CAJ | 학술논문

目的观察电刺激迷走神经对脓毒症大鼠凝血功能的影响.方法采用经左侧股静脉注射脂多糖(LPS,10mg/kg)复制脓毒症模型.将雄性SD大鼠96只随机分成4组:生理盐水组(SHAM组)、脓毒症组(LPS组)、迷走神经切断组(VGX组)、电刺激迷走神经组(VNS组).将左侧迷走神经远端与双铂电极连接,于模型制备成功即刻行电刺激(5 V,2 ms,1 Hz)20 min.于注射脂多糖前(0 h),注入后2、4、6 h各个时间点取6只动物,经腹主动脉取血查血浆凝血酶原时间(PT)、活化部分凝血酶原时间(aPTT)、血浆凝血酶时间(TT)、血浆纤维蛋白原(Fbg)和肿瘤坏死因子-α(TNF-α)水平.结果在予以LPS 2 h后,LPS组(316.34±23.96)ng/L和VGX组(325.77±39.77)ng/L血浆TNF-α水平较VNS组(252.72±30.36)ng/L升高(P＜0.05);6 h时,LPS组(10.68±0.66)s和VGX组(10.72±0.57)s与VNS组(9.67±1.04)s比较PT时间延长(P＜0.05);2 h时,LPS组(23.4 ±0.5)s和VGX组(23.9±0.5)s与VNS组(18.4±1.1)s比较aPTT时间延长(P＜0.05);4 h时,LPS组(32.0±1.0)s和VGX组(32.7±0.8)s与VNS组(28.7±1.9)s比较,TT时间延长(P＜0.05);4 h时,LPS组(1.909±0.224)g/L和VGX组(1.822±0.329)g/L与VNS组(2.376±0.138)g/L比较,Flg浓度降低(P＜0.05).结论电刺激迷走神经不仅可以有效地抑制脓毒症大鼠血浆TNF-α水平,抑制炎症反应,而且还可以改善脓毒症大鼠的凝血功能紊乱.
목적 관찰전자격미주신경대농독증대서응혈공능적영향.방법 채용경좌측고정맥주사지다당(LPS,10mg/kg)복제농독증모형.장웅성SD대서96지수궤분성4조:생리염수조(SHAM조)、농독증조(LPS조)、미주신경절단조(VGX조)、전자격미주신경조(VNS조).장좌측미주신경원단여쌍박전겁련접,우모형제비성공즉각행전자격(5 V,2 ms,1 Hz)20 min.우주사지다당전(0 h),주입후2、4、6 h각개시간점취6지동물,경복주동맥취혈사혈장응혈매원시간(PT)、활화부분응혈매원시간(aPTT)、혈장응혈매시간(TT)、혈장섬유단백원(Fbg)화종류배사인자-α(TNF-α)수평.결과 재여이LPS 2 h후,LPS조(316.34±23.96)ng/L화VGX조(325.77±39.77)ng/L혈장TNF-α수평교VNS조(252.72±30.36)ng/L승고(P＜0.05);6 h시,LPS조(10.68±0.66)s화VGX조(10.72±0.57)s여VNS조(9.67±1.04)s비교PT시간연장(P＜0.05);2 h시,LPS조(23.4 ±0.5)s화VGX조(23.9±0.5)s여VNS조(18.4±1.1)s비교aPTT시간연장(P＜0.05);4 h시,LPS조(32.0±1.0)s화VGX조(32.7±0.8)s여VNS조(28.7±1.9)s비교,TT시간연장(P＜0.05);4 h시,LPS조(1.909±0.224)g/L화VGX조(1.822±0.329)g/L여VNS조(2.376±0.138)g/L비교,Flg농도강저(P＜0.05).결론 전자격미주신경불부가이유효지억제농독증대서혈장TNF-α수평,억제염증반응,이차환가이개선농독증대서적응혈공능문란.
Objective To investigate the effect of vagus nerve stimulation on coagulation parameters in septic rats. Methods Sepsis model was reproduced by intravenously sublethal dose of lipopolysaccharide (LPS). Ninety-six male Sprague-Dawley rats were randomly divided into four groups: saline group (SHMA); lipopolysaccharide group (LPS); Vogotomy group (VGX) and vagus nerve stimulation grou (VNS). The distal end of the left vagus nerve was electrically stimulated for 20 min after injection of LPS with predefined settings (5 V, 2 ms, 1 Hz) as described previously. Prothrombin time (PT), activated partial thromboplastin time (aPTT), thrombin time (TT), fibrinogen (Fbg) and tumor necrosis factor-α (TNF-α) were measured before injection (0 h) and 2, 4 and 6 h thereafter. Results At the 2nd h after injection of LPS, the plasma TNF-α levels were significantly higher in LPS group and VGX group than those in VNS group[( 316.34 ± 23.96), (325.77 ± 39.77) vs ( 252.72 ± 30.36 ) ng/L, P ＜ 0.05]. In LPS group and VGX group the PT was significantly longer than VNS group at the 6th h after injection ofLPS[( 10.68 ± 0.66), ( 10.72 ± 0.57) vs (9.67 ± 1.04) s,P ＜ 0.05]. At the 2nd h in LPS group and VGX group the aPTT was significantly longer than VNS group[( 23.4 ± 0.5 ), ( 23.9 ± 0.5 ) vs ( 18.4 ±1.1) s,P＜0.05]. At the 4th h in LPS group and VGX group the TT was significantly longer than VNS group[(32.0 ± 1.0), (32.7 ±0.8) vs (28.7 ± 1.9) s,P ＜0.05]. At the 4th h in LPS group and VGX group the levels of Fbg were significantly decreased as compared with VNS group[( 1.909 ± 0.224 ),( 1.822 ± 0.329) vs (2.376 ± 0.138 ) g/L, P ＜ 0.05]. Conclusion Electrical stimulation of the vagus nerve can not only significantly reduce serum TNF-α levels but also improve the coagulation dysfunction in septic rats.