Suppr超能文献

在再梗死患者或接受再灌注治疗的患者中,人类梗死心肌中的C反应蛋白和补体沉积更为广泛。

C-reactive protein and complement depositions in human infarcted myocardium are more extensive in patients with reinfarction or upon treatment with reperfusion.

作者信息

Nijmeijer R, Krijnen P A J, Assink J, Klaarenbeek M A R, Lagrand W K, Veerhuis R, Visser C A, Meijer C J L M, Niessen H W M, Hack C E

机构信息

ICaR-VU, Amsterdam, the Netherlands.

出版信息

Eur J Clin Invest. 2004 Dec;34(12):803-10. doi: 10.1111/j.1365-2362.2004.01425.x.

Abstract

BACKGROUND

Impaired perfusion of the heart induces a local inflammatory response, which involves deposition of C-reactive protein and complement activation products C3d and C5b-9. We investigated whether reperfusion or reinfarction enhances these phenomena in humans.

MATERIALS AND METHODS

Depositions of C-reactive protein and complement were quantified in tissue samples of infarcted myocardium from 76 patients who had died after acute myocardial infarction. The extent of depositions in patients treated with reperfusion or suffering from reinfarction was compared with that in patients who had no reperfusion or reinfarction.

RESULTS

Patients with reinfarction had significantly more extensive depositions of C-reactive protein and complement (C3d and C5b-9) in the infarcted myocardium than patients without reinfarction. Similarly, patients who received reperfusion therapy had more extensive depositions also than those who had not received this therapy.

CONCLUSIONS

Both reinfarction and reperfusion therapy significantly increase the extent of C-reactive protein and complement depositions in human myocardial infarcts.

摘要

背景

心脏灌注受损会引发局部炎症反应,其中涉及C反应蛋白的沉积以及补体激活产物C3d和C5b - 9。我们研究了再灌注或再梗死是否会增强人类的这些现象。

材料与方法

对76例急性心肌梗死后死亡患者梗死心肌组织样本中的C反应蛋白和补体沉积进行定量分析。将接受再灌注治疗或发生再梗死患者的沉积程度与未接受再灌注或未发生再梗死的患者进行比较。

结果

与未发生再梗死的患者相比,发生再梗死的患者梗死心肌中C反应蛋白和补体(C3d和C5b - 9)的沉积明显更广泛。同样,接受再灌注治疗的患者的沉积也比未接受该治疗的患者更广泛。

结论

再梗死和再灌注治疗均显著增加人类心肌梗死中C反应蛋白和补体沉积的程度。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验