葡萄籽原花青素对DOCA-盐高血压小鼠心室重构的影响

目的研究葡萄籽原花青素(GSP)对DOCA-盐型高血压小鼠心室重构保护作用并初步探讨其机制。方法皮下注射去氧皮质酮(DOCA)同时予高盐饮水形成DOCA-盐型高血压小鼠模型。实验分为对照组、模型组和GSP 130 mg.kg-1组。计算小鼠心脏重量指数以及肾脏重量指数,HE染色和V-G染色观察心肌病理形态学改变,比色法测定血清中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量以及心肌羟脯氨酸(Hyp)含量。结果与空白对照组相比,DOCA-盐型高血压模型组小鼠心重指数、肾重指数、心肌细胞横截面积(CSA)、心肌胶原纤维明显升高,血清MDA含量升高,SOD活性降低,心肌组织羟脯氨酸含量增加。与模型组相比,GSP 130 mg.kg-1组小鼠心重指数、肾重指数、CSA、心肌胶原沉积明显降低,血清MDA含量降低,SOD活性增加,心肌组织Hyp含量减少。结论 GSP能明显改善DOCA-高盐高血压小鼠心室重构,其机制可能与抗氧化应激有关。     

替米沙坦对异丙肾上腺素所致心肌肥厚大鼠GATA4表达的影响

目的 探讨替米沙坦对异丙肾上腺素所致心肌肥厚大鼠GATA4表达的影响.方法 应用对大鼠背部行皮下注射异丙肾上腺素(ISO)的方法制备心肌肥厚的动物模型,将动物分为对照组、模型组、替米沙坦干预组,分别注射生理盐水及ISO;10天后测量左心室重量/体重(LVW/BW)及全心重量/体重(HW/BW);应用免疫组化及RT-PCR的方法分别观察对照组、模型组、替米沙坦干预组大鼠左心室中GATA4含量及表达.结果 ①与对照组相比,经异丙肾上腺素注射后的大鼠左心室LVW/BW及HW/BW明显增高.②经异丙肾上腺素注射并应用替米沙坦干预后的大鼠LVW/BW及HW/BW高于对照组,但明显低于模型组.③免疫组化结果及RT-PCR结果均显示替米沙坦干预组中GATA4蛋白含量、GATA4 Mrna表达低于对照组,但明显高于模型组.结论 ①皮下注射异丙肾上腺素(ISO)能成功制备大鼠的心肌肥厚.②转录因子GATA4对ISO所致心肌肥厚大鼠中的心肌肥厚起抑制作用,是心肌细胞的保护者.③替米沙坦可能对ISO所致的心肌肥厚大鼠通过GATA4对基因调控从而抑制心肌重构起着协同作用.     

环维黄杨星D对大鼠心肌肥厚的保护作用及机制研究

目的:探讨环维黄杨星D(Cvb-D)对甲状腺素诱导大鼠心肌肥厚的保护作用及机制.方法:除正常对照组外,各组每日均腹腔注射左旋甲状腺素(L-Thy)1 mg·kg-1,连续14 d,制备大鼠心肌肥厚模型.末次给药24 h后处死大鼠,计算大鼠心脏质量指数(全心质量/体质量,HW/BW)和左心室质量指数(左心室质量/体质量,LVW/BW),观察心肌组织病理形态学改变,并测定心肌组织中一氧化氮(NO)、一氧化氮合成酶(NOS)、超氧化物歧化酶(SOD)、丙二醛(MDA)的含量,评价Cvb-D对大鼠心肌肥厚的影响及可能机制.结果:与对照组比较,L-Thy模型组大鼠心脏质量指数明显升高,病理切片可见心肌肥厚改变,心肌NO、NOS和SOD含量显著降低,MDA显著增加.与模型组相比,Cvb-D中、高剂量组(12,24 mg·kg-1)均能明显降低小鼠HW/BW和LVW/BW,病理切片可见损害较模型组减轻,心肌NO、NOS、SOD含量显著升高(P<0.05),MDA含量显著下降(P<0.01).结论:环维黄杨星D对L-Thy诱导的大鼠心肌肥厚具有一定的保护作用,其作用机制可能与其抗心肌氧化损伤有关.     

