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首页> 外文期刊>Taiwan Veterinary Journal >TELETHONIN AS AN EARLY IMMUNOHISTOCHEMICAL MARKER IN LIGATION-INDUCED ISCHEMIC MYOCARDIAL INJURY
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TELETHONIN AS AN EARLY IMMUNOHISTOCHEMICAL MARKER IN LIGATION-INDUCED ISCHEMIC MYOCARDIAL INJURY

机译：Telethonin作为结扎诱导的缺血性心肌损伤的早期免疫组织化学标志物

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In this study, acute myocardial injuries or necrosis were experimentally induced in calves and pigs by ligation of either the left anterior descending coronary artery or left circumflex branch for 30min without reperfusion. Various antibodies directed to structural and functional proteins of the sarcomere, as well as activated proteinases, were employed in immunohistochemistry to compare for their potentials to detect early myocardial injury. For comparison, the histological criteria (designated as “Method A”) of cardiomyocyte necrosis such as nuclear pyknosis, sarcoplasmic fragmentation, flocculation, and/or the presence of a contraction band, and inflammatory infiltration were also scored. Additional criteria (designated “Method B”) of changes in late reversible stage of cell injury such as irregular nuclear shape or hyperchromasia, sarcomplasmic hypereosinophilia with either swelling or atrophy in diameter, and perinuclear vacuolation likely of swollen organelles, were also scored. In this setting, telethonin (T-cap), cardiac troponin I (cTnI), the current gold standard, and Method B, were superior to others in detecting ligation-induced ischemic injury. Other markers were either less specific, or less sensitive, or inconclusive for the current application. In conclusion, telethonin may serve as an early immunohistochemical marker in ligation-induced ischemic myocardial injury due to a combination of biomechanical stress, hypoxia, and possibly additional factor as matrix metalloproteinase activation.
机译：在本研究中，通过结扎左冠状动脉前降支或左回旋支30分钟而不进行再灌注，在小牛和猪中实验性地诱导急性心肌损伤或坏死。各种针对肌节结构和功能蛋白的抗体，以及激活的蛋白酶，被用于免疫组织化学，以比较它们检测早期心肌损伤的潜力。为了进行比较，还对心肌细胞坏死的组织学标准（指定为“方法A”）进行了评分，如核固缩、肌浆碎裂、絮凝和/或收缩带的存在，以及炎症浸润。此外，还对可逆性晚期细胞损伤的其他标准（称为“方法B”）进行了评分，如核形状不规则或染色过度、肌浆嗜酸性粒细胞增多伴直径肿胀或萎缩，以及可能由肿胀的细胞器引起的核周空泡化。在这种情况下，telethonin（T-cap）、心肌肌钙蛋白I（cTnI）和方法B在检测结扎诱导的缺血性损伤方面优于其他方法。其他标记要么不那么特异，要么不那么敏感，要么对当前的应用不确定。总之，telethonin可作为结扎诱导的缺血性心肌损伤的早期免疫组化标记物，该损伤是由生物力学应激、缺氧以及基质金属蛋白酶激活等可能的额外因素共同作用所致。

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