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首页> 外文期刊>Pulmonary pharmacology & therapeutics >Up-regulation of arginase II contributes to pulmonary vascular endothelial cell dysfunction during experimental pulmonary embolism.
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Up-regulation of arginase II contributes to pulmonary vascular endothelial cell dysfunction during experimental pulmonary embolism.

机译：在实验性肺栓塞过程中，精氨酸酶II的上调导致了肺血管内皮细胞功能障碍。

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摘要

Pulmonary embolism (PE) causes pulmonary hypertension by mechanical obstruction and constriction of non-obstructed vasculature. We tested if experimental PE impairs pulmonary vascular endothelium-dependent dilation via activation of arginase II. Experimental PE was induced in male Sprague-Dawley rats by infusing 25 mum microspheres in the right jugular vein, producing moderate pulmonary hypertension. Shams received vehicle injection. Pulmonary arterial rings were isolated after 18 h and isometric tensions were determined. Dilations were induced with acetylcholine, calcium ionophore A23187 or nitroglycerin (NTG) in pre-contracted rings (phenylephrine). Protein expression was assessed by Western blot and immunohistochemistry. Arginase activity was inhibited by intravenous infusion of N(w)-hydroxy-nor-l-arginine (nor-NOHA). l-Arginine supplementation was also given. Endothelium-dependent dilation responses were significantly reduced in PE vs. vehicle-treated animals (ACh: 50 +/- 9% vs. 93 +/- 3%; A23187: 19 +/- 7% vs. 85 +/- 7%, p < 0.05), while endothelium-independent dilations (NTG) were unchanged. Endothelial nitric oxide synthase (eNOS) protein content was unchanged by PE. Expression of arginase II increased 4.5-fold and immunohistochemistry revealed increased arginase II staining. Nor-NOHA treatment and l-arginine supplementation significantly improved pulmonary artery ring endothelium-dependent dilation in PE (ACh: 58 +/- 6% PE, 88 +/- 6% PE + nor-NOHA, 84 +/- 4% PE + l-arginine). Experimental PE impairs endothelium-dependent pulmonary artery dilation, while endothelium-independent dilation remains unchanged. The data support the conclusion that up-regulation of arginase II protein expression contributes to pulmonary artery endothelial dysfunction in this model of experimental PE.
机译：肺栓塞（PE）通过机械性阻塞和非阻塞性血管的收缩引起肺动脉高压。我们测试了实验性PE是否通过精氨酸酶II的激活来损害肺血管内皮依赖性的扩张。在雄性Sprague-Dawley大鼠中，通过向右颈静脉内注入25个妈妈的微球体诱导实验性PE，产生中度肺动脉高压。子接受了车辆注射。 18小时后分离出肺动脉环并确定等轴测张力。在预收缩的环（去氧肾上腺素）中用乙酰胆碱，钙离子载体A23187或硝酸甘油（NTG）诱导扩张。通过蛋白质印迹和免疫组织化学评估蛋白质表达。静脉内输注N（w）-羟基-正-1-精氨酸（nor-NOHA）可抑制精氨酸酶活性。还补充了l-精氨酸。与媒介物处理的动物相比，PE的内皮依赖性舒张反应明显降低（ACh：50 +/- 9％vs. 93 +/- 3％; A23187：19 +/- 7％vs. 85 +/- 7％ ，p <0.05），而内皮依赖性扩张（NTG）不变。内皮细胞一氧化氮合酶（eNOS）蛋白含量未见改变。精氨酸酶II的表达增加了4.5倍，免疫组织化学显示精氨酸酶II染色增加了。 Nor-NOHA治疗和l-精氨酸补充可显着改善PE中肺动脉环内皮依赖性扩张（ACh：58 +/- 6％PE，88 +/- 6％PE + nor-NOHA，84 +/- 4％PE + l-精氨酸）。实验性PE损害内皮依赖性肺动脉扩张，而内皮依赖性扩张保持不变。数据支持以下结论：在此实验性PE模型中，精氨酸酶II蛋白表达的上调可导致肺动脉内皮功能障碍。

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