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首页> 外文期刊>American Journal of Veterinary Research >Evaluation of the induction of vasoactive mediators from equine digital vein endothelial cells by endotoxin.
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Evaluation of the induction of vasoactive mediators from equine digital vein endothelial cells by endotoxin.

机译：评估内毒素对马数字静脉内皮细胞诱导血管活性介质的作用。

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OBJECTIVE: To determine the effect of endotoxin (lipopolysaccharide [LPS]) on vasoactive mediator production by cultured equine digital vein endothelial cells (EDVECs). SAMPLE POPULATION: EDVECs obtained from forelimb digital veins of 7 healthy adult horses. PROCEDURES: EDVECs were incubated with or without LPS (1 microg/mL) for 0, 2, 4, 6, 22, and 24 hours. The EDVECs were incubated for 18 hours with LPS (10 pg/mL to 1 microg/mL) with or without ibuprofen, cycloheximide, or L-nitroarginine methyl ester. Medium concentrations of prostacyclin, cyclic guanosine monophosphate, endothelin-1, and thromboxane A(2) were determined. Changes in inducible nitric oxide synthase and cyclooxygenase-2 expression were determined. RESULTS: LPS stimulated mean 4.2- and 14.1-fold increases in EDVEC prostacyclin and cyclic guanosine monophosphate production, respectively, after 22 hours. These effects were LPS concentration-dependent (LPS concentrations that induced a response halfway between the maximum response and baseline of 1.50 and 1.22 ng/mL, respectively). The LPS-induced cyclic guanosine monophosphate production was significantly inhibited (to basal concentrations) by L-nitroarginine methyl ester, and prostacyclin production was inhibited by cycloheximide and ibuprofen. Production of thromboxane A(2) by EDVECs was not detected. Endothelin-1 accumulated in the medium, but LPS did not enhance its production. Inducible nitric oxide synthase expression in EDVECs was not detected with the available antibodies, whereas LPS stimulated cyclooxygenase-2 expression in a time- and concentration-dependent manner. CONCLUSIONS AND CLINICAL RELEVANCE: LPS stimulated vasoactive mediator production by equine endothelial cells, which may play a role in LPS-induced digital hypoperfusion.
机译：目的：研究内毒素（脂多糖[LPS]）对培养的马数字静脉内皮细胞（EDVEC）血管活性介质产生的影响。样本人群：从7头健康成年马的前肢数字静脉中获得的EDVEC。程序：将EDVECs与或不与LPS（1 microg / mL）孵育0、2、4、6、22和24小时。将EDVECs与含或不含布洛芬，环己酰亚胺或L-硝基精氨酸甲酯的LPS（10 pg / mL至1 microg / mL）一起孵育18小时。确定了中等浓度的前列环素，环鸟苷单磷酸，内皮素-1和血栓烷A（2）。确定诱导型一氧化氮合酶和环氧合酶2表达的变化。结果：22小时后，LPS刺激EDVEC前列环素和环状鸟苷单磷酸产量分别平均增加4.2和14.1倍。这些影响是LPS浓度依赖性的（LPS浓度分别在最大响应和基线之间分别在1.50和1.22 ng / mL的中间诱导一个响应）。 L-硝基精氨酸甲酯可显着抑制LPS诱导的环状鸟苷单磷酸的产生（达到基础浓度），而环己酰亚胺和布洛芬则抑制前列环素的产生。未检测到EDVECs产生血栓烷A（2）。内皮素-1在培养基中积累，但脂多糖并没有提高其产量。可用抗体未检测到EDVECs中的诱导型一氧化氮合酶表达，而LPS以时间和浓度依赖性方式刺激了环氧合酶2表达。结论和临床意义：LPS刺激马内皮细胞产生血管活性介质，这可能在LPS诱导的数字灌注不足中起作用。

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