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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，脓毒症的介体，其固有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：在败血症性休克中，心血管衰竭是由炎症介质的释放引起的。我们以前发现白细胞释放的溶菌酶（Lzm-S）导致了败血症性休克犬模型中发生的心肌抑制和动脉血管舒张。为了引起血管舒张，Lzm-S产生过氧化氢（H（2）O（2）），它激活平滑肌可溶性鸟苷酸环化酶（sGC）途径，尽管H（2）O（2）生成的机制尚不清楚。为了引起心肌抑制，Lzm-S与心内膜内皮结合，导致一氧化氮（NO）的形成和随后心肌sGC的激活，尽管最初的信号事件尚不清楚。在这项研究中，我们检查了Lzm-S产生的心肌抑制是否也由H（2）O（2）的产生引起，以及Lzm-S是否可以固有地产生H（2）O（2）。用于其他蛋白质类型。在犬心室小梁准备中，我们发现过氧化物黑曲霉过氧化氢酶会分解H（2）O（2），阻止Lzm-S引起的收缩减少。我们还发现化合物I，一种在H（2）O（2）代谢过程中形成的过氧化氢酶，可能有助于由Lzm-S引起的NO生成。在无组织的实验中，我们分别使用荧光测定法（Ultra Amplex红H（2）O（2）测定）和电化学传感器技术来测量H（2）O（2）的产生。我们发现Lzm-S可以生成H（2）O（2），此外，单重态氧猝灭叠氮化钠可以减弱这一生成。这项研究表明，Lzm-S，败血症的介体，能够固有地产生H（2）O（2）。此外，这一代可能会激活H（2）O（2）依赖的途径，导致败血性休克中的心血管衰竭。

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