卡维地洛对高血压大鼠左心室重构的影响

目的 探讨卡维地洛对高血压大鼠左心室重构的保护机制.方法 将30只健康雄性SD大鼠随机分为空白对照组(n=10)及模型组(n=20),模型组以经典的二肾一夹方法建立高血压模型,成功后随机分为模型对照组及卡维地洛治疗组,每组10只.卡维地洛治疗组予卡维地洛(50 mg/kg)灌胃给药,空白对照组及模型对照组给予相同体积的生理盐水灌胃,1/d.8周后麻醉处死动物,称取心脏重量(HW)和左心室重量(LvW),计算HW/体重(BW)为心脏指数(CI),LVW/BW为左心室指数(LVI);应用HE染色、Masson三色染色和VanGieson染色法检测心肌细胞横径(CTD)、心肌纤维沉积百分比(CFDP)、心肌胶原体积比例(CVF)和心肌血管周围胶原与管腔面积比例(PVCA);用Western blot方法检测心肌结缔组织生长因子(CTGF)及Ⅰ、Ⅲ型胶原的表达.结果 与空白对照组比较,模型组血压、LvW、CIh和LVI明显升高(P＜0.05);与模型对照组比较,卡维地洛治疗组血压、LvW、CIh和LVI明显降低(P＜0.05).与空白对照组比较,模型对照组CTD、CFDP、CVF和PVCA明显升高(P＜0.05);与模型对照组比较,卡维地洛治疗组CTD、CFDP、CVF和PVCA明显降低(P＜0.05).与空白对照组比较,模型对照组CTGF、Ⅰ型及Ⅲ型胶原蛋白表达明显增多(P＜0.05);与模型对照组比较,卡维地洛治疗组的CTGF及Ⅰ、Ⅲ型胶原的表达明显减少(P＜0.05).结论 卡维地洛通过降低心肌间质CTGF和Ⅰ型、Ⅲ型胶原蛋白的沉积而抑制高血压引起的大鼠左心室重构.     

卡维地洛对高血压大鼠左心室重构的影响

目的 探讨卡维地洛对高血压大鼠左心室重构的保护机制.方法 将30只健康雄性SD大鼠随机分为空白对照组(n=10)及模型组(n=20),模型组以经典的二肾一夹方法建立高血压模型,成功后随机分为模型对照组及卡维地洛治疗组,每组10只.卡维地洛治疗组予卡维地洛(50 mg/kg)灌胃给药,空白对照组及模型对照组给予相同体积的生理盐水灌胃,1/d.8周后麻醉处死动物,称取心脏重量(HW)和左心室重量(LvW),计算HW/体重(BW)为心脏指数(CI),LVW/BW为左心室指数(LVI);应用HE染色、Masson三色染色和VanGieson染色法检测心肌细胞横径(CTD)、心肌纤维沉积百分比(CFDP)、心肌胶原体积比例(CVF)和心肌血管周围胶原与管腔面积比例(PVCA);用Western blot方法检测心肌结缔组织生长因子(CTGF)及Ⅰ、Ⅲ型胶原的表达.结果 与空白对照组比较,模型组血压、LvW、CIh和LVI明显升高(P＜0.05);与模型对照组比较,卡维地洛治疗组血压、LvW、CIh和LVI明显降低(P＜0.05).与空白对照组比较,模型对照组CTD、CFDP、CVF和PVCA明显升高(P＜0.05);与模型对照组比较,卡维地洛治疗组CTD、CFDP、CVF和PVCA明显降低(P＜0.05).与空白对照组比较,模型对照组CTGF、Ⅰ型及Ⅲ型胶原蛋白表达明显增多(P＜0.05);与模型对照组比较,卡维地洛治疗组的CTGF及Ⅰ、Ⅲ型胶原的表达明显减少(P＜0.05).结论 卡维地洛通过降低心肌间质CTGF和Ⅰ型、Ⅲ型胶原蛋白的沉积而抑制高血压引起的大鼠左心室重构.     

