Early structural changes of the heart after experimental polytrauma and hemorrhagic shock.
Early structural changes of the heart after experimental polytrauma and hemorrhagic shock.
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DOI：
10.1371/journal.pone.0187327
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Huber-Lang MS
中科院分区：
文献类型：
--
作者：
Braun CK;Kalbitz M;Halbgebauer R;Eisele P;Messerer DAC;Weckbach S;Schultze A;Braumüller S;Gebhard F;Huber-Lang MS
越来越多的证据表明，创伤后的全身炎症会导致心肌细胞的结构和功能受损，并导致心功能障碍，从而恶化多发伤患者的预后。本研究采用临床相关的多发伤啮齿动物模型，研究了多发伤合并失血性休克后4h心脏组织的结构和分子变化。我们测定了血浆中的全身炎症介质(角质形成细胞趋化因子、巨噬细胞趋化蛋白1)、激活补体成分C3a和心肌肌钙蛋白I，并通过标准的组织形态学和免疫组织化学方法评估了小鼠心脏的组织标本，以了解细胞和亚细胞损伤以及持续的细胞凋亡。通过免疫组织化学和Western blotting研究缝隙连接蛋白43的空间分布和数量变化。我们的结果显示，多发伤后4h和诱导低血容量后2小时，血浆角质形成细胞趋化因子和心肌肌钙蛋白I水平均显著升高。虽然我们没有检测到任何形态变化，但免疫组织化学检测显示，组织高迁移率族蛋白1的水平增加，这既是一种损伤相关分子，也是一种主动释放的危险反应信号。此外，合并多发伤和失血性休克后，心脏缝隙连接蛋白Cx43有明显的偏侧化。这些结果表明，在多发伤和失血性休克后早期，心肌细胞远隔损伤的分子表现，心脏缝隙连接明显破坏。心脏传导系统的一个重要组成部分的这种破坏可能会导致心律失常，从而导致心脏功能障碍。
Evidence is emerging that systemic inflammation after trauma drives structural and functional impairment of cardiomyocytes and leads to cardiac dysfunction, thus worsening the outcome of polytrauma patients. This study investigates the structural and molecular changes in heart tissue 4 h after multiple injuries with additional hemorrhagic shock using a clinically relevant rodent model of polytrauma. We determined mediators of systemic inflammation (keratinocyte chemoattractant, macrophage chemotactic protein 1), activated complement component C3a and cardiac troponin I in plasma and assessed histological specimen of the mouse heart via standard histomorphology and immunohistochemistry for cellular and subcellular damage and ongoing apoptosis. Further we investigated spatial and quantitative changes of connexin 43 by immunohistochemistry and western blotting. Our results show significantly increased plasma levels of both keratinocyte chemoattractant and cardiac troponin I 4 h after polytrauma and 2 h after induction of hypovolemia. Although we could not detect any morphological changes, immunohistochemical evaluation showed increased level of tissue high-mobility group box 1, which is both a damage-associated molecule and actively released as a danger response signal. Additionally, there was marked lateralization of the cardiac gap-junction protein connexin 43 following combined polytrauma and hemorrhagic shock. These results demonstrate a molecular manifestation of remote injury of cardiac muscle cells in the early phase after polytrauma and hemorrhagic shock with marked disruption of the cardiac gap junction. This disruption of an important component of the electrical conduction system of the heart may lead to arrhythmia and consequently to cardiac dysfunction.
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影响因子：
3.5
作者：
Mehta, NJ;Khan, IA;Smith, PR
通讯作者：
Smith, PR
影响因子：
4.1
作者：
Martins-Marques, Tania;Catarino, Steve;Girao, Henrique
通讯作者：
Girao, Henrique
DOI：
10.1016/j.injury.2007.10.003
发表时间：
2007-12-01
影响因子：
2.5
作者：
Lenz, Andreas;Franklin, Glen A.;Cheadle, William G.
通讯作者：
Cheadle, William G.
影响因子：
3.7
作者：
Altmann DR;Korte W;Maeder MT;Fehr T;Haager P;Rickli H;Kleger GR;Rodriguez R;Ammann P
通讯作者：
Ammann P
DOI：
10.1016/j.aat.2013.03.007
发表时间：
2013-03-01
期刊：
Acta anaesthesiologica Taiwanica : official journal of the Taiwan Society of Anesthesiologists
影响因子：
--
作者：
Asavarut, Paladd;Zhao, Hailin;Ma, Daqing
通讯作者：
Ma, Daqing