Background: While intravascular imaging, particularly optical coherence tomography (OCT), improves percutaneous coronary intervention (PCI) outcomes, its interpretation is operator-dependent. General-purpose artificial intelligence (AI) shows promise but lacks domain-specific reliability. We evaluated the performance of CA-GPT, a novel large model deployed on an AI-OCT system, against that of the general-purpose ChatGPT-5 and junior physicians for OCT-guided PCI planning and assessment. Methods: In this single-center analysis of 96 patients who underwent OCT-guided PCI, the procedural decisions generated by the CA-GPT, ChatGPT-5, and junior physicians were compared with an expert-derived procedural record. Agreement was assessed using ten pre-specified metrics across pre-PCI and post-PCI phases. Results: For pre-PCI planning, CA-GPT demonstrated significantly higher median agreement scores (5[IQR 3.75-5]) compared to both ChatGPT-5 (3[2-4], P<0.001) and junior physicians (4[3-4], P<0.001). CA-GPT significantly outperformed ChatGPT-5 across all individual pre-PCI metrics and showed superior performance to junior physicians in stent diameter (90.3 Conclusion: The CA-GPT-based AI-OCT system achieved superior decision-making agreement versus a general-purpose large language model and junior physicians across both PCI planning and assessment phases. This approach provides a standardized and reliable method for intravascular imaging interpretation, demonstrating significant potential to augment operator expertise and optimize OCT-guided PCI.

Background Excessive myocardial oxidative stress could lead to the congestive heart failure. NADPH oxidase is involved in the pathological process of left ventricular (LV) remodeling and dysfunction. β3-Adrenergic receptor (AR) could regulate cardiac dysfunction proved by recent researches. The molecular mechanism of β3-AR regulating oxidative stress, especially NADPH oxidase, remains to be determined. Methods Cardiac hypertrophy was constructed by the transverse aortic constriction (TAC) model. ROS and NADPH oxidase subunits expression were assessed after β3-AR agonist (BRL) or inhibitor (SR) administration in cardiac hypertrophy. Moreover, the cardiac function, fibrosis, heart size, oxidative stress, and cardiomyocytes apoptosis were also detected. Results β3-AR activation significantly alleviated cardiac hypertrophy and remodeling in pressure-overloaded mice. β3-AR stimulation also improved heart function and reduced cardiomyocytes apoptosis, oxidative stress, and fibrosis. Meanwhile, β3-AR stimulation inhibited superoxide anion production and decreased NADPH oxidase activity. Furthermore, BRL treatment increased the neuronal NOS (nNOS) expression in cardiac hypertrophy. Conclusion β3-AR stimulation alleviated cardiac dysfunction and reduced cardiomyocytes apoptosis, oxidative stress, and fibrosis by inhibiting NADPH oxidases. In addition, the protective effect of β3-AR is largely attributed to nNOS activation in cardiac hypertrophy.

目的 研究对比ST段抬高型心肌梗死( STEMI)患者不同时期经皮冠状动脉介入术( PCI)并置入药物洗脱支架(DES)的近远期预后.方法 回顾性分析2016年2月至2018年12月接受PCI并置入DES治疗的200例STEMI患者的病历资料.按照接受PCI时间的不同分为早期组(发病3 ～14 d实施PCI)110 例,晚期组(发病15 ～35 d实施PCI)90例.比较2组一般资料、临床诊治情况、住院期间主要不良心血管事件( MACE)发生情况,随访2年MACE发生情况.结果 早期组前壁心肌梗死人数占比低于晚期组,差异有统计学意义(P＜0. 05).早期组与晚期组患者各项诊治情况相关指标比较,差异均无统计学意义(P＞0. 05).早期组住院期间MACE总发生率2. 73% ,低于晚期组的11. 11% ,差异有统计学意义(P＜0. 05).早期组与晚期组随访2年内MACE发生情况比较,差异无统计学意义(P＞0. 05).结论 早期PCI并置入DES的STEMI患者近期预后优于晚期PCI患者,但2组患者远期预后并无明显差异.

