比索洛尔对异丙肾上腺素引起的大鼠心肌纤维化的干预研究

目的探讨异丙肾上腺素引起的心肌纤维化和比索洛尔对其抑制作用。方法52只Wistar(WS)大鼠随机分为3组:(1)异丙肾上腺素组20只,腹部皮下注射异丙肾上腺1mg/Kg/d;(2)比索洛尔组20只,预先用比索洛尔2mg/Kg/d灌胃,3天后加用异丙肾上腺素1mg/Kg/d皮下注射;(3)对照组12只,腹部皮下注射生理盐水1ml/d。3组均连续腹部皮下注射10天。第15天杀死全部大鼠,分别计算出每只大鼠的心室/体重指数;心室胶原蛋白浓度。结果与对照组相比,异丙肾上腺素组心室/体重指数为6.28±1.10mg/g,明显增加(P<0.01);心室组织胶原蛋白浓度为8.717±0.795ng/mg,明显升高(P<0.05)。与异丙肾上腺素组相比,比索洛尔组心室/体重指数为5.53±0.87mg/g,心室组织胶原蛋白浓度为7.897±0.107ng/mg,均明显下降(P<0.05)。结论大剂量异丙肾上腺素可引起大鼠心肌纤维化,比索洛尔可以有效抑制这一过程。     

地尔硫卓对异丙肾上腺素诱导的大鼠心肌纤维化的保护作用研究

目的:研究地尔硫卓对异丙肾上腺素(ISO)诱导的大鼠心肌纤维化的保护作用,并探讨其可能的作用机制。方法:30只,SD大鼠,随机分为正常对照组、模型组和地尔硫卓组,每组各10只。除正常对照组外,各组均通过皮下注射2 mg·kg~(-1)·d~(-1)异丙肾上腺素的方法诱导大鼠心肌纤维化模型,连续注射10 d。地尔硫卓组灌胃给予10 mg·kg~(-1)·d~(-1)地尔硫卓,连续灌胃4周,正常组和模型组给予等体积0.9%氯化钠溶液。采用心电图和血流动力学指标评估大鼠心功能的变化。心肌组织行苏木精-伊红(HE)染色和Masson染色以观察其形态和胶原沉积情况的变化。免疫组织化学法观察I型和III型胶原蛋白的表达情况。试剂盒测定心肌组织中超氧化物歧化酶,谷胱甘肽过氧化物酶和丙二醛含量的变化。蛋白免疫印迹法检测大鼠心肌组织中核因子κB(NF-κB)、转录生长因子β1(TGF-β1)以及结缔组织生长因子(CTGF)等蛋白的表达变化。结果:地尔硫卓能显著抑制ISO引起的心电图的改变,包括S-T段、T波和QRS波振幅的变化,同时明显抑制心率和左心室舒张末压,显著提高左心室收缩压和左心室内压上升及下降最大变化速率(P<0.05)。HE染色和Masson结果显示,地尔硫卓能改善ISO引起的心肌结构紊乱和胶原过度沉积,显著降低胶原容积分数(P<0.05)。免疫组化结果显示,地尔硫卓能显著降低ISO诱导的Collagen I和Collagen III表达的上调(P<0.05)。地尔硫卓能显著增加SOD、GSH-Px的水平,降低MDA的水平(P<0.05)。蛋白免疫印迹的结果显示,地尔硫卓能恢复因ISO而上调的NF-κB、TGF-β1、CTGF等蛋白的表达水平(P<0.05)。结论:地尔硫卓通过抗氧化应激和抑制NF-κB信号通路来改善ISO诱导的大鼠心肌纤维化。     

大鼠实验性糖尿病对异丙肾上腺素所致心肌坏死的影响

异丙肾上腺素(ISP)是一种强有力的心脏毒性物质。给动物注射一定剂量可引起明显心肌坏死。糖尿病时可发生心肌病改变,为探讨糖尿病心肌对致损伤因素的反应特点,本实验研究了糖尿病状态对ISP所致心肌坏死的影响。由于甲状腺功能状态可影响儿茶酚胺的反应性,故同时也探讨了糖尿病大鼠血清甲状腺激素水平对这种心肌坏死的影响。     