淫羊藿苷对异丙肾上腺素致大鼠急性心肌缺血的影响

目的探讨淫羊藿苷对异丙肾上腺素(ISO)致大鼠急性心肌缺血的作用。方法淫羊藿苷(12、6、3mg·kg-1)静脉注射给药5d,采用ISO(30mg·kg-1,每日1次,连续2d)sc诱导大鼠急性心肌缺血模型,观察大鼠心电图的变化,测定血清中乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)、丙二醛(MDA)和一氧化氮(NO)的含量,测定心脏指数(HW/BW和LVW/BW)和心肌梗死面积(IS/V%)。结果和模型组相比,淫羊藿苷(12、6、3mg·kg-1)均能有效对抗心电图T波和J点的变化,降低血清中LDH、SOD、MDA和NO的含量(P<0.01或P<0.05),降低心脏指数(P<0.01或P<0.05)和心肌梗死面积(P<0.01)。结论淫羊藿苷对ISO所致大鼠急性心肌缺血有一定的保护作用。     

α-硫辛酸抗心肌肥厚作用

目的研究α 硫辛酸（α LA）抗异丙肾上腺素致大鼠心肌肥厚的作用。方法24只大鼠随机分为模型组、对照组、硫辛酸组,每组8只。模型组和硫辛酸组建立心肌肥厚模型,硫辛酸组同时给予α 硫辛酸盐液腹腔注射,100 mg&#8226;kg－1&#8226;d－1,qd。测定大鼠全心质量指数（HW/BW）、左心室质量指数（LVW /BW,即LVI）,放射免疫分析法和逆转录聚合酶链反应（RT PCR）检测大鼠心肌组织血管紧张肽Ⅱ（AngⅡ）、AT1R含量及AT1mRNA表达水平,硫代巴比妥酸法测定丙二醛（MDA）含量,黄嘌呤氧化酶法测定超氧化物歧化酶（SOD）活性。结果与对照组比较,模型组大鼠HW/BW、LVI明显升高,心肌AngⅡ、AT1R含量及AT1mRNA表达水平增高,心肌和血清MDA含量增高,SOD含量降低（P＜0.01）;与模型组比较,硫辛酸组各心脏指标均明显减低,心肌组织MDA、AngⅡ、AT1R含量及AT1mRNA表达水平降低,SOD含量增高（P＜0.01）。结论氧化应激参与心肌肥厚的发生发展,α LA通过抗氧化作用抑制心肌肥厚的发生发展。     

小鼠不同心肌肥厚模型标志性基因表达变化的比较

目的探索小鼠不同心肌肥厚模型间肥厚性标志基因心房利尿钠肽(ANP)、脑利尿钠肽(BNP)、β-肌球蛋白重链(β-MHC)基因表达的差异。方法取C57BL/6小鼠,采用肾上腹主动脉缩窄(AAC)、动静脉瘘(AVF)和异丙肾上腺素(ISO)分别建立小鼠心肌肥厚模型。造模结束,称取各小鼠体重(BW)、心脏重量(HW)和左室重量(LVW),计算心脏重量指数(HW/BW)和左心室指数(LVW/BW);HE染色观察心肌病理组织形态学变化;免疫组织化学染色观察心肌组织ANP、BNP和β-MHC蛋白表达;采用Real-time PCR检测心肌ANP、BNP和β-MHC mRNA表达。结果与对照组比较,3种模型的HW/BW和LVW/BW升高,光镜下观察各模型小鼠心肌呈现不同程度的肥厚性变化,ANP、BNP和β-MHC在蛋白和mRNA表达水平均不同程度增加;与AAC组比较,AVF和ISO组心肌组织ANP、BNP和β-MHC在蛋白和mRNA表达水平均降低。结论 3种心肌肥厚模型造模成功,AAC模型心肌组织在同时表达肥厚性标志基因ANP、BNP和β-MHC时优于AVF和ISO。     