目的 研究美托洛尔与益心舒胶囊联用对急诊冠心病心力衰竭患者心功能及用药安全性的影响.方法 选择2017年2月至2019年10月收治的急诊冠心病心力衰竭患者90例,采用随机数字表法分为联用组和单纯组,每组45例.单纯组给予美托洛尔治疗,联用组给予美托洛尔及益心舒胶囊治疗.比较2组临床疗效,治疗前后心功能变化情况,不良反应发生情况,治疗前后血清Treg以及白介素-10(IL-10)水平变化情况.结果 联用组治疗总有效率为97.78％高于单纯组的86.87％(P<0.05).联用组LVEF水平高于单纯组,而LVESD、LVEDD水平均低于单纯组(P<0.05).联用组总不良反应发生率为4.44％低于单纯组的17.78％(P<0.05).联用组血清Treg水平高于单纯组,而IL-10水平低于单纯组(P<0.05).结论 美托洛尔与益心舒胶囊联用在改善急诊冠心病心力衰竭患者心功能方面效果显著,且用药安全性较佳,有利于改善患者血清Treg以及IL-10水平,值得推广应用.

目的 探讨褪黑素在高糖诱导的原代心肌细胞损伤中的作用,并明确SIRT1在其中的作用及其机制.方法 将原代心肌细胞分为对照组(Con组)、褪黑素对照组(Con+Mel组)、高糖组(HG组)、高糖+褪黑素组(HG+Mel组)和SIRT1抑制剂理组(HG+Mel+EX527组).采用Cell Counting Kit-8(CCK-8)试剂盒检测细胞活性,丙二醛(MDA)和超氧化物歧化酶(SOD)试剂盒检测细胞氧化应激水平,TUNEL染色检测细胞凋亡,免疫印迹检测SIRT1、Beclin1、Atg5、cleaved Caspase-3、Bax和Bcl-2蛋白表达水平.结果 与Con组相比,HG组原代心肌细胞活力减低,氧化应激水平升高,细胞凋亡水平增加,SIRT1表达下调(P<0.05).给予褪黑素干预后,与Con组相比,Con+Mel组SIRT1表达量增加(P<0.05),而两组间细胞活力、氧化应激水平和细胞凋亡水平无显著差异(P>0.05).与HG组相比,HG+Mel组原代心肌细胞SIRT1表达量提高(P<0.05),细胞活力增加(P<0.05),氧化应激水平和细胞凋亡水平下降(P<0.05).免疫印迹结果显示,与Con组相比,HG组原代心肌细胞自噬相关蛋白Beclin1和Atg5表达减低(P<0.05),Con+Mel组Beclin1和Atg5表达明显上升(P<0.05);与HG组相比,HG+Mel组Beclin1和Atg5表达上升(P<0.05).此外,给予SIRT1特异性抑制剂EX527干预后,相比于HG+Mel组,HG+Mel+EX527组细胞凋亡比率增加(P<0.05),凋亡蛋白cleaved Caspase-3和Bax上调(P<0.05),抗凋亡蛋白Bcl-2下调(P<0.05),细胞自噬蛋白Beclin1和Atg5表达减低(P<0.05).结论 褪黑素可能通过上调SIRT1信号增强细胞自噬,改善高糖诱导的原代心肌细胞损伤.

Objective Puerarin was reported to protect against myocardial ischemia/reperfusion (IR) injury. The current study aims to investigate the protective effects of puerarin against myocardial IR injury and the underlying mechanisms. Methods The hearts were subjected to the ligation of the left anterior descending coronary artery and reperfusion. Before reperfusion, pretreatment with puerarin (100 mg/kg), with or without the AMPK inhibitor Compound c (0.25 mg/kg). Myocardial infarct size, the serum creatine kinase-MB (CK-MB) activity, cardiac function, apoptotic cell death, and the endoplasmic reticulum stress, as well as activation of the AMPK/NRF2 pathway were observed. Results Treatment with puerarin significantly decreased the myocardial infarct size, the serum CK-MB activity and notably alleviated IR-induced cardiac dysfunction. Moreover, puerarin reduced myocardial IR-induced apoptotic cell death. In addition, puerarin inhibited myocardial IR-induced endoplasmic reticulum stress and activated the AMPK/NRF2 pathway. More importantly, the AMPK inhibitor Compound c prevented these puerarin-induced cardioprotective effects and activation of the AMPK/NRF2 pathway, as well as apoptosis and the endoplasmic reticulum stress activation. Conclusion Our results show that puerarin alleviates myocardial IR injury by