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赵桂香,刘志强,古丽扎尔·吐尔逊.截肢手术创伤对大鼠心脏电生理?心功能及eNOS 通路的影响[J].中国比较医学杂志,2019,29(8):79~87.
截肢手术创伤对大鼠心脏电生理?心功能及eNOS 通路的影响
Effects of amputation trauma on cardiac electrophysiology, cardiac function, and the endothelial nitric oxide synthase pathway in rats
投稿时间:2019-01-02  
DOI:10.3969/j. issn. 1671 -7856. 2019. 08. 013
中文关键词:  截肢手术创伤  心功能  心电图  内皮型一氧化氮合酶  一氧化氮  大鼠
英文关键词:amputation trauma  cardiac function  electrocardiogram  endothelial nitric oxide synthase  nitric oxide  rat
基金项目:
作者单位E-mail
赵桂香 新疆医科大学第六附属医院心血管内科,乌鲁木齐 830002 zq217218219@ 163.com 
刘志强 新疆医科大学第一附属医院心内管内科,乌鲁木齐 830054  
古丽扎尔·吐尔逊 新疆喀什疏勒县解放军第947 医院特诊科,新疆喀什 844200  
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中文摘要:
      目的 探究大鼠经截肢创伤后心脏电生理?心功能变化情况及其与内皮型一氧化氮合酶/ 一氧化氮(eNOS/ NO)通路的关系?方法 建立左后肢创伤模型,将大鼠分为正常组(仅麻醉)?截肢对照组?截肢0. 25 h?截肢0. 5 h?截肢0. 75 h?截肢1. 5 h,每组12 只?采用心电图(ECG)检测大鼠心率?QT 间期?PR 间期变化;超声检测左室射血分数(LVEF)?左室短轴缩短率(LVFS);右侧颈动脉插管检测左心室收缩压(LVSP)?左心室内压升高最高速率(+dp/ dt max)?左心室内压降低最高速率(-dp/ dtmax);试剂盒检测血清和心肌组织丙二醛(MDA)?超氧化物歧化酶(SOD)?一氧化氮(NO)?髓过氧化物酶(MPO)?肿瘤坏死因子-ɑ(TNF-ɑ)和白介素-6(IL-6)水平;苏木精—伊红染色法(HE)染色观察心肌组织形态学变化;末端标记法(TUNEL)染色法观察心肌组织细胞凋亡情况;蛋白免疫印迹法检测心肌组织中eNOS?B 淋巴细胞瘤-2 蛋白(Bcl-2)?Bcl-2 相关X 蛋白(Bax)蛋白表达?结果 与正常组相比,截肢0. 5 h,截肢0. 75 h 心率升高?QT 间期降低,LVSP?+dp/ dmax?-dp/ dmax?LVEF?LVFS 降低,MPO?MDA?TNF-ɑ?IL-6 升高,SOD 降低,细胞排列疏松呈坏死状,伴有大量炎性细胞浸润;心肌细胞凋亡指数升高,心肌组织Bcl-2 蛋白表达降低?Bax 蛋白表达升高,NO 水平?eNOS 蛋白表达降低,呈时间依赖性,差异具有显著性( P <0. 05);与截肢0. 75 h 相比,截肢1. 5 h 心率降低,QT 间期?PR 间期升高,LVSP?+dp/ dmax?-dp/ dmax?LVEF?LVFS升高,MPO?MDA?SOD?TNF-ɑ?IL-6 降低,心肌病理损伤程度有所减轻;心肌细胞凋亡指数降低,Bcl-2 蛋白表达升高,Bax 蛋白表达降低,NO 水平?eNOS 蛋白表达升高,差异具有显著性( P <0. 05)?结论 截肢手术创伤可使大鼠发生缺血性心电图改变,心功能受损及过度氧化应激?炎症损伤,其机制可能与eNOS/ NO 通路受到抑制有关?
英文摘要:
      Objective To investigate the changes in cardiac electrophysiology and cardiac function in rats afterlimb amputation and their relationships with the endothelial nitric oxide synthase/ nitric oxide ( eNOS/ NO) pathway.Methods Seventy-two healthy 8-week old male Wistar rats were divided into the normal group (anesthesia only),amputation control, amputation 0. 25 h, amputation 0. 5 h, amputation 0. 75 h, and amputation 1. 5 h groups (n=12 ratsper group). The left hind limb trauma model was established by amputation surgery. Changes in heart rate, QT interval,and PR interval were detected by electrocardiogram; the left ventricular ejection fraction (LVEF) and left ventricular shortaxis shortening rate (LVFS) were measured by echocardiography; the left ventricular systolic pressure (LVSP), thehighest rate of increase of left ventricular pressure (+dp/ dt max), and the highest rate of decrease of left ventricularpressure (-dp/ dt max) were measured by right carotid artery intubation; the level of malondialdehyde (MDA) in themyocardium was measured with thiobarbituric acid; the level of superoxide dismutase (SOD) was detected by pyrogallolcolorimetry; Green’s method was used to detect the nitric oxide (NO) levels; levels of myeloperoxidase (MPO), tumornecrosis factor-ɑ (TNF-α), and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay; hematoxylinand eosin staining was used to observe the histopathological changes in the myocardium; myocardial cell apoptosis wasobserved by TUNEL staining; and the expression of eNOS, Bcl-2, and Bcl-2-related X protein (Bax) in the myocardiumwas detected by western blotting. Results Compared with the normal group, the following changes were observed 0. 5 hand 0. 75 h after amputation: the heart rate increased, the QT interval decreased, LVSP, +dp/ dmax, -dp/ dmax, LVEF,and LVFS decreased, MPO, MDA, SOD, TNF-α, and IL-6 increased, and the myocardial cells were loosely arranged,necrotic, and accompanied with a large amount of inflammatory cell infiltration. Moreover, at these same time points, thefollowing significant changes were observed in a time-dependent manner ( P < 0. 05): an increased apoptotic index ofcardiomyocytes, decreased expression of Bcl-2 protein in the myocardium, increased expression of Bax protein, anddecreased NO level and eNOS protein expression. Compared with 0. 75 h after amputation group, the heart rate decreased at0. 5 h after amputation, the QT interval and PR interval increased, LVSP, +dp/ dmax, -dp/ dmax, LVEF, and LVFSincreased, MPO, MDA, SOD, TNF-α, and IL-6 decreased, and the degree of myocardial pathological injury wasalleviated. Moreover, significant differences were seen as following: a decreased apoptotic index of cardiomyocytes,increased Bcl-2 and eNOS protein expression, increased NO levels, and decreased Bax protein expression ( P <0. 05).Conclusions Amputation trauma causes ischemic electrocardiogram changes, cardiac function damage, excessiveoxidative stress, and inflammatory damages in rats. The underlying mechanism may be related to inhibition of the eNOS/ NO pathway.
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