辛伐他汀对慢性心力衰竭兔心肌PPARγ mRNA、蛋白表达及核因子κB表达、活性的影响

目的观察辛伐他汀对兔慢性心力衰竭模型心肌肥厚、心功能的影响,探讨辛伐他汀抑制心肌肥厚、改善心功能的机制。方法24只新西兰白兔分为4组,1组为假手术组。2、3、4组给予主动脉瓣返流及腹主动脉缩窄术,其中2组为心衰对照组;3组:早干预组,术后给予辛伐他汀5mg·kg-1·d-1灌胃连续8wk;4组:晚干预组,术后4wk给予辛伐他汀5mg·kg-1·d-1灌胃连续4wk。观察开始及结束时左室舒张末压(LVEDP)。实验结束时,观察左心室重量(LVW)、心脏重量(HW),计算左心室重量指数(LVW/BW)、心脏重量指数(HW/BW)。RT-PCR分析各组PPARγmRNA表达。Western blot分析心肌细胞核PPARγ和p65蛋白表达,电泳迁移率变动试验分析p65活性。结果早、晚干预组LVW、HW、HW/BW均低于心衰对照组(P<0.05,P<0.01),早干预组(LVW/BW)低于心衰对照组(P<0.01)。早、晚干预组左室舒张末压低于心力衰竭组(P<0.01)。心衰对照组心肌组织PPARγ蛋白和mRNA表达低于假手术组(P<0.01),p65蛋白表达及活性高于假手术组(P<0.01)。辛伐他汀干预后,早干预组、晚干预组PPARγ蛋白和mRNA表达增加(P<0.01),p65蛋白表达及活性降低(P<0.01)。结论辛伐他汀抑制心肌肥厚、改善心功能,其机制与增加PPARγ表达、降低p65蛋白表达及活性有关。     

血脂康对自发性高血压大鼠心肌重构的作用及其可能机制

目的观察血脂康(Xuezhikang,XZK)对自发性高血压大鼠(spontaneously hypertensive rats,SHR)左室肥厚和心肌间质纤维化的影响,探究其可能机制。方法 30只SHR,♂,随机分为3组,血脂康(300 mg.kg 1.d 1)治疗组(XZK组,n=10),辛伐他汀(5 mg.kg 1.d 1)治疗组(SIM组,n=10),SHR对照组(SHR组,n=10),同时入组同龄Wistar-Kyoto大鼠为正常对照组(WKY组,n=10),均予等容量0.9%生理盐水灌胃。12周后,分离心脏,左室称重并计算左室重量指数(LVWI),心肌组织固定包埋后Masson染色并计算心肌胶原容积分数(CVF)及心肌血管周围胶原面积(PVCA),测定血清Ⅰ型前胶原羧基末端前肽(PⅠCP)浓度、心肌组织超氧歧化酶(SOD)活性及丙二醛(MDA)浓度。结果与SHR组相比,XZK组和SIM组可以显著降低LVWI(P<0.05)、CVF(P<0.01)、PVCA(P<0.01)及血清PⅠCP浓度(P<0.01),但SOD活力及MDA浓度差异无统计学意义。结论血脂康能够显著减轻SHR的左室肥厚,降低心肌间质纤维化程度,并与血压和胆固醇水平的变化无关,血脂康表现出与辛伐他汀相同的抗心肌重构作用,作用机制可能与心肌SOD活性和MDA浓度相关不大。     