虾青素对肝纤维化大鼠的保护作用及机制研究*

目的 研究虾青素抑制肝纤维化作用是否与影响TGF-β1/Smad/ERK通路有关。方法 将50只大鼠随机分为正常组、模型组、秋水仙碱组（0.1 mg·kg^-1）、虾青素Ⅰ组（2 mg·kg^-1）和虾青素Ⅱ组（4 mg·kg^-1）,每组10只。采用皮下注射CCl₄法制备肝纤维化大鼠模型。在造模成功后,给予正常组和模型组动物生理盐水、而在药物干预组则分别给予秋水仙碱和虾青素灌胃,连续给药6 w。分别采用免疫组化法和Western blot法检测肝组织Ⅰ型胶原、Smad2、转化生长因子-β1（TGF-β1）和p-ERK蛋白表达,采用RT-PCR法检测肝组织CollagenⅠ、Smad2、TGF-β1 和p-ERK mRNA水平。结果 正常组、虾青素Ⅰ组和虾青素Ⅱ组肝组织Ⅰ型胶原蛋白分别为（0.4±0.1）、（1.4±0.3）和（1.2±0.3）,均显著低于模型组【（1.7±0.4）,P<0.05】,Smad2分别为（0.5±0.1）、（1.3±0.4）和（0.8±0.4）,显著低于模型组【（1.6±0.3）,P<0.05】,TGF-β1蛋白分别为（0.5±0.1）、（1.4±0.4）和（1.2±0.3）,显著低于模型组【（1.7±0.4）,P<0.05】,p-ERK蛋白分别为（0.4±0.1）、（1.3±0.4）和（0.9±0.3）,显著低于模型组【（1.6±0.5）,P<0.05】;正常组、虾青素Ⅰ组和虾青素Ⅱ肝组织Ⅰ型胶原 mRNA水平分别为（1.0±0.1）、（2.0±0.4）和（1.8±0.5）,均显著低于模型组【（2.4±0.4）,P<0.05】,Smad2 mRNA水平分别为（1.0±0.1）、（2.0±0.5）和（1.8±0.4）,显著低于模型组【（2.5±0.6）,P<0.05】,TGF-β1 mRNA水平分别为（1.0±0.1）、（2.1±0.4）和（1.6±0.3）,均显著低于模型组【（2.5±0.5）,P<0.05】,p-ERK mRNA水平分别为（1.1±0.1）、（2.1±0.4）和（1.8±0.3）,均明显低于模型组【（2.6±0.5）,P<0.05】。结论 虾青素可抑制肝纤维化进展,其机制可能与调控TGF-β1/Smad/ERK通路表达有关。     

Rho激酶抑制剂对异丙肾上腺素诱导大鼠心肌肥厚的影响

目的 研究Rho激酶抑制剂对异丙肾上腺素(isoproterenol,Iso)诱导大鼠心肌肥厚的影响及其机制.方法 40只雄性Wistar大鼠随机分为5组:空白对照组、Iso模型组、法舒地尔(fasudil,Fas)低剂量组、高剂量组及卡托普利(captopril,Cap)组,每组8只.除空白对照组外,各组皮下注射Iso建立大鼠心肌肥厚模型.给药结束后分别测定各组大鼠体重(BW)、心脏重量(HW),计算心脏重量指数(HW/BW);测定左室收缩压(LVSP)、左室舒张末压(LVEDP)、左心室压力上升及下降最大速率(±dp/dtmax)等指标;取心肌组织作病理学检测;RT-PCR测定心肌组织RhoA、Rho激酶mRNA表达.结果 Iso模型组大鼠HW/BW增大;LVEDP增加,而LVSP、±dp/dtmax下降;心肌细胞直径增大、胶原纤维增生;左心室组织RhoA、Rho激酶mRNA表达上调.使用Fas和Cap干预,上述指标均出现不同程度的改善.结论 肾上腺素β受体兴奋所诱导的心肌肥厚伴有Rho激酶信号通路的激活,Rho激酶抑制剂可改善Iso所致心肌肥厚动物模型的心功能和病理学变化.     

白细胞介素8对异丙肾上腺素所致大鼠心肌细胞坏死的影响

近年发现白细胞介素8(IL-8)具有抑制中性粒细胞与血管内皮细胞粘附的作用,本工作用重组IL-8治疗异丙肾上腺素(ISO)所致大鼠心肌坏死。与单纯ISO组比较,重组IL-8治疗明显减轻ISO引起的心肌坏死,使心肌丙二醛含量减少、降低心肌髓过氧化物酶活性,使血浆内皮素放免活性明显降低。实验结果提示,IL-8可以通过抑制白细胞粘附和浸润,抑制内皮素释放,防治缺血心肌坏死。     

