CAJ | 학술논문

目的：探讨加参方通过抑制血管紧张素Ⅱ（AngⅡ）改善心梗模型大鼠心室重构的相关机制。方法：结扎SD大鼠冠状动脉前降支，建立心肌梗死模型，随机分为加参方3 g组、加参方6 g组、氯沙坦组、模型组，另设假手术组。药物干预组在心梗发生24 h后灌胃给药，其中加参方3 g组和6 g组给药剂量分别为3 g生药·kg-1·d-1和6 g生药·kg-1·d-1；氯沙坦组给药剂量为10 mg·kg-1·d-1；假手术组和模型组给予相同体积蒸馏水灌胃。4周后观察大鼠左室收缩末期内径（LVESD）、左室舒张末期内径（LVEDD）、左室后壁厚度（PWT）、左室射血分数（LVEF）、左室短轴缩短率（LVFS）和左室重量指数（LVWI）；胶原蛋白的分布和含量；血浆脑钠肽（BNP）、心肌组织匀浆中AngⅡ的含量等指标变化。结果：大鼠心梗后4周，与模型组相比，加参方6 g剂量组能够明显缩小心肌梗死范围，显著降低LVWI，明显抑制LVEDD和LVESD的扩大，提高LVEF和LVFS（P<0.05）；在缺血危险区，与模型组比较，加参方能明显降低胶原蛋白的含量（P<0.05），该作用呈剂量依赖性；血浆BNP、心肌组织匀浆中AngⅡ含量也明显低于模型组（P<0.05）。结论：加参方能改善心梗模型大鼠心室重构，其相关机制与抑制AngⅡ、改善心梗后早期左室形态学的重构、改善心肌纤维化和心脏的收缩功能有关。
목적：탐토가삼방통과억제혈관긴장소Ⅱ（AngⅡ）개선심경모형대서심실중구적상관궤제。방법：결찰SD대서관상동맥전강지，건립심기경사모형，수궤분위가삼방3 g조、가삼방6 g조、록사탄조、모형조，령설가수술조。약물간예조재심경발생24 h후관위급약，기중가삼방3 g조화6 g조급약제량분별위3 g생약·kg-1·d-1화6 g생약·kg-1·d-1；록사탄조급약제량위10 mg·kg-1·d-1；가수술조화모형조급여상동체적증류수관위。4주후관찰대서좌실수축말기내경（LVESD）、좌실서장말기내경（LVEDD）、좌실후벽후도（PWT）、좌실사혈분수（LVEF）、좌실단축축단솔（LVFS）화좌실중량지수（LVWI）；효원단백적분포화함량；혈장뇌납태（BNP）、심기조직균장중AngⅡ적함량등지표변화。결과：대서심경후4주，여모형조상비，가삼방6 g제량조능구명현축소심기경사범위，현저강저LVWI，명현억제LVEDD화LVESD적확대，제고LVEF화LVFS（P<0.05）；재결혈위험구，여모형조비교，가삼방능명현강저효원단백적함량（P<0.05），해작용정제량의뢰성；혈장BNP、심기조직균장중AngⅡ함량야명현저우모형조（P<0.05）。결론：가삼방능개선심경모형대서심실중구，기상관궤제여억제AngⅡ、개선심경후조기좌실형태학적중구、개선심기섬유화화심장적수축공능유관。
This study was aimed to observe the effect ofJia-Shen prescription (JSP) on angiotensinⅡ (AngⅡ) inhibition, ventricular remodeling in myocardial infarction (MI) rat model. The anterior descending coronary artery of Sprague-Dawley rat was ligated to establish the MI rat model. Rats were randomly divided into the 3 g JSP group, 6 g JSP group, losartan group, model group, and the sham-operation group. Intragastric administration of medication was given 24 h after MI. In the 3 g and 6 g JSP group, JSP was given at the dose of 3 g·kg-1·day-1 and 6 g·kg-1day-1, respectively. Losartan was given at the dose of 10 mg·kg-1·day-1 in the losartan group. Same volume of distilled water was given to the sham-operation and model group. Four weeks later, the left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD), posterior wall thickness (PWT), left ventricular ejection fraction (LVEF), left ventricular fractional shorten (LVFS), left ventricular weight index (LVWI), the distribution and content of collagen, plasma brain natriuretic peptide (BNP) and the AngⅡ content in myocardial tissues homogenate were observed. The results showed that 4 weeks after MI, compared to the model group, 6 g PJP reduced myocardial infarct size, LVWI, LVEDD and LVESD, and enhanced LVEF and LVFS (P< 0.05). In ischemic regions, compared to the model group, JSP can obviously reduce the content of collagen (P < 0.05). This effect had dose-dependent relationship. Plasma BNP and AngⅡ content in myocardial tissues homogenate were also obviously lower than the model group (P< 0.05). It was concluded that JSP can improve the ventricular remodeling of MI rat model. Its action mechanism may be through the AngⅡ inhibition, in order to improve the early stage left ventricular morphological remodeling, myocardial fibrosis and cardiac contractile function.