小檗碱对肾性高血压心肌肥厚模型大鼠左心室重塑的影响

The purpose of this study is to evaluate the effects and the underline mechanisms of berberine on the cardiac function and left ventricular remodeling in rats with renovascular hypertension. The renovascular hypertensive model was established by the two-kidney, two-clip （2K2C） method in Sprague-Dawley （SD） rats. Two weeks after surgery, all the operated SD rats were randomly assigned into four groups： （1） renovascular hypertensive model group; （2） berberine 5 mg · kg^-1 group; （3） berberine 10 mg · kg^-1 group ; （4） captopril 45 mg · kg^-1 group ; and the sham operated rats were used as control. Four weeks after the drugs were administered, the cardiac function was assessed. The ratios of heart weight to body weight （HW/BW）, left ventricular weight to body weight （LVW/BW） and right ventricular weight to body weight （RVW/BW） were compared between groups. Coronal sections of the left ventricular tissue （LV） were prepared for paraffin sections, picrosirius red and HE staining was performed. The left ventricular wall thickness （LVWT）, interventricular septal thickness （IVST）, the parameters of myocardial fibrosis indicated by interstitial collagen volume fraction （ICVF） and perivascular collagen area （ PVCA ） were assessed. Nitric oxide （ NO ）, adenosine cyclophosphate （ cAMP ） and guanosine cyclophosphate （cGMP） concentrations of left ventricular tissue were measured. Berberine 5 mg· kg^-1 and 10 mg · kg^-1 increased the left ventricular± dp/dt max. and HR. Berberine 10 mg · kg^-1 decreased HW/BW and LVW/BW. The image analysis showed that both 5 and 10 mg · kg^-1 of berberine decreased LVWT, ICVF and PVCA, while increased the NO and cAMP contents in left ventricular tissue. Berberine could improve cardiac contractility of 2K2C model rats, and inhibit left ventricular remodeling especially myocardial fibrosis in renovascular hypertension rats. And such effects may partially associate with the increased NO and cAMP content in left ventricular tissue.     

Lipotab, a polyherbal formulation, attenuates isoprenaline-induced left ventricular remodeling and heart failure in rats

The present study was designed to evaluate the effect of Lipotab, a polyherbal formulation on isoprenaline (ISO)-induced left ventricular (LV) remodeling and heart failure (HF). HF in Wistar albino rats was produced by two consecutive injections of ISO (150 mg/kg, s.c.) at an interval of 24 h. After 15 days of 2nd ISO injection, HF was indicated by rise in left ventricular end-diastolic pressure (LVEDP), lowering of maximal rate of rise of LV pressure divided by LV systolic pressure (LVdP/dtmax/P; cardiac contractility) and maximal rate of fall of LV pressure (LVdP/dtmin), fall in cardiac output (CO), cardiac hypertrophy (heart to body weight ratio) and histopathological changes in heart. HF rats showed a significant increase in serum malondialdehyde (MDA), reduction in serum reduced glutathione (GSH) content and a significant rise in tumor necrosis factor-α (TNF-α) level. Prior treatment with Lipotab (275 mg/kg/day, p.o.) was significantly able to preserve LV functions. Post treatment with Lipotab (275 mg/kg/day, p.o.) also improved LV functions but did not prevent the fall in LVdP/ dtmin, CO and cardiac hypertrophy. Lipotab significantly prevented fall in GSH levels, rise in level of MDA and TNF-α in serum of HF rats. Histopathological examination confirmed hemodynamic and biochemical findings. Results of the present study indicate that Lipotab prevents ISO-induced LV remodeling and consequent HF in rats through its antioxidant and anti-inflammatory activity.     

