Lipoteichoic Acid from Staphylococcus aureus Depresses Contractile Function of Human Arteries In Vitro Due to the Induction of Nitric Oxide synthase
Lipoteichoic Acid from Staphylococcus aureus Depresses Contractile Function of Human Arteries In Vitro Due to the Induction of Nitric Oxide synthase
复制标题
金黄色葡萄球菌中的脂磷壁酸通过诱导一氧化氮合酶抑制体外人体动脉的收缩功能
DOI：
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发表时间：
1996
影响因子：
5.7
通讯作者：
N. Yoshimura
中科院分区：
文献类型：
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作者：
I. Tsuneyoshi;Y. Kanmura;N. Yoshimura
本研究的目的是阐明革兰氏阳性菌在脓毒症发生中的作用。在本研究中，我们研究了从金黄色葡萄球菌细胞壁中提取的脂磷壁酸（LTA）对去甲肾上腺素（NE）引起的人胃网膜动脉环收缩的影响。LTA减弱了对NE的收缩反应。这种衰减在暴露于LTA几小时后开始，并且在暴露10小时后达到最大值，无论是否存在内皮。环鸟苷酸含量的LTA处理环高于对照环，是否有功能性内皮。这些LTA介导的反应显着减少一氧化氮（NO）合酶和鸟苷酸环化酶的抑制剂。所有这些表明，血管对NE的低反应性的主要潜在原因是大量产生的NO。此外，放线菌酮，诱导型NO合酶的抑制剂，防止NE引起的收缩LTA引起的衰减。因此，我们的研究结果提供了强有力的支持证据，在由革兰氏阳性菌的一个减少收缩反应升压药物的成因的重要因素是他们的诱导型NO合酶在平滑肌中的诱导。（Anesth Analg 1996;82：948-53）
The aim of this study was to clarify the role of Gram-positive organisms in the genesis of sepsis. In the present study, we investigated the effect of lipoteichoic acid (LTA) from the cell wall of Staphylococcus aureus on contractions elicited by norepinephrine (NE) in rings cut from human gastroepiploic arteries. LTA diminished the contractile response to NE. This attenuation began after several hours exposure to LTA, and reached its maximum after 10 h of exposure, whether or not endothelium was present. The cyclic guanosine monophosphate content of LTA-treated rings was higher than that of control rings, whether there was a functional endothelium. These LTA-mediated responses were reduced significantly by inhibitors of nitric oxide (NO) synthase and guanylate cyclase. All of this indicates that the main underlying cause of the vascular hyporeactivity to NE was a massive generation of NO. In addition, cycloheximide, an inhibitor of inducible NO synthase, prevented the attenuation of NE-induced contractions caused by LTA. Thus, our results offer strong supporting evidence that the important factor in the genesis by Gram-positive organisms of a diminished contractile response to pressor drugs is their induction of inducible NO synthase in smooth muscle. (Anesth Analg 1996;82:948-53)
影响因子：
15.9
作者：
WAKABAYASHI, G;GELFAND, JA;DINARELLO, CA
通讯作者：
DINARELLO, CA