苯肾上腺素对腹主动脉缩窄诱导心肌间质纤维化的影响

目的观察苯肾上腺素对腹主动脉缩窄导致心肌纤维化的作用及可能机制。方法雄性昆明(KM)小鼠42只,体重24~30 g,其中28只采用腹主动脉缩窄术(AAC)建立压力超负荷诱导心肌反应性纤维化的动物模型,8周后将模型小鼠随机分为4组,AAC组、苯肾上腺素(PE)组(AAC+PE组)、哌唑嗪(Praz)组(AAC+Praz组)和普萘洛尔(Prop)组(AAC+Prop组),每组7只,其中AAC+PE组给予PE 0.65 mg/(kg·d)腹腔注射,AAC+Praz组予Praz 5 mg/(kg·d)灌胃,AAC+Prop组给予Prop 10 mg/(kg·d)灌胃,AAC组给等量生理盐水灌胃,连续4周;另设空白对照组及假手术组各7只,其中假手术组只分离腹主动脉而不结扎,二组均给予等量生理盐水持续灌胃。给药4周后处死动物,取左心室游离壁组织,HE染色观察组织细胞形态学变化,胶原容积分数(CVF)、羟脯氨酸(Hyp)含量测定及Ⅰ、Ⅲ型胶原蛋白免疫组化染色观察心肌胶原,Western blot方法测定α-平滑肌肌动蛋白(α-SMA)、转化生长因子β1(TGF-β1)、p-Smad2和p-Smad3蛋白表达。结果 ACC术后12周小鼠心脏均发生明显纤维化,与空白对照组相比,CVF、Hyp含量显著升高(P0.01),Ⅰ、Ⅲ型胶原表达增多(P0.01),α-SMA、TGF-β1、p-Smad2及p-Smad3蛋白表达增加(P0.01),假手术组CVF、Hyp含量以及α-SMA、TGF-β1、p-Smad2、p-Smad3蛋白表达和Ⅰ、Ⅲ型胶原含量变化不明显。与AAC组比较,AAC+PE组和AAC+Prop组左心室CVF、Hyp含量及Ⅰ、Ⅲ型胶原表达均明显减少(P0.01),α-SMA、TGF-β1、p-Smad2和p-Smad3的蛋白表达水平降低(P0.05),而AAC+Praz组上述各指标无明显变化(P0.05);AAC+PE组与AAC+Prop组相比,上述指标均无统计学差异(P0.05)。结论苯肾上腺素可能通过TGF-β1/Smads信号通路改善压力超负荷介导的小鼠心肌间质纤维化,其作用与普萘洛尔相似。     

Calpain 1在黄芪甲苷抑制异丙肾上腺素诱导的大鼠心肌凋亡中的作用

目的探讨Calpain 1在黄芪甲苷抑制异丙肾上腺素诱导的大鼠心肌凋亡中的作用。方法 SD大鼠48只,随机分为6组,每组8只:正常对照组、异丙肾上腺素组、异丙肾上腺素+普萘洛尔40 mg/(kg·d)组、异丙肾上腺素+黄芪甲苷20 mg/(kg·d)组、异丙肾上腺素+黄芪甲苷40 mg/(kg·d)组、异丙肾上腺素+黄芪甲苷80mg/(kg·d)组。给药组连续灌胃2周,并于灌胃1天后腹腔注射异丙肾上腺素10 mg/(kg·d)2周。2周后,采用TUNEL检测心肌凋亡,电镜观察心肌线粒体病变,Western blot检测心肌线粒体Calpain 1、凋亡诱导因子(AIF)的蛋白表达和心肌组织多聚ADP核糖聚合酶1(PARP1)的蛋白表达。结果与正常对照组相比,异丙肾上腺素组凋亡率明显增加;心肌线粒体肿胀、膜融合消失、嵴断裂;心肌线粒体中Calpain 1表达增加,AIF表达减少;心肌组织中PARP1表达增加。与异丙肾上腺素组相比,异丙肾上腺素+黄芪甲苷40 mg/(kg·d)组、异丙肾上腺素+80mg/(kg·d)组表现为心肌凋亡率减少;心肌线粒体结构相对完整;心肌线粒体Calpain 1表达减少,AIF表达增加;心肌组织PARP1表达减少,且呈一定的剂量依赖性。结论黄芪甲苷对异丙肾上腺素诱导的心肌凋亡有一定的保护作用,其机制可能与抑制线粒体Calpain 1表达,从而减少线粒体AIF释放至胞浆并转位至核有关。     

