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脓毒性休克患儿的炎症、心肌功能障碍及死亡率:一项观察性研究。

Inflammation, myocardial dysfunction, and mortality in children with septic shock: an observational study.

作者信息

Carmona Fabio, Manso Paulo H, Silveira Vanessa S, Cunha Fernando Q, de Castro Margaret, Carlotti Ana P C P

机构信息

Ribeirao Preto Medical School, University of Sao Paulo, Avenida dos Bandeirantes 3900, Ribeirao Preto, SP, 14049-900, Brazil,

出版信息

Pediatr Cardiol. 2014 Mar;35(3):463-70. doi: 10.1007/s00246-013-0801-6. Epub 2013 Oct 4.

DOI:10.1007/s00246-013-0801-6
PMID:24091885
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7100657/
Abstract

We aimed to investigate whether nuclear factor kappa-B activation, as evaluated by gene expression of its inhibitor (I-κBα) and cytokine serum levels, was associated with myocardial dysfunction and mortality in children with septic shock. Twenty children with septic shock were prospectively enrolled and grouped according to ejection fraction (EF) <45% (group 1) or EF ≥45% (group 2) on the first day after admission to the pediatric intensive care unit. No interventions were made. In the first day, patients from group 1 (n = 6) exhibited significantly greater tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-10 plasma levels. However, I-κBα gene expression was not different in both groups. Mortality and number of complications were significantly greater in group 1. Patients who died had greater plasma concentrations of TNF-α. In conclusion, TNF-α and IL-10 are involved in myocardial dysfunction accompanying septic shock in children, and TNF-α is associated with mortality.

摘要

我们旨在研究通过其抑制剂(I-κBα)的基因表达和细胞因子血清水平评估的核因子κB激活是否与感染性休克患儿的心肌功能障碍和死亡率相关。前瞻性纳入20例感染性休克患儿,并在入住儿科重症监护病房后的第一天根据射血分数(EF)<45%(第1组)或EF≥45%(第2组)进行分组。未进行干预。在第一天,第1组(n = 6)的患者表现出显著更高的肿瘤坏死因子-α(TNF-α)和白细胞介素(IL)-10血浆水平。然而,两组的I-κBα基因表达没有差异。第1组的死亡率和并发症数量显著更高。死亡患者的TNF-α血浆浓度更高。总之,TNF-α和IL-10参与儿童感染性休克伴发的心肌功能障碍,且TNF-α与死亡率相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1594/7100657/acf780845a15/246_2013_801_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1594/7100657/b35f466ce96e/246_2013_801_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1594/7100657/1c746090c968/246_2013_801_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1594/7100657/acf780845a15/246_2013_801_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1594/7100657/b35f466ce96e/246_2013_801_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1594/7100657/1c746090c968/246_2013_801_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1594/7100657/acf780845a15/246_2013_801_Fig3_HTML.jpg

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Prazosin protects myocardial cells against anoxia-reoxygenation injury via the extracellular signal‑regulated kinase signaling pathway.哌唑嗪通过细胞外信号调节激酶信号通路保护心肌细胞对抗缺氧/复氧损伤。
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