Endothelial nitric oxide synthase is downregulated during hyperdynamic sepsis.
Endothelial nitric oxide synthase is downregulated during hyperdynamic sepsis.
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高动力脓毒症期间内皮一氧化氮合酶下调。
DOI：
10.1016/s0304-4165(96)00139-0
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Chaudry,IH
中科院分区：
文献类型：
--
作者：
Zhou,M;Wang,P;Chaudry,IH
虽然研究表明，内皮源性一氧化氮（NO）的释放被抑制在内毒素休克或多微生物脓毒症，它仍然是未知的，是否内皮源性NO释放的减少在脓毒症的高动力阶段是由于内皮NO合酶的下调。为了研究这一点，成年大鼠通过盲肠结扎和穿孔（CLP）进行脓毒症。CLP后10 h（即，高动力性脓毒症）或假手术后，切除主动脉，并使用抗内皮（组成型）NO合酶（E-NOS）的单克隆抗体来确定大鼠主动脉内皮细胞中E-NOS的免疫组织化学存在和电子显微镜定位。采用图像分析法定量测定主动脉E-NOS。在其他动物组中，主动脉在CLP后10小时分离，并测定血管对内皮依赖性血管扩张剂乙酰胆碱和内皮非依赖性血管扩张剂硝酸甘油的反应。结果表明，E-NOS阴性的内皮细胞数量从假手术组的7%增加到脓毒症组的22%。CLP后10 h，E-NOS标记的内皮细胞从20%减少到8%。E-NOS阳性细胞面积由假手术组的26.1±1.0 μm2/标准帧减少到脓毒症组的22.3±0.9 μm2/标准帧。此外，乙酰胆碱诱导的，但不是硝酸甘油诱导的血管舒张显着抑制在10小时后，脓毒症的发病。这些结果综合起来表明，血管内皮细胞中E-NOS的减少至少部分地导致内皮细胞功能障碍（即，减少的内皮源性NO释放）。
Although studies have shown that endothelium-derived nitric oxide (NO) release is depressed during endotoxic shock or polymicrobial sepsis, it remains unknown whether the decreased release of endothelium-derived NO during the hyperdynamic stage of sepsis is due to downregulation of endothelial NO synthase. To study this, adult rats were subjected to sepsis by cecal ligation and puncture (CLP). At 10 h after CLP (i.e., hyperdynamic sepsis) or sham operation, the aorta was removed and a monoclonal antibody against endothelial (constitutive) NO synthase (E-NOS) was used to determine the immunohistochemical presence and electron microscopic localization of E-NOS in rat aortic endothelial cells. Image analysis was used to quantify aortic E-NOS. In additional groups of animals, the aorta was isolated at 10 h after CLP and the vascular responses to an endothelium-dependent vasodilator, acetylcholine, and an endothelium-independent vasodilator, nitroglycerine, were determined. The results indicate that the number of E-NOS negative endothelial cells increased from 7% in shams to 22% in septic animals. E-NOS densely labeled endothelial cells were significantly reduced from 20% to 8% at 10 h after CLP. The E-NOS positive area in aortic endothelial cells was reduced from 26.1±1.0 μm2/standard frame in sham to 22.3±0.9 μm2/standard frame in septic animals. Moreover, acetylcholine-induced but not nitroglycerine-induced vascular relaxation was significantly depressed at 10 h after the onset of sepsis. These results, taken together, indicate that the decreased E-NOS in the vascular endothelial cell is at least in part responsible for endothelial cell dysfunction (i.e., the reduced endothelium-derived NO release) observed during the early, hyperdynamic stage of polymicrobial sepsis.
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脓毒症综合征患者一氧化氮生成增加的证据。
DOI：
--
发表时间：
1993
期刊：
Circulatory shock
影响因子：
--
作者：
T. Evans;A. Carpenter;H. Kinderman;J. Cohen
通讯作者：
J. Cohen
内毒素增强肝再灌注损伤对大鼠主动脉内皮依赖性舒张的影响
影响因子：
3.1
作者：
Rosemary McKenna;R. Laskey;Ying Wang;H. Jaeschke;W. Mathews
通讯作者：
W. Mathews
在血管壁中发现一氧化氮。
影响因子：
--
作者：
R. Palmer
通讯作者：
R. Palmer
内毒素和 TNF α 直接刺激慢性内毒素血症大鼠培养的大鼠肝细胞中一氧化氮的形成。
DOI：
--
发表时间：
1992
期刊：
Biochemical and Biophysical Research Communications - BBRC
影响因子：
--
作者：
R. Pittner;J. A. Spitzer
通讯作者：
J. A. Spitzer
有证据表明，L-精氨酸/一氧化氮依赖性组织环鸟苷酸含量升高与内毒素抑制血管反应性有关
影响因子：
7.3
作者：
I. Fleming;G. Julou‐Schaeffer;G. Gray;J. Parratt;J. Stoclet
通讯作者：
J. Stoclet