卡托普利和低剂量阿司匹林相互作用对心衰大鼠左室重建的影响

目的：观察联用卡托普利和低剂量阿司匹林对心衰大鼠左室重建的影响。方法：采用冠状动脉结扎致急性心肌梗死和心梗后慢性心力衰竭大鼠模型，按照正交设计试验方案服药5周，测定左室重量／体重比（LVW／BW），心肌组织胶原VG染色，图像分析系统测量心肌胶原容积分数（ICVF），血管周围胶原面积（PVCA）。结果：与正常组，假手术组相比，急性心梗模型组，慢性心衰模型组LVW／BW，ICVF，PVCA均显著升高（P＜0．01），卡托普利显著逆转左室肥厚（P＜0．05），减轻间质纤维化（P＜0．05），阿司匹林对其无影响（P＞0．05），但二者联用存在显著的相互作用（P＜0．01，P＜0．05），且表现为拮抗效应。卡托普利对血管周围纤维化无显著性作用（P＞0．05），但与阿司匹林存在显著的相互作用（P＜0．05），其拮抗低剂量阿司匹林对血管周围纤维化的显著不利作用（P＜0．05），结论：低剂量阿司匹林减弱卡托普利逆转左室肥厚及减轻间质纤维化的作用，其本身对血管周围纤维化的发生也存在不利影响。     

Effects of Chinese herb medicine Radix Scrophulariae on ventricular remodeling

The effects and mechanism of the extract of Radix Scrophulariae (ERS), a traditional Chinese herb, on experimental ventricular remodeling in rats was studied. Rats were separated randomly into 5 groups: sham, model, captopril (40 mg x kg(-1)) and ERS (8, 16 g x kg(-1)). The experimental ventricular remodeling was induced with ligating the left anterior descending branch of the coronary artery of the rats. The sham group was conducted the same procedure without ligation. After 4 weeks treatment with intragastric administration of the corresponding drugs, the left ventricular weight index (LVWI) and heart weight index (HWI) were determined. The concentrations of angiotensin II (Ang II) and hydroxyproline (Hyp) in myocardium were detected. Myocardium tissue was stained with HE and picric acid/Sirius red for cardiocyte cross-section area and collagen content measurements. Real-time RT-PCR was used to detect the gene expressions of AT1R, TNF-alpha and TGF-beta1 mRNA. ERS could significantly reduce the LVWI, HWI, decrease the content of Ang II, Hyp, diminish cardiocyte cross-section area and ameliorate collagen deposition. In addition, ERS could down regulate the gene expressions of AT1R, TNF-alpha and TGF-beta1 mRNA in myocardium. ERS has beneficial effect against ventricular remodeling. The mechanism may be related to decreasing the level of Ang II and cardiac fibrosis, modulating some gene expressions associated with cardiac hypertrophy.     

大豆异黄酮对心肌梗死大鼠心室重构的影响(英文)

目的：观察大豆异黄酮对心肌梗死大鼠心室重构的影响。方法：雄性SD大鼠,结扎冠状动脉左前降支,造成心肌梗死。实验分为6组：假手术组,心肌梗死模型组,卡托普利组,大豆异黄酮低、中、高剂量组。在结扎冠状动脉后3h开始,分别灌胃给予0.5%羧甲基纤维素钠(CMC-Na),0.5%CMC-Na,卡托普利50mg·kg~(-1)和大豆异黄酮30,90,270 mg·kg~(-1),qd,共35 d。给药容积均为10 mL·kg~(-1)。最后一次给药后24 h,测定心率(HR)、左室舒张末期压(LVEDP)、左室收缩压峰值(Peak)、左室压最大上升速率/下降速率(±dp/dt_(max))和心肌最大缩短速率(V_(max)),测定全心室质量和体重比(TVW/BW),用天狼猩红染色,在图像分析系统下测量梗死范围(IS)、左心室内径(LVD)、室间隔厚度(ST),心肌间质胶原容积系数(ICVF)和血管周围胶原容积系数(PCVF)。结果：卡托普利、大豆异黄酮90 mg·kg~(-1)和270 mg·kg~(-1)组大鼠的梗死范围分别是(31±s4)%,(32±3)%和(31±5)%,均显著小于心肌梗死模型组大鼠[(38.9±2.9)%,P＜0.01]。心肌梗死组大鼠的TVW/BW,LVD,ICVF和PCVF均比假手术组明显增加(P＜0.01),增加的TVW/BW,LVD,ICVF和PCVF用卡托普利和大豆异黄酮90 mg·kg~(-1),270 mg·kg~(-1)治疗后明显减少[P＜0.01,P＜0.05(SI 90 mg·kg~(-1)组的LVD)]。心肌梗死大鼠的ST显著减小(P＜0.01),而给予卡托普利和大豆异黄酮可增加ST(P＜0.01)。结扎LAD后,大鼠的Peak,±dp/dt_(max)和V_(max)明显降低(P＜0.01),而LVEDP明显升高(P＜0.01),降低的Peak,±dp/dt_(max)和V_(max)在给予卡托普利、大豆异黄酮90 mg·kg~(-1)和270 mg·kg~(-1)后明显升高(P＜0.01)；而升高的LVEDP仅在给予卡托普利治疗后降低。结论：大豆异黄酮能够改善心肌梗死大鼠的心功能和心室重构。     

