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首页> 外文期刊>American Journal of Physiology >Lysozyme, a mediator of sepsis that intrinsically generates hydrogen peroxide to cause cardiovascular dysfunction.
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Lysozyme, a mediator of sepsis that intrinsically generates hydrogen peroxide to cause cardiovascular dysfunction.

机译：溶菌酶，一种败血症的介质，其内在地产生过氧化氢以引起心血管功能障碍。

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In septic shock, cardiovascular collapse is caused by the release of inflammatory mediators. We previously found that lysozyme (Lzm-S), released from leukocytes, contributed to the myocardial depression and arterial vasodilation that develop in canine models of septic shock. To cause vasodilation, Lzm-S generates hydrogen peroxide (H(2)O(2)) that activates the smooth muscle soluble guanylate cyclase (sGC) pathway, although the mechanism of H(2)O(2) generation is not known. To cause myocardial depression, Lzm-S binds to the endocardial endothelium, resulting in the formation of nitric oxide (NO) and subsequent activation of myocardial sGC, although the initial signaling event is not clear. In this study, we examined whether the myocardial depression produced by Lzm-S was also caused by the generation of H(2)O(2) and whether Lzm-S could intrinsically generate H(2)O(2) as has been described for other protein types. In a canine ventricular trabecular preparation, we found that the peroxidizing agent Aspergillus niger catalase, that would breakdown H(2)O(2), prevented Lzm-S- induced decrease in contraction. We also found that compound I, a species of catalase formed during H(2)O(2) metabolism, could contribute to the NO generation caused by Lzm-S. In tissue-free experiments, we used a fluorometric assay (Ultra Amplex red H(2)O(2) assay) and electrochemical sensor techniques, respectively, to measure H(2)O(2) generation. We found that Lzm-S could generate H(2)O(2) and, furthermore, that this generation could be attenuated by the singlet oxygen quencher sodium azide. This study shows that Lzm-S, a mediator of sepsis, is able to intrinsically generate H(2)O(2). Moreover, this generation may activate H(2)O(2)-dependent pathways leading to cardiovascular collapse in septic shock.
机译：在化脓性休克中，心血管塌陷是由炎症介质的释放引起的。我们以前发现从白细胞释放的溶菌酶（LZM-S）导致心肌抑郁和动脉血管血管血管血管血管血管血管血管血管血管血管血管血管血管血管血管血管舒张。为了引起血管沉积，LZM-S产生过氧化氢（H（2）O（2）），其激活平滑肌可溶性胍基酸环酶（SGC）途径，尽管H（2）O（2）产生的机制不知道。为了引起心肌凹陷，LZM-S与心内膜内皮结合，导致形成一氧化氮（NO）并随后激活心肌SGC，尽管初始信号传导事件尚不清楚。在这项研究中，我们检查了LZM-S产生的心肌抑制也是由H（2）O（2）的产生引起的，并且LZM-S是否可以本质上产生H（2）O（2），如所描述的那样对于其他蛋白质类型。在犬腔室间胫胚制剂中，我们发现过氧化剂曲霉过氧化物过氧化氢酶，即破碎H（2）O（2），预防LZM-S诱导的收缩。我们还发现化合物I，在H（2）O（2）代谢期间形成的一种过氧化氢酶，可以有助于LZM-S引起的不一致。在无组织实验中，我们使用荧光测定（超倍向红H（2）O（2）测定）和电化学传感器技术，以测量H（2）O（2）代。我们发现LZM-S可以产生H（2）O（2），而且，此外，该一代可以通过单线氧猝灭剂叠氮化钠衰减。本研究表明，LZM-S，脓毒症的介质，能够本质地产生H（2）O（2）。此外，该一代可以激活H（2）O（2）依赖性途径，导致脓毒症休克的心血管塌陷。

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