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猪多发性创伤后的心脏抑制 - 创伤后结构和功能改变的特征。

Cardiac Depression in Pigs after Multiple Trauma - Characterization of Posttraumatic Structural and Functional Alterations.

机构信息

Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University of Ulm, Ulm, Germany.

Division of Neonatology and Pediatric Critical Care, University of Ulm, Ulm, Germany.

出版信息

Sci Rep. 2017 Dec 19;7(1):17861. doi: 10.1038/s41598-017-18088-1.

Abstract

The purpose of this study was to define the relationship between cardiac depression and morphological and immunological alterations in cardiac tissue after multiple trauma. However, the mechanistic basis of depressed cardiac function after trauma is still elusive. In a porcine polytrauma model including blunt chest trauma, liver laceration, femur fracture and haemorrhage serial trans-thoracic echocardiography was performed and correlated with cellular cardiac injury as well as with the occurrence of extracellular histones in serum. Postmortem analysis of heart tissue was performed 72 h after trauma. Ejection fraction and shortening fraction of the left ventricle were significantly impaired between 4 and 27 h after trauma. H-FABP, troponin I and extracellular histones were elevated early after trauma and returned to baseline after 24 and 48 h, respectively. Furthermore, increased nitrotyrosine and Il-1β generation and apoptosis were identified in cardiac tissue after trauma. Main structural findings revealed alteration of connexin 43 (Cx43) and co-translocation of Cx43 and zonula occludens 1 to the cytosol, reduction of α-actinin and increase of desmin in cardiomyocytes after trauma. The cellular and subcellular events demonstrated in this report may for the first time explain molecular mechanisms associated with cardiac dysfunction after multiple trauma.

摘要

本研究旨在明确多发伤后心脏抑制与心肌形态和免疫改变之间的关系。然而,创伤后心脏功能抑制的机制基础仍难以捉摸。在包括钝性胸部创伤、肝脏裂伤、股骨骨折和出血的猪多发伤模型中,进行了连续经胸超声心动图检查,并与细胞性心肌损伤以及血清中外源组蛋白的发生相关联。创伤后 72 小时进行心脏组织的死后分析。创伤后 4 至 27 小时,左心室射血分数和缩短分数明显受损。H-FABP、肌钙蛋白 I 和细胞外组蛋白在创伤后早期升高,并分别在 24 和 48 小时后恢复至基线。此外,在创伤后的心肌组织中还发现了硝基酪氨酸和 Il-1β生成以及细胞凋亡的增加。主要的结构发现揭示了连接蛋白 43(Cx43)的改变和 Cx43 与封闭蛋白 1 的共转位到细胞质,以及肌动蛋白-α的减少和结蛋白的增加。本报告中展示的细胞和亚细胞事件可能首次解释了与多发伤后心脏功能障碍相关的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f2b/5736586/8fa184b4f862/41598_2017_18088_Fig1_HTML.jpg

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