Protective effects of hydroxysafflor yellow A on acute and chronic congestive cardiac failure mediated by reducing ET-1, NOS and oxidative stress in rats

The present study was conducted to investigate whether hydroxysafflor yellow A (HSYA) has a protective effect on acute and chronic heart failure (AHF/CHF) induced by ligation of the left anterior descending coronary artery for 3 h and 8 weeks, respectively. The rats were divided into the following groups: sham operation, coronary artery ligation (CAL), CAL+HSYA (100 mg kg(-1) by gavage) and CAL+diltiazem (20 mg kg(-1) by gavage). In the AHF model, heart function, as determined by haemodynamic studies and echocardiography, was improved significantly by pretreatment with HSYA or diltiazem. Significant reductions in elevated serum creatine phosphokinase, lactate dehydrogenase, malondialdehyde (MDA), glutamic oxalacetic transaminase, glutamic pyruvic transaminase and blood viscosity were observed, and the activity of serum superoxide dismutase (SOD) was enhanced (all P<0.01). In the CHF model, HSYA and diltiazem restored abnormal heart function, and completely suppressed the elevated plasma atrial natriuretic polypeptide (ANP) and endothelin-1 (ET-1), serum and left-ventricular tissue inducible nitric oxide (NO) synthase (iNOS), NO and MDA, and improved the decrease in SOD. HSYA and diltiazem improved cardiac performance in AHF and reduced cardiac remodelling in CHF by reducing tissue weight indices: left ventricular weight/body weight (BW), right ventricular weight/BW, kidney weight/BW and lung weight/BW, and attenuating increases in infarct size, inner diameter of the left ventricle and collagen volume fraction in non-infarcted areas, and the decrease in mean wall thickness of infarcted myocardium. These results suggest that HSYA exerted beneficial actions in cardiac performance in models of both AHF and CHF, mainly by suppressing ET-1, iNOS and oxidative stress in infarcted tissue.     

5-HT_(2B)受体阻断剂对心肌肥厚大鼠心肌5-HT含量及5-HT_(2B)受体表达的影响

目的观察5-HT2B受体阻断剂对去甲肾上腺素(norepinephrine,NE)诱导的心肌肥厚大鼠心肌中5-羟色胺(5-hydrotriptamine,5-HT)含量及5-HT2B受体表达的影响。方法雄性SD大鼠24只,随机分为3组,8只/组,分别为对照组、肥厚组、实验组。采用腹腔注射NE(1.5 mg/kg,2次/d,28 d)的方法建立心肌肥厚模型,自第15天起实验组腹腔注射SB204741(5-HT2B受体阻断剂;2 mg/kg,2次/d),连续注射14 d。对照组腹腔注射相同体积的生理盐水(2次/d,28 d)。检测各组左心室重量与体重之比(LVW/BW)、心肌组织中5-HT的含量及5-HT2B受体的表达情况。结果在NE诱导心肌肥厚过程中,应用SB204741干预可显著减轻心肌肥厚的程度,降低心肌组织中5-HT的含量,并抑制5-HT2B受体表达的上调。结论应用5-HT2B受体阻断剂可减轻NE诱导心肌肥厚的程度,降低心肌组织中5-HT的含量,并抑制5-HT2B受体表达的上调。