曲美他嗪对异丙肾上腺素所致大鼠心肌肥厚的影响

目的探讨曲美他嗪（TMZ）对异丙肾上腺素（ISO）致大鼠心肌肥厚的影响及可能的作用机制。方法30只Sprague-Ddwley（SD）大鼠,随机分为3组。正常对照组、ISO组、TMZ组,每组10只。通过大剂量注射ISO制成心肌肥厚模型,以TMZ干预,观察心肌组织病理学变化和心肌细胞超微结构改变,计算心脏质量/体质量（HW/BW）,测定心肌三磷酸腺苷（ATP）、丙二醛（MDA）、超氧化物歧化酶（SOD）和血清乳酸脱氢酶（LDH）、肌酸激酶（CK）含量。结果TMZ组与ISO组比较,HW/BW、LDH、CK、SOD和ATP有显著差异（P<0.05）,而与正常对照组比较无显著差异。TMZ组心肌组织病理损伤程度及细胞超微结构改变程度,较ISO组明显减轻,而接近正常对照组。结论TMZ可拮抗ISO所致的大鼠心肌肥厚,其机制可能与改善心肌能量代谢、提高组织对缺氧的耐受力、消除氧自由基等有关。     

异丙肾上腺素诱导的急性心肌损伤大鼠一氧化氮系统的变化

目的建立异丙肾上腺素(ISO)诱导的急性心肌损伤大鼠模型,观察急性心肌损伤大鼠NO系统的变化。方法将SD大鼠随机分为两组,对照组和模型组。模型组连续3d皮下注射ISO(150mg·kg-1·d-1)。通过血清肌酸激酶(CK)和乳酸脱氢酶(LDH)的活性和Ⅱ导联心电图来判定心肌损伤与否。用荧光定量RT-PCR来分析三种一氧化氮(eNOS、nNOS、iNOS)以及肿瘤坏死因子-α(TNF-α)的mRNA转录水平。结果模型组血清CK、LDH的活性显著增加(P<0.001),ST段明显上抬。与正常组相比,模型组eNOS和nNOS的转录水平显著降低(P<0.001);而iNOS和TNF-α的转录水平显著升高(P<0.001)。结论ISO诱导的心肌损伤大鼠NO系统发生的主要变化为三种NOS转录水平的改变。     

非诺贝特对大鼠心肌损伤保护作用的实验观察

目的探讨非诺贝特对异丙基肾上腺素所致大鼠急性心肌缺血性损伤的保护作用。方法应用异丙基肾上腺素复制大鼠急性心肌缺血性损伤的动物模型,Wister大鼠随机分为3组,正常对照组、模型组(Iso)、非诺贝特保护组(FF),观察非诺贝特对大鼠心肌的形态学,血清肌酸激酶和乳酸脱氢酶(CK,LDH)以及一氧化氮(NO)的影响。结果非诺贝特能对抗异丙基肾上腺素所致的大鼠急性心肌缺血性损伤,可使其病理损伤性改变减轻,抑制CK和LDH的释放,增加NO的产生。结论非诺贝特对异丙基肾上腺素所致大鼠急性心肌缺血性损伤具有保护作用。     

Protective effects of melatonin against myocardial injury induced by isoproterenol in rats

This study was performed to determine whether melatonin could have a protective effect against myocardial injury (MI) induced by isoproterenol (ISO) in rats. Twenty-four rats were divided into three treatment groups: (1) control (n = 8): saline solution. (2) ISO (n = 8): ISO only. (3) melatonin + ISO (n = 8). Melatonin (10 mg/kg/day, i.p.) was administered 30 min before the initiation of ISO (150 mg/kg/day, s.c.). Drugs and saline were given at 14:00 hr for two consecutive days. At the end of the second day, blood samples were taken from the abdominal aorta shortly after the rats were anesthetized for the purpose of measuring cardiac troponins T (cTnT) and I (cTnI); hearts were removed, preserved and examined microscopically. Additionally, based on the histological changes in myocardial tissue, the rats were divided into three groups: no change, mild changes and moderate and/or marked changes. The mean cTnT and cTnI values were significantly increased in ISO group compared with control group [(1.29 +/- 0.22 ng/mL versus 0.46 +/- 0.07 ng/mL, P < 0.0001) and (0.56 +/- 0.11 ng/mL versus 0.21 +/- 0.01 ng/mL, P < 0.001)], respectively, and were significantly reduced in the ISO + melatonin group (0.65 +/- 0.06 ng/mL for cTnT and 0.25 +/- 0.01 ng/mL for cTnI) compared with the ISO only group (P < 0.01), respectively. cTnT and cTnI values were significantly increased in rats with moderate and/or marked cardiac changes compared with hearts where there were mild changes and no change (P < 0.05). ISO + melatonin group showed less histological changes than the ISO group (P < 0.01). In conclusion, this study revealed a protective effect of melatonin against ISO-induced MI in rats, and its potential clinical application in the treatment of MI.     

