Auguet M, Lonchampt M O, Delaflotte S, Goulin-Schulz J, Chabrier P E, Braquet P
Institut Henri Beaufour, Les Ulis, France.
FEBS Lett. 1992 Feb 3;297(1-2):183-5. doi: 10.1016/0014-5793(92)80356-l.
Inducible vascular nitric oxide synthase accounts for the contractile impairment observed in endotoxemia. We provide evidence that lipoteichoic acid (LTA) from Staphylococcus aureus, a micro-organism without endotoxin, also induces nitric oxide synthase. Our study demonstrates that on endothelium-free rings of rat aorta. LTA-like lipopolysaccharide induces a loss of contractility restored by Methylene blue and NG-nitro-L-arginine-methyl ester (LNAME). Moreover in cultured vascular smooth muscle cells, LTA produces a dose-dependent increase in intracellular cyclic GMP which is antagonized by LNAME and prevented by dexamethasone.
诱导型血管一氧化氮合酶是内毒素血症中观察到的收缩功能障碍的原因。我们提供的证据表明，来自无内毒素的微生物金黄色葡萄球菌的脂磷壁酸（LTA）也可诱导一氧化氮合酶。我们的研究表明，在大鼠主动脉无内皮环上，LTA样脂多糖会导致收缩力丧失，亚甲蓝和NG-硝基-L-精氨酸甲酯（LNAME）可恢复这种收缩力。此外，在培养的血管平滑肌细胞中，LTA会使细胞内环磷酸鸟苷呈剂量依赖性增加，LNAME可拮抗这种增加，地塞米松可预防这种增加。
