CAJ | 학술논문

目的探讨趋化因子Fractalkine(FKN)、肿瘤坏死因子-α(TNF-α)与慢性肺源性心脏病(简称肺心病)的关系,揭示川芎嗪抑制肺动脉高压的作用机制.方法将35例确诊为慢性肺心病患者随机分为川芎嗪组(19例)及常规治疗组(16例),并选取18名健康体检者为健康组.常规治疗组给予常规治疗(哌拉西林/他唑巴坦针3.375 g静脉滴注,每天2次;左氧氟沙星针0.6 g静脉滴注,每天1次;氨溴索针60 mg静脉滴注,每天1次;多索茶碱针0.2 g静脉滴注,每天1次,均连用10～14天,并纠正酸碱失衡及电解质紊乱),川芎嗪组在常规治疗基础上加用盐酸川芎嗪(商品名:川青,每支120 mg,240 mg加入生理盐水注射液250 mL中静脉滴注,每天1次,连用10～14天),分别于治疗前后采用酶联免疫法检测血清FKN、TNF-α水平,应用多普勒超声仪检测治疗前后肺动脉压(mPAP)的变化.结果 (1)治疗前常规治疗组、川芎嗪组血清FKN及TNF-α水平差异无统计学意义(P＞0.05),但均高于健康组(均P＜0.01);(2)川芎嗪组治疗后FKN、TNF-α及mPAP水平显著低于治疗前,且低于常规治疗组治疗后(P＜0.05,P＜0.01).(3)FKN与TNF-α水平呈显著正相关(r=0.662,P＜0.01).结论 (1)慢性肺心病患者存在FKN及TNF-α的高表达状态;(2)川芎嗪能抑制慢性肺心痛患者FKN与TNF-α的表达,这可能是其降低肺动脉压的重要作用机制之一.
목적 탐토추화인자Fractalkine(FKN)、종류배사인자-α(TNF-α)여만성폐원성심장병(간칭폐심병)적관계,게시천궁진억제폐동맥고압적작용궤제.방법 장35례학진위만성폐심병환자수궤분위천궁진조(19례)급상규치료조(16례),병선취18명건강체검자위건강조.상규치료조급여상규치료(고랍서림/타서파탄침3.375 g정맥적주,매천2차;좌양불사성침0.6 g정맥적주,매천1차;안추색침60 mg정맥적주,매천1차;다색다감침0.2 g정맥적주,매천1차,균련용10～14천,병규정산감실형급전해질문란),천궁진조재상규치료기출상가용염산천궁진(상품명:천청,매지120 mg,240 mg가입생리염수주사액250 mL중정맥적주,매천1차,련용10～14천),분별우치료전후채용매련면역법검측혈청FKN、TNF-α수평,응용다보륵초성의검측치료전후폐동맥압(mPAP)적변화.결과 (1)치료전상규치료조、천궁진조혈청FKN급TNF-α수평차이무통계학의의(P＞0.05),단균고우건강조(균P＜0.01);(2)천궁진조치료후FKN、TNF-α급mPAP수평현저저우치료전,차저우상규치료조치료후(P＜0.05,P＜0.01).(3)FKN여TNF-α수평정현저정상관(r=0.662,P＜0.01).결론 (1)만성폐심병환자존재FKN급TNF-α적고표체상태;(2)천궁진능억제만성폐심통환자FKN여TNF-α적표체,저가능시기강저폐동맥압적중요작용궤제지일.
Objective To reveal the relationship of chronic pulmonary heart disease(CPHD)with the chemotactic factor Fractalkine(FKN)and tumor necrosis factor-α(TNF-α),and to explore the action mechanism of tetramethylpyrazine(TMP)for suppressing pulmonary hypertension.Methods Patients with CPHD were randomly assigned to two groups,19 in Group A and 16 in Group B,and a control group(group C)consisting of 18 healthy adults was setup.Conventional treatment were given to all patients,which consisted of Piperacillin 3.375 g iv dripping twice a day,Levofloxacin 0.6 g + Ambroxol 60 mg + Doxofylline 0.2 g iv dripping once e day,all for 10-14 days,and acid-base and electrolytesim balance in patients were monitored and corrected.At the same time,TMP(trade name: Chuanqing,containing 120 mg of TMP in a 2 mL ampoule)was given additionally to patients in Group B at the dosage of 240 mg/d by adding in 250 mL of normal saline via iv dripping.Serum levels of FKN and TNF-α were detected before and after treatment by enzyme-linked immunoassay,and the change of mean pulmonary arterial pressure(mPAP)was measured as well.Results Before treatment,difference of FKN and TNF-α levels between the two patients' groups were insignificant(P＞0.05),but all higher than those in Group C respectively(P＜0.01).While after treatment,the two indices and mPAP levels in Group B were statistically lower than those before treatment,also than those in Group A.Regression analysis showed a positive correlation between TNF-α and FKN(r =0.662,P＜0.001).Conclusions A high blood FKN and TNF-α expression state exists in CPHD patients,which could be suppressed by TMP,and these suppressive effects may be one of the important mechanisms responsible for the pulmonary arterial pressure lowering action of TMP.