左旋卡尼汀对异丙肾上腺素致心肌损害的影响

目的:观察左旋卡尼汀对异丙肾上腺素致心肌损害的保护作用并探讨其机制。方法:采用大鼠皮下注射异丙肾上腺素造成心肌损害模型。心肌切片,HE染色,光镜下观察心肌损害程度;分离心肌线粒体,测定膜脂流动性（LFU）。结果:注射左旋卡尼汀可减轻心肌损害程度;改善线粒体的损伤,改善LFU。结论:左旋卡尼汀能减轻异丙肾对心肌的损害,对线粒体膜脂流动性损伤具有明显的保护作用。     

Effects of phospholipase inhibitors and calcium antagonists on the changes in myocardial phospholipids induced by isoproterenol

Summary To investigate the change in myocardial phospholipids after the administration of isoproterenol and its prevention by pretreatment with phospholipase inhibitors and calcium antagonists, we determined the phospholipid species in the heart of female Wistar rats. Isoproterenol (40 mg/kg) was administered 24 h before excising the heart, and chlorpromazine, mepacrine (phospholipase inhibitors), nifedipine, verapamil (calcium antagonists) and propranolol (-adrenoceptor blocker) were injected intraperitoneally 30 min prior to isoproterenol administration. The phospholipid species were quantified using silica gel precoated thin-layer rods and the hydrogen flame ionization method. Isoproterenol induced significant increases in heart/body weight ratio, myocardial protein/heart weight ratio and lysophosphatidylcholine (LPC), and significant decreases in myocardial total phosphorus, creatine kinase (CK) activity, phosphatidylethanolamine and phosphatidylcholine (PC). The significant decrease in PC and increase in LPC indicated the degradation of myocardial phospholipids. Pretreatment with nifedipine (30 mg/kg), verapamil (50 mg/kg) or propranolol (20 mg/kg) completely prevented the occurrence of myocardial injury through the preservation of myocardial phospholipid composition, total phosphorus, CK activity and heart/body and protein/heart weight ratios. On the other hand, chlorpromazine (30 mg/kg) and mepacrine (50 mg/kg) partially prevented myocardial damage through the preservation of myocardial phospholipid composition, total phosphorus and CK activity. Results suggest that not only calcium influx but also phospholipase activation plays an important role in the development of myocardial injury induced by isoproterenol.     

Mechanism of isoproterenol induced myocardial damage

To study the harmful effects of isoproterenol on myocardium rats were injected with isoproterenol 10 or 0.1 mg.kg-1 or with isoproterenol 10 mg.kg-1 after an injection of propranolol 20 mg.kg-1. Endogenous phospholipase activity in heart homogenate and tissue adenosine triphosphate concentrations were determined 1, 7, and 15 h after isoproterenol injection. The activities of three segments (NADH-cytochrome c reductase, succinate-cytochrome c reductase, and cytochrome c oxidase) of the electron transport chain in heart mitochondria were also measured in the same manner. In the group given isoproterenol 0.1 mg.kg-1 the tissue adenosine triphosphate concentration was decreased after 1 h but returned to control value after 15 h. No significant change in phospholipase activity or in the activities of the three segments in mitochondria was observed throughout the study. In the group given isoproterenol 10 mg.kg-1 the tissue adenosine triphosphate concentration was significantly decreased after 1 h and did not return to control values after 15 h. Phospholipase activity was increased and the activities of NADH-cytochrome c reductase and cytochrome c oxidase were significantly decreased after 15 h. The activity of succinate-cytochrome c reductase was not affected. In the propranolol group, pretreatment with propranolol protected against a reduction in adenosine triphosphate after isoproterenol 10 mg.kg-1. Propranolol also prevented activation of phospholipase and maintained the activities of the three segments of mitochondria throughout the study. In an in vitro study mitochondria prepared from intact rat hearts were incubated with 0.1 unit phospholipase A2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of erdosteine on inflammation and fibrosis in rats with pulmonary fibrosis induced by bleomycin

