287-2_15","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 19
摘要
在心脏匀浆中添加1 mM NADH的匀浆(带60天)中,与对照匀浆相比,增厚匀浆(带60天)的抗氰呼吸作用更大,特别是当匀浆在100%氧气中孵育时。肥大心脏的肌纤维间线粒体比肌下线粒体产生更多的超氧自由基,两者均大于非带状组。在肥大心脏制备的完整线粒体中,H2O2的形成比对照心脏更明显。此外,在缺氧和再氧条件下灌注离体心脏,肥大心脏在线粒体水平上的脂质氧化和功能损伤大于对照心脏。这些结果与在超载心脏中发现的线粒体功能减少有关,表明活性氧参与了主动脉带带延长引起的心脏损伤的形成。
Oxygen radicals and tissue damage in heart hypertrophy.
Cyanide-resistant respiration in heart homogenates supplemented with 1 mM NADH was greater in hypertrophied homogenates (60 days banding) with respect to control homogenates, particularly when the homogenates were incubated in 100% oxygen. The intermyofibrillar mitochondria from hypertrophied hearts produced more superoxide radicals than sub-sarcolemmal mitochondria, and both values were greater than in the unbanded group. H2O2 formation was more evident in the intact mitochondria prepared from hypertrophied hearts than in those of the control hearts. Moreover, the perfusion of isolated hearts in anoxic and reoxygenated conditions caused a greater lipoperoxidative and functional damage at the mitochondrial level in hypertrophied hearts than in the control hearts. These results, correlate with the reduction in mitochondrial function found in the overloaded hearts, suggest an involvement of the reactive species of oxygen in the formation of cardiac damage induced by prolonged aortic banding.