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本文引用的文献

1
Effects of trauma, hemorrhagic shock, and chronic stress on lung vascular endothelial growth factor.创伤、失血性休克及慢性应激对肺血管内皮生长因子的影响
J Surg Res. 2017 Apr;210:15-21. doi: 10.1016/j.jss.2016.10.023. Epub 2016 Nov 2.
2
Clonidine reduces norepinephrine and improves bone marrow function in a rodent model of lung contusion, hemorrhagic shock, and chronic stress.可乐定可降低去甲肾上腺素水平,并改善肺挫伤、失血性休克和慢性应激啮齿动物模型中的骨髓功能。
Surgery. 2017 Mar;161(3):795-802. doi: 10.1016/j.surg.2016.08.043. Epub 2016 Oct 11.
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Daily propranolol prevents prolonged mobilization of hematopoietic progenitor cells in a rat model of lung contusion, hemorrhagic shock, and chronic stress.在大鼠肺挫伤、失血性休克和慢性应激模型中,每日服用普萘洛尔可防止造血祖细胞的长期动员。
Surgery. 2015 Sep;158(3):595-601. doi: 10.1016/j.surg.2015.06.031. Epub 2015 Jul 21.
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Propranolol attenuates hemorrhage and accelerates wound healing in severely burned adults.普萘洛尔可减轻严重烧伤成人的出血并加速伤口愈合。
Crit Care. 2015 May 4;19(1):217. doi: 10.1186/s13054-015-0913-x.
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Can mesenchymal stem cells reverse chronic stress-induced impairment of lung healing following traumatic injury?间充质干细胞能否逆转创伤后慢性应激诱导的肺愈合损伤?
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Novel role of PKR in inflammasome activation and HMGB1 release.PKR 在炎症小体激活和 HMGB1 释放中的新作用。
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An official American Thoracic Society workshop report: features and measurements of experimental acute lung injury in animals.美国胸科学会官方工作组报告:动物实验性急性肺损伤的特征和测量。
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Mobilization of bone marrow cells to the site of injury is necessary for wound healing.将骨髓细胞动员至损伤部位对伤口愈合是必要的。
J Trauma. 2009 Aug;67(2):315-21; discussion 321-2. doi: 10.1097/TA.0b013e3181a5c9c7.
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Central sympatholytics prolong survival in experimental sepsis.中枢交感神经抑制剂可延长实验性脓毒症的生存时间。
Crit Care. 2009;13(1):R11. doi: 10.1186/cc7709. Epub 2009 Feb 6.
10
Hematopoietic progenitor cells mobilize to the site of injury after trauma and hemorrhagic shock in rats.在大鼠遭受创伤和失血性休克后,造血祖细胞会迁移至损伤部位。
J Trauma. 2007 Sep;63(3):596-600; discussion 600-2. doi: 10.1097/TA.0b013e318142d231.

可乐定可恢复血管内皮生长因子的表达,并改善严重创伤后的组织修复。

Clonidine restores vascular endothelial growth factor expression and improves tissue repair following severe trauma.

作者信息

Loftus Tyler J, Thomson Andrew J, Kannan Kolenkode B, Alamo Ines G, Millar Jessica K, Plazas Jessica M, Whitley Elizabeth E, Efron Philip A, Mohr Alicia M

机构信息

University of Florida Health, Department of Surgery and Sepsis and Critical Illness Research Center, Gainesville, FL, USA.

University of Florida, College of Medicine, Gainesville, FL, USA.

出版信息

Am J Surg. 2017 Oct;214(4):610-615. doi: 10.1016/j.amjsurg.2017.06.019. Epub 2017 Jun 23.

DOI:10.1016/j.amjsurg.2017.06.019
PMID:28666582
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5603405/
Abstract

BACKGROUND

We hypothesized that clonidine and propranolol would increase VEGF and VEGF-receptor expression and promote lung healing following severe trauma and chronic stress.

METHODS

Sprague-Dawley rats were subjected to lung contusion (LC), lung contusion/hemorrhagic shock (LCHS), or lung contusion/hemorrhagic shock/daily restraint stress (LCHS/CS). Clonidine and propranolol were administered daily. On day seven, lung VEGF, VEGFR-1, VEGFR-2, and HMGB1 were assessed by PCR. Lung injury was assessed by light microscopy (*p < 0.05).

RESULTS

Clonidine increased VEGF expression following LCHS (43%) and LCHS/CS (46%). Clonidine increased VEGFR-1 and R-2 expression following LCHS/CS (203%* and 47%, respectively). Clonidine decreased HMGB1 and TNF-alpha expression following LCHS/CS (22% and 58%*, respectively.) Clonidine decreased inflammatory cell infiltration and total Lung Injury Score following LCHS/CS. Propranolol minimally affected VEGF and did not improve lung healing.

CONCLUSIONS

Clonidine increased VEGF and VEGF-receptor expression, decreased HMGB1 expression, decreased lung inflammation, and improved lung tissue repair.

摘要

背景

我们推测可乐定和普萘洛尔会增加血管内皮生长因子(VEGF)及其受体的表达,并促进严重创伤和慢性应激后的肺愈合。

方法

将斯普拉格-道利大鼠进行肺挫伤(LC)、肺挫伤/失血性休克(LCHS)或肺挫伤/失血性休克/每日束缚应激(LCHS/CS)处理。每天给予可乐定和普萘洛尔。在第7天,通过聚合酶链反应(PCR)评估肺组织中的VEGF、血管内皮生长因子受体-1(VEGFR-1)、血管内皮生长因子受体-2(VEGFR-2)和高迁移率族蛋白B1(HMGB1)。通过光学显微镜评估肺损伤情况(*p < 0.05)。

结果

可乐定可增加LCHS组(增加43%)和LCHS/CS组(增加46%)的VEGF表达。可乐定可增加LCHS/CS组的VEGFR-1和VEGFR-2表达(分别增加203%和47%)。可乐定可降低LCHS/CS组的HMGB1和肿瘤坏死因子-α(TNF-α)表达(分别降低22%和58%)。可乐定可减少LCHS/CS组的炎症细胞浸润和降低肺损伤总评分。普萘洛尔对VEGF的影响极小,且未改善肺愈合情况。

结论

可乐定可增加VEGF及其受体的表达,降低HMGB1表达,减轻肺部炎症,并改善肺组织修复。