We aimed to investigate the levels of some chemokines, inflammatory cell counts in bronchoalveolar lavage (BAL) fluid, histopathological changes in lung tissue, to determine the effect of erdosteine on acute inflammatory changes and fibrosis in a rat fibrosis model induced by bleomycine (BLM). Forty-five Wistar male rats were taken into the study. On day 0, intratracheal saline to control group (group 1, n= 15), intratracheal BLM 7.5 U/kg to BLM (group 2, n= 15) and erdosteine group (group 3, n= 15) was administered. In group 3, oral erdosteine (10 mg/kg/day) was applied two days before BLM. On day 0, 14, and 29th five rats in each groups were sacrificed, BAL fluid was performed. Malonyldialdehyde (MDA), macrophage inflammatory protein (MIP)-1alpha, MIP-2 levels in BAL fluid, hydroxyproline levels in lung tissue were measured. Histopathological examination was performed. When BLM group compared to erdosteine group, the levels of MDA, MIP-1alpha, MIP-2, and neutrophil counts, the hydroxyproline (OH-P) level of lung tissue were decreased in erdosteine group on acute inflammatory phase (day 14) (p< 0.001, p= 0.017, p= 0.009, p< 0.001, p= 0.009, respectively), and late fibrosis phase (day 29) except BAL MIP-2 (p= 0.022, p= 0.025, p= 0.01, p< 0.001, respectively). Fibrosis level was significantly lower in erdosteine group than BLM group on day 29 (p= 0.01). We conclude that erdosteine may prevent the acute lung inflammation and fibrosis by suppressing the accumulation of neutrophils, inhibition of lipid peroxydation, chemokine production, and release.     

生脉注射液对大鼠心肌纤维化作用的影响

目的:观察生脉注射液对异丙肾上腺素(Iso)引起大鼠心肌纤维化的干预作用,并探讨其抗心肌纤维化的可能机制。方法:将48只SD大鼠随机分为对照组、模型组、卡托普利组和生脉注射液组(生脉组),每组各12只,采用Iso 5mg.kg-1.d-1皮下注射制造心肌纤维化模型,给予生脉注射液100mg.kg-1.d-1灌胃。测算大鼠左室射血分数(LVEF)、左室质量指数(LVMI)和胶原容积积分(CVF),应用分光光度法检测羟脯氨酸(Hyp)、丙二醛(MDA)和超氧化物岐化酶(SOD)活性,运用反转录聚合酶链式反应半定量分析结缔组织生长因子(CTGF)mRNA水平。结果:与模型组相比,生脉组CVF、Hyp、LVMI及MDA含量降低,SOD活性增强,CTGF的过度表达被抑制(均P<0.01)。结论:生脉注射液能明显改善心室重构和心肌纤维化,这可能与其抗氧化、抑制CTGF过度表达有关。     

丹酚酸B对大鼠缺血心肌组织溶酶体功能的影响

目的探讨丹酚酸B(Sal B)对异丙肾上腺素(ISO)所致大鼠心肌缺血模型心肌溶酶体功能的影响。方法 SD大鼠随机分为空白组,模型组,丹参注射液组和Sal B 12.8、6.4、3.2 mg/kg组。除空白组外,各组大鼠尾静脉注射ISO建立急性心肌缺血模型,连续给药7 d后,PowerLab数据采集分析系统测定各组大鼠心电图变化;试剂盒测定血清中溶酶体相关膜蛋白2(Lamp-2)、组织蛋白酶D(Cat-D)的活性,心脏匀浆中一氧化氮合酶(NOS)、一氧化氮(NO)、Cat-D和溶酶体匀浆中Cat-D的活性;HE染色法检测心肌梗死面积。结果与空白对照组比较(P0.05或P0.01),模型组大鼠心电图T波水平显著升高,血清中Lamp-2、Cat-D的水平显著升高,心脏匀浆中NOS、NO、Cat-D含量升高,溶酶体匀浆中Cat-D含量降低,心肌梗死面积明显增多。Sal B 12.8、6.4 mg/kg组和丹参注射液组能够显著降低心电图T波升高值,降低血清lamp2、Cat-D和心脏匀浆中NOS、NO、Cat-D含量,升高心脏溶酶体匀浆Cat-D含量,与模型组比较(P0.05或P0.01)。结论 Sal B对心肌缺血的保护作用与溶酶体的膜稳定性及水解酶的活性功能有一定的关系。