Effects of Pseudomonas aeruginosa endotoxin on vasodilation in the intact spinotrapezius muscle.
Effects of Pseudomonas aeruginosa endotoxin on vasodilation in the intact spinotrapezius muscle.
复制标题
铜绿假单胞菌内毒素对完整斜方肌血管舒张的影响。
DOI：
10.1152/jappl.2001.91.1.351
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Rubinstein,I
中科院分区：
文献类型：
--
作者：
Suzuki,H;Ikezaki,H;Chandiwala,R;Hong,D;Rubinstein,I
本研究的目的是确定短期暴露于临床相关浓度的铜绿假单胞菌是否会损害完整的斜方肌微循环中阻力小动脉的血管反应性，如果是的话，确定介导这一反应的机制。活体显微镜下，我们发现OFP灌胃60min。铜绿素-内毒素(0.03-3.0μg/ml)对金黄地鼠斜方肌具有即刻、深度和持久的浓度依赖性的血管扩张作用(P<；0.05)。这种反应在OFP灌胃后是可逆的。停用铜绿假单胞菌内毒素。用非选择性一氧化氮合酶(NO)抑制剂NG-硝基-L-精氨酸甲酯(10.0μM)(而不是NG-硝基-d-精氨酸甲酯)预处理可消除P。铜绿假单胞菌内毒素诱导血管扩张，并引起微小的，但显著的血管收缩。吲哚美辛对NP无明显影响。铜绿假单胞菌内毒素对乙酰胆碱和硝酸甘油引起的脊髓斜方肌血管扩张无明显影响。总而言之，这些数据表明，短期暴露于临床相关浓度的OFP。铜绿假单胞菌脂多糖可在体内引起骨骼肌立即、有效、持久和可逆的NO依赖、前列腺素非依赖的血管扩张。我们认为，这种反应可能在P患者外周循环中观察到的严重血管运动障碍的病理生理学中起重要作用。铜绿假单胞菌感染综合征。
The purpose of this study was to determine whether short-term exposure to clinically relevant concentrations ofPseudomonas aeruginosalipopolysaccharide (LPS) impairs vasoreactivity of resistance arterioles in the intact spinotrapezius muscle microcirculation and, if so, to determine the mechanisms mediating this response. Using intravital microscopy, we found that 60-min suffusion ofP. aeruginosaLPS (0.03–3.0 μg/ml) on the in situ hamster spinotrapezius muscle elicited an immediate, profound, and prolonged concentration-dependent vasodilation (P< 0.05). This response was reversible once suffusion ofP. aeruginosaLPS was stopped. Pretreatment withNG-nitro-l-arginine methyl ester (10.0 μM), a nonselective nitric oxide (NO) synthase inhibitor, but notNG-nitro-d-arginine methyl ester, abrogatedP. aeruginosaLPS-induced vasodilation and elicited a small, albeit significant, vasoconstriction. Indomethacin had no significant effects onP. aeruginosaLPS-induced responses.P. aeruginosaLPS had no significant effects on acetylcholine- and nitroglycerin-induced vasodilation in the spinotrapezius muscle. Collectively, these data indicate that short-term exposure to clinically relevant concentrations ofP. aeruginosaLPS evokes an immediate, potent, prolonged, and reversible NO-dependent, prostaglandin-independent vasodilation in skeletal muscles in vivo. We suggest this response could play an important role in the pathophysiology of the profound vasomotor dysfunction observed in the peripheral circulation of patients withP. aeruginosasepsis syndrome.