中国现代医学杂志
中國現代醫學雜誌
중국현대의학잡지
CHINA JOURNAL OF MODERN MEDICINE
2004年
13期
23-26
,共4页
胥方元%何成松%邹树芳%干锦华%孔古娅
胥方元%何成鬆%鄒樹芳%榦錦華%孔古婭
서방원%하성송%추수방%간금화%공고아
卡托普利%肺动脉高压%野百合碱%内皮素-1
卡託普利%肺動脈高壓%野百閤堿%內皮素-1
잡탁보리%폐동맥고압%야백합감%내피소-1
captopril%pulmonary hypertension%monocrotaline%endothelin - 1
目的探讨卡托普利(CPT)对野百合碱(MCT)诱发大鼠慢性炎性肺动脉高压的影响.方法将33只雄性Wister大鼠随机分为正常对照组、肺动脉高压模型组、CPT治疗组,每组11只.予MCT(50 mg/kg)复制大鼠肺动脉高压模型后,分别给CPT组及模型组大鼠连续灌胃CPT25 mg/(kg·d)或等量生理盐水21 d,采用改良右心导管术测定肺血流动力学参数,以非平衡法测定静脉血浆内皮素-1(ET-1)水平;处死大鼠后,称量肺湿重(wW)、右心室自由壁(RV)和左心室加室间隔(LV+S)重,计算右心肥厚指数(RV/LV+S).结果CPT能明显降低肺动脉高压模型大鼠的平均肺动脉压、wW、RV/LV+S及血浆ET-1水平(P<0.05,或P<0.01).结论长期使用CPT能有效降低MCT所致肺动脉高压,改善心功能,其作用机制可能与显著降低血浆ET-1水平有关.
目的探討卡託普利(CPT)對野百閤堿(MCT)誘髮大鼠慢性炎性肺動脈高壓的影響.方法將33隻雄性Wister大鼠隨機分為正常對照組、肺動脈高壓模型組、CPT治療組,每組11隻.予MCT(50 mg/kg)複製大鼠肺動脈高壓模型後,分彆給CPT組及模型組大鼠連續灌胃CPT25 mg/(kg·d)或等量生理鹽水21 d,採用改良右心導管術測定肺血流動力學參數,以非平衡法測定靜脈血漿內皮素-1(ET-1)水平;處死大鼠後,稱量肺濕重(wW)、右心室自由壁(RV)和左心室加室間隔(LV+S)重,計算右心肥厚指數(RV/LV+S).結果CPT能明顯降低肺動脈高壓模型大鼠的平均肺動脈壓、wW、RV/LV+S及血漿ET-1水平(P<0.05,或P<0.01).結論長期使用CPT能有效降低MCT所緻肺動脈高壓,改善心功能,其作用機製可能與顯著降低血漿ET-1水平有關.
목적탐토잡탁보리(CPT)대야백합감(MCT)유발대서만성염성폐동맥고압적영향.방법장33지웅성Wister대서수궤분위정상대조조、폐동맥고압모형조、CPT치료조,매조11지.여MCT(50 mg/kg)복제대서폐동맥고압모형후,분별급CPT조급모형조대서련속관위CPT25 mg/(kg·d)혹등량생리염수21 d,채용개량우심도관술측정폐혈류동역학삼수,이비평형법측정정맥혈장내피소-1(ET-1)수평;처사대서후,칭량폐습중(wW)、우심실자유벽(RV)화좌심실가실간격(LV+S)중,계산우심비후지수(RV/LV+S).결과CPT능명현강저폐동맥고압모형대서적평균폐동맥압、wW、RV/LV+S급혈장ET-1수평(P<0.05,혹P<0.01).결론장기사용CPT능유효강저MCT소치폐동맥고압,개선심공능,기작용궤제가능여현저강저혈장ET-1수평유관.
Objective:To investigate the effect of captopril on monocrotaline - induced pulmonary hypertension in rats. Methods:Adult male Waister rats were given a single dose of monocrotaline(50 mg/kg) to induce the mold of pulmoanry hypertension. 33 cases were randmonly divided into normal control group, mold group and captopril treatment group(n = 11 ). Then treated with gastric infusion of normal saline, captopril respectively for 21 days. The parameter of pulmonary hemodynamics was monitored by Gould 3 400 polygrph system through the cannulation of polyvinyl tube. Right ventricle and left ventricle added with interventricular septum weight ratio, the lung wet weight were measured. The level of plasma endothetin - 1 was determined by the method of nonequilibrium. Results: Captopril significantly inhibited the progression of pulmonary artery pressure(P <0.01 ). It decreased the right heart index, and reduced the lung wet weight and the level of plasma endothelin - 1 (P <0.05 ,or P <0,01 ). Conclusions:Captopril is able to reduce the pulmonary hypertension and improve the heart function. Its mechanisms may be related to reducing the level of plasma endothelin - 1.