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Inflammatory response mechanisms exacerbating hypoxemia in coexistent pulmonary fibrosis and sleep apnea.炎症反应机制加剧并存的肺纤维化和睡眠呼吸暂停中的低氧血症。
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[Obesity is a risk factor of young onset of acute aortic dissection and postoperative hypoxemia].肥胖是急性主动脉夹层年轻发病及术后低氧血症的危险因素。
Kyobu Geka. 2013 Jun;66(6):437-44.
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Obesity and respiratory infections: does excess adiposity weigh down host defense?肥胖与呼吸道感染:过多的体脂是否会削弱宿主防御?
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Obesity, inflammation and the immune system.肥胖、炎症与免疫系统。
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9
[The clinical study of modified total aortic arch replacement and stent elephant trunk technique treatment for patients with DeBakey I thoracic aortic dissection].[改良全主动脉弓置换术及支架象鼻技术治疗DeBakey I型胸主动脉夹层的临床研究]
Zhonghua Wai Ke Za Zhi. 2011 Mar 1;49(3):236-9.
10
Reduction of the PaO2/FiO2 ratio in acute aortic dissection – relationship between the extent of dissection and inflammation –.急性主动脉夹层中 PaO2/FiO2 比值降低与夹层范围和炎症的关系——。
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肥胖是斯坦福A型急性主动脉夹层术前低氧血症的一个风险因素。

Obesity is a risk factor for preoperative hypoxemia in Stanford A acute aortic dissection.

作者信息

Wu Zhiyong, Wang Zhiwei, Wu Hongbing, Hu Rui, Ren Wei, Hu Zhipeng, Chang Jinxing

机构信息

Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei, P.R. China.

出版信息

Medicine (Baltimore). 2020 Mar;99(11):e19186. doi: 10.1097/MD.0000000000019186.

DOI:10.1097/MD.0000000000019186
PMID:32176045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7440331/
Abstract

Obese individuals are apt to develop Stanford A acute aortic dissection (AAD) complicated with acute lung injury (ALI), but the mechanism is still not well defined. We aim to investigate whether oxidative stress and inflammatory are involved in the aortic dissection lung injury caused by obesity.Seventy-nine patients were categorized into AAD with obesity group (n = 17) and AAD without obesity group (n = 62) according to body mass index (BMI). Inflammatory reactions including interleukin 1β (IL-1β), tumor necrosis factor-α (TNF-α), IL-6, C-reactive protein (CRP) and white blood cell (WBC) count, and oxidative stress including malondialdehyde (MDA), superoxide dismutase were determined using enzyme-linked immunosorbent assays and chemiluminescence. All the patients received ascending aorta replacement combined with total arch replacement and stented elephant trunk. The postoperative complications were recorded.The incidence of preoperative hypoxemia (94.1% vs 35.5%, P < .01) and postoperative ALI (88.2% vs 40.3%, P < .01) in obese patients was significantly higher than that in non-obese patients. Besides, the ICU stay (119.2 ± 59.2 vs 87.8 ± 31.2 h, P < .01) and hospitalization duration (18.8 ± 8.5 vs 14.3 ± 8.1d, P = .048) were increased in the obese patients with AAD. The expression of IL-1β, TNF-α, IL-6, CRP, and WBC was remarkably increased (P < .01) in obese group compared with non-obese group.Oxidative stress and inflammatory response may be involved in the process of ALI of aortic dissection caused by obesity, which provides new ideas for the treatment of ALI of the aortic dissection.

摘要

肥胖个体易于发生合并急性肺损伤(ALI)的斯坦福A型急性主动脉夹层(AAD),但其机制仍未完全明确。我们旨在研究氧化应激和炎症是否参与肥胖所致的主动脉夹层肺损伤。根据体重指数(BMI),将79例患者分为肥胖合并AAD组(n = 17)和非肥胖AAD组(n = 62)。采用酶联免疫吸附测定法和化学发光法测定包括白细胞介素1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、IL-6、C反应蛋白(CRP)和白细胞(WBC)计数在内的炎症反应,以及包括丙二醛(MDA)、超氧化物歧化酶在内的氧化应激指标。所有患者均接受升主动脉置换联合全弓置换及支架象鼻手术。记录术后并发症。肥胖患者术前低氧血症(94.1% 对35.5%,P <.01)和术后ALI(88.2% 对40.3%,P <.01)的发生率显著高于非肥胖患者。此外,肥胖合并AAD患者的重症监护病房(ICU)住院时间(119.2 ± 59.2对87.8 ± 31.2小时,P <.01)和住院时间(18.8 ± 8.5对14.3 ± 8.1天,P =.048)增加。与非肥胖组相比,肥胖组IL-1β、TNF-α、IL-6、CRP和WBC的表达显著增加(P <.01)。氧化应激和炎症反应可能参与肥胖所致主动脉夹层ALI的过程,这为主动脉夹层ALI的治疗提供了新思路。