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浅低温体外循环心脏不停跳条件下瓣膜置换的肺保护☆
引用本文:谢晓勇,何 巍,郑宝石,冯 旭,周 涛,叶仕高,冯震博. 浅低温体外循环心脏不停跳条件下瓣膜置换的肺保护☆[J]. 中国组织工程研究, 2012, 16(18): 3267-3271. DOI: 10.3969/j.issn.1673-8225.2012.18.009
作者姓名:谢晓勇  何 巍  郑宝石  冯 旭  周 涛  叶仕高  冯震博
作者单位:1广西医科大学,广西壮族自治区南宁市530021;2广西医科大学第一附属医院心胸外科,广西壮族自治区南宁市 530021
摘    要:
背景:浅低温体外循环心脏不停跳瓣膜置换可减轻术后肺损伤,与其可减轻中性粒细胞在肺部积聚,降低肿瘤坏死因子α、白细胞介素8等炎性因子水平有关,但其他方面的作用机制有待于进一步研究。目的:进一步探讨浅低温体外循环心脏不停跳二尖瓣置换术肺保护机制。方法:纳入二尖瓣置换患者40例,随机数字表法均分为2组。实验组采用浅低温体外循环心脏不停跳治疗,对照组采用中低温心脏停跳体外循环治疗。分别于开胸后和体外循环后30 min两个时点采集肺组织及静脉血,检测肺组织核转录因子κB表达水平及血液黏附分子CD11b/CD18荧光阳性百分率;体外循环前、体外循环30 min、停机时、停机后3,6,12 h取静脉血测定中性粒细胞弹性蛋白酶浓度;体外循环前、停机时、停机后1,8 h查动脉血气分析,计算呼吸指数。结果与结论:①两组肺组织核转录因子κB蛋白表达、CD11b/CD18荧光阳性百分率在体外循环后30 min明显升高(P < 0.01);但对照组明显高于实验组(P < 0.05)。②两组血清中性粒细胞弹性蛋白酶浓度在体外循环 30 min、停机时、停机后3,6 h 4个时点明显升高(P < 0.01,P < 0.05),但对照组明显高于实验组(P < 0.01,P < 0.05)。③两组呼吸指数在体外循环停机时、停机后1,8 h各时点升高(P < 0.01,P < 0.05),但对照组高于实验组(P < 0.05)。提示浅低温体外循环心脏不停跳瓣膜置换可通过抑制肺部核转录因子кB活性,降低中性粒细胞表面CD11b/CD18表达及减少中性粒细胞释放弹性蛋白酶等机制,减轻术后肺损伤。 

关 键 词:浅低温体外循环心脏不停跳  二尖瓣置换  肺保护机制  肺损伤  体外循环  
收稿时间:2011-10-14

Lung protective mechanism of mitral valve replacement with beating-heart via mild hypothermic cardiopulmonary bypass
Xie Xiao-yong,He Wei,Zheng Bao-shi,Feng Xu,Zhou Tao,Ye Shi-gao,Feng Zhen-bo. Lung protective mechanism of mitral valve replacement with beating-heart via mild hypothermic cardiopulmonary bypass[J]. Chinese Journal of Tissue Engineering Research, 2012, 16(18): 3267-3271. DOI: 10.3969/j.issn.1673-8225.2012.18.009
Authors:Xie Xiao-yong  He Wei  Zheng Bao-shi  Feng Xu  Zhou Tao  Ye Shi-gao  Feng Zhen-bo
Affiliation:1Guangxi Medical University, Nanning  530021, Guangxi Zhuang Autonomous Region, China; 2Department of Cardiothoracic Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning  530021, Guangxi Zhuang Autonomous Region, China
Abstract:
BACKGROUND: Mitral valve replacement on beating-heart with mild hypothermic cardiopulmonary bypass (CPB) can lessen pulmonary injury after operation, which is relative to its lightening accumulation of polymorphonuclear neutrophil in lung and reducing the serum levels of tumor necrosis factor α and interleukin-8. But other mechanism of its lung protection should research further.OBJECTIVE: To further explore the lung protective mechanism of mitral valve replacement with beating-heart with mild hypothermic CPB.METHODS: A total of 40 patients underwent mitral valve replacements which were randomly divided into experimental group and control group. Patients in the experimental group were performed with the operation on beating-heart with mild hypothermic CPB, while the patients in the control group received the operation on arrested heart with moderate hypothermia CPB. The protein expression level of nuclear factor-кB in lung tissue and positive percentage of adhesion molecule CD11b/CD18 in blood was detected after opening chest and 30 minutes after CPB. The serum level of Neutrophil elastase was measured before CPB, 30 minutes during CPB, at the end of CPB and 3, 6 and 12 hours after CPB. Arterial blood gas analysis was preformed and respiratory index was calculated before CPB, at the end of CPB and 1 and 8 hours after CPB.RESULTS AND CONCLUSION: The protein expression level of nuclear factor-кB in lung tissue and positive percentage of CD11b/CD18 in blood of two groups was increased significantly at 30 minutes after CPB (P < 0.01), but the levels in the control group were higher than that in the experimental group (P < 0.05). The serum levels of Neutrophil elastase in two groups were increased significantly at 30 minutes during CPB, at the end of CPB, 3 and 6 hours after CPB (P < 0.01, P < 0.05), but the level in the control group was higher than that in the experimental group (P < 0.01, P < 0.05). The level of respiratory index in two groups was significantly increased at the end of CPB, 1 and 8 hours after CPB (P < 0.01, P < 0.05), but the level in the experimental group was significantly lower than that in the control group (P < 0.05). It indicates that mitral valve replacement on beating-heart with mild hypothermic cardiopulmonary bypass can reduce the lung injury through the inhibition of nuclear factor-кB activity, decreasing the expression of CD11b/CD18 on the surface of neutrophils and reduce the release of neutrophils.
Keywords:
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