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体外循环对血管内皮细胞的急性损伤 (PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第1期
页码:
82-84/87
栏目:
临床研究
出版日期:
2007-01-01

文章信息/Info

Title:
Vascular endothelial cells injury and activation during cardiopulmonary bypass
作者:
顾春虎1; 王云雅2; 易定华1; 俞世强1;  张近宝1;  陈文生1; 孙国成1
第四军医大学附属西京医院:1. 心脏外科, 2. 核医学科,陕西 西安 710032
Author(s):
GU Chunhu1;  WANG Yunya2;  YI Dinghua1;  YU Shiqiang1;  ZHANG Jinbao1;  CHEN Wensheng1;  SUN Guocheng1
1.Department of Cardiology Surgery, 2.Department of Nuclear Medicine, Xijing Hospital, Fourth Military Medical University, Xi′an 710032, Shaanxi, China
关键词:
体外循环; 血栓调节蛋白; 血管性假血友病因子; 内皮素1;  一氧化氮
Keywords:
cardiopulmonary bypass;  thrombomodulin;  von Willebrand factor;  endothelial1;  nitric oxide
分类号:
Q274；R654.1
DOI:
-
文献标识码:
A
摘要:
目的 观察体外循环(CPB) 对全身血管内皮的急性损伤/活化。方法 实验分组：Ⅰ组：60 例先天性心脏病心内畸形矫治术患者； Ⅱ组: 60例瓣膜病患者。于术中CPB前、CPB 30 min、CPB后 0、4、24、48、72 h 共7个时点采集静脉血,动态观察患者血浆中血栓调节蛋白( thrombomodulin,TM)、血管性假血友病因子(von Willebrand factor,vWF)、内皮素1(endothelin1，ET1)和一氧化氮（nitric oxide，NO）的变化。结果 与CPB前相比，Ⅰ、Ⅱ组患者TM、vWF 在CPB 30 min 显著升高, CPB结束时升至最高点［TM：（5.7±1.3）μg/L vs （6.6±1.0）μg/L；vWF：（18±3）μkat/L vs （23±4）μkat/L, 均P< 0.01］,而后下降,但CPB后72 h 仍未恢复到CPB前水平(P< 0.05)。ET1 在整个过程中先降后升, 与CPB前相比［Ⅰ组：（92±5）ng/L，Ⅱ组：（106±6）ng/L］，CPB后4 h降至最低［Ⅰ组：（70±5）ng/L，Ⅱ组：（78±3）ng/L, 均P< 0.01］，而后逐渐上升，CPB后72 h明显高于CPB前［Ⅰ组：（101±7）ng/L，Ⅱ组：（122±7）ng/L，均P<0.01］。NO含量在CPB后4 h 降至最低水平［Ⅰ组：（42±6）μmol/L，Ⅱ组：（43±5）μmol/L］，CPB后72 h NO含量［Ⅰ组：（58±6）μmol/L，Ⅱ组：（62±10）μmol/L］恢复至CPB前水平［Ⅰ组：（57±6）μmol/L，Ⅱ组：（63±7）μmol/L］。结论 CPB可导致血管内皮细胞的广泛损伤/活化，这种损伤大约72 h恢复。
Abstract:
AIM To investigate vascular endothelial cell injury and activation during cardiopulmonary bypass (CPB). METHODS One hundred and twenty patients treated with surgical procedures were divided in two groups: 60 cases with congenital heart disease in groupⅠ and 60 cases with valve disease in groupⅡ. Blood samples of each patient were taken to detect the levels of thrombomodulin (TM), von Willebrand Factor (vWF) and endothelial1(ET1) before CPB, at 30 min during CPB, and at 0 h, 4 h, 24 h, 48 h, 72 h after the termination of CPB. RESULTS The TM and vWF levels of groupⅠand group Ⅱ significantly increased at 30 min during CPB, rose to the peak 0 h after the termination of CPB［TM:（5.7±1.3）μg/L, （6.6±1.0）μg/L; vWF:（18±3）μkat/L, （23±4）μkat/L, respectively］, as compared with before CPB (P<0.01) and did not return to normal till 72 h after the termination of CPB. Compared with the concentration of ET1 before CPB ［groupⅠ: （92±5）ng/L, groupⅡ:（106±6）ng/L］, the concentration of ET1 dropped to the lowest level 4 h after the termination of CPB ［groupⅠ: （70±5）ng/L, groupⅡ: （78±3）ng/L, P<0.01］ and increased gradually to a peak level 72 h after the termination of CPB ［groupⅠ: （101±7）ng/L, groupⅡ: （122±7）ng/L, P<0.01］. The concentration of NO also dropped to the lowest level 4 h after the termination of CPB［groupⅠ:（42±6）μmol/L, groupⅡ: （43±5）μmol/L］ and returned to normal level 72 h after CPB ［groupⅠ: （57 ±6）μmol/L, groupⅡ: （63±7）μmol/L］. CONCLUSION CPB induces the injury and activation of vascular endothelial cells, which may be recovered about 72 h after CPB.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2005-09-20.基金项目：陕西省卫生厅基金项目资助（No.2006D42）作者简介：顾春虎,博士,主治医生Email：guchunhu@fmmu.edu.cn
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