天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2013年
8期
802-805
,共4页
王士凯%王海燕%薛彦菊%梁江久
王士凱%王海燕%薛彥菊%樑江久
왕사개%왕해연%설언국%량강구
心力衰竭%心室重构%利钠肽,脑%大鼠, Wistar%氟伐他汀%血管性血友病因子
心力衰竭%心室重構%利鈉肽,腦%大鼠, Wistar%氟伐他汀%血管性血友病因子
심력쇠갈%심실중구%리납태,뇌%대서, Wistar%불벌타정%혈관성혈우병인자
heart failure%ventricular remodeling%natriuretic peptide,brain%rats,Wistar%fluvastatin%Von Wille-brand factor
目的研究氟伐他汀对慢性心衰大鼠心室重构和心功能的保护作用，并探讨其对血管性血友病因子（VWF）的影响。方法皮下注射异丙基肾上腺素（170 mg/kg）2次,建立心力衰竭大鼠模型，将18只慢性心衰大鼠随机分为氟伐他汀组(20 mg ·kg-1·d-1)、安慰剂组和正常对照组，安慰剂组和正常对照组给予等量生理盐水。灌胃灌药6周后，超声心动图观察各组大鼠心脏结构和功能的变化，测定心室质量分数，酶联免疫吸附试验（ELISA）检测血浆VWF和B型脑钠肽（BNP)的含量，逆转录多聚酶链反应（RT-PCR）检测心脏组织VWF mRNA的表达。结果与正常对照组相比较，安慰剂组和氟伐他汀组左心室舒张末期内径（LVEDD）和左心室收缩末期内径（LVESD）均显著增加，左心室射血分数（LVEF）和左室射血分数缩短率（LVFS）均显著降低（P＜0.05），左心室湿质量/体质量（LVRW）及右室湿质量/体质量（RVRW）显著增加，心脏组织VWF mRNA表达明显增强（P＜0.01）；与安慰剂组相比，氟伐他汀组LVEDD、LVRW及RVRW均降低，心脏组织VWF mRNA表达明显降低（P＜0.01），LVEF和LVFS均显著增加（P＜0.05）；VWF与BNP呈高度正相关（r=0.996）。结论氟伐他汀能改善心室重构及心功能，其作用机制可能与调节VWF的水平、改善内皮功能有关。
目的研究氟伐他汀對慢性心衰大鼠心室重構和心功能的保護作用，併探討其對血管性血友病因子（VWF）的影響。方法皮下註射異丙基腎上腺素（170 mg/kg）2次,建立心力衰竭大鼠模型，將18隻慢性心衰大鼠隨機分為氟伐他汀組(20 mg ·kg-1·d-1)、安慰劑組和正常對照組，安慰劑組和正常對照組給予等量生理鹽水。灌胃灌藥6週後，超聲心動圖觀察各組大鼠心髒結構和功能的變化，測定心室質量分數，酶聯免疫吸附試驗（ELISA）檢測血漿VWF和B型腦鈉肽（BNP)的含量，逆轉錄多聚酶鏈反應（RT-PCR）檢測心髒組織VWF mRNA的錶達。結果與正常對照組相比較，安慰劑組和氟伐他汀組左心室舒張末期內徑（LVEDD）和左心室收縮末期內徑（LVESD）均顯著增加，左心室射血分數（LVEF）和左室射血分數縮短率（LVFS）均顯著降低（P＜0.05），左心室濕質量/體質量（LVRW）及右室濕質量/體質量（RVRW）顯著增加，心髒組織VWF mRNA錶達明顯增彊（P＜0.01）；與安慰劑組相比，氟伐他汀組LVEDD、LVRW及RVRW均降低，心髒組織VWF mRNA錶達明顯降低（P＜0.01），LVEF和LVFS均顯著增加（P＜0.05）；VWF與BNP呈高度正相關（r=0.996）。結論氟伐他汀能改善心室重構及心功能，其作用機製可能與調節VWF的水平、改善內皮功能有關。
목적연구불벌타정대만성심쇠대서심실중구화심공능적보호작용，병탐토기대혈관성혈우병인자（VWF）적영향。방법피하주사이병기신상선소（170 mg/kg）2차,건립심력쇠갈대서모형，장18지만성심쇠대서수궤분위불벌타정조(20 mg ·kg-1·d-1)、안위제조화정상대조조，안위제조화정상대조조급여등량생리염수。관위관약6주후，초성심동도관찰각조대서심장결구화공능적변화，측정심실질량분수，매련면역흡부시험（ELISA）검측혈장VWF화B형뇌납태（BNP)적함량，역전록다취매련반응（RT-PCR）검측심장조직VWF mRNA적표체。결과여정상대조조상비교，안위제조화불벌타정조좌심실서장말기내경（LVEDD）화좌심실수축말기내경（LVESD）균현저증가，좌심실사혈분수（LVEF）화좌실사혈분수축단솔（LVFS）균현저강저（P＜0.05），좌심실습질량/체질량（LVRW）급우실습질량/체질량（RVRW）현저증가，심장조직VWF mRNA표체명현증강（P＜0.01）；여안위제조상비，불벌타정조LVEDD、LVRW급RVRW균강저，심장조직VWF mRNA표체명현강저（P＜0.01），LVEF화LVFS균현저증가（P＜0.05）；VWF여BNP정고도정상관（r=0.996）。결론불벌타정능개선심실중구급심공능，기작용궤제가능여조절VWF적수평、개선내피공능유관。
Objective To study the protective effect of fluvastatin on cardiac remodeling and cardiac function, and to investigate its effect on Von Willebrand factor (VWF). Methods The rat model of cardiac heart failure (CHF) was in-duced by isoproterenol injection (170 mg/kg) via subcutaneous. Eighteen model rats were randomly divided into fluvastatin (20 mg ·kg-1·d-1) group, placebo group and control group. Rats were treated with normal saline in placebo group and control group. After 6-week treatment, the structure and function of hearts were measured by echocardiography in three groups. The ventricular weight index, the serum levels of VWF and B-type natriuretic peptide (BNP) were measured by ELISA assay. The levels of VWF mRNA in cardiac muscle were measured by RT-PCR. Results Compared with control group, the val-ues of left ventricular end-diastolic diameter (LVEDD) and left ventricular end systolic diameter (LVESD) were significantly increased in placebo group and fluvastatin group, while values of left ventricular ejection fraction (LVEF) and left ventricular ejection fraction shortening (LVFS) were significantly decreased (P<0.05). The values of left ventricular wet weight/body weight (LVRW) and right ventricular wet weight/body weight (RVRW) were increased in placebo group and fluvastatin group. The expression of VWF mRNA in cardiac tissues was enhanced significantly (P<0.01). Compared with placebo group, the values of LVEDD, LVRW and RVRW were significantly decreased in fluvastatin group. The expression of VWF mRNA in cardiac tissues was significantly decreased (P<0.01), and the values of LVEF and LVFS were significant increased in fluvas-tatin group (P<0.05). The level of VWF was positively corrected with BNP(r=0.996). Conclusion Fluvastatin could im-prove the cardiac function and cardiac remodeling, which may be by reducing the level of VWF and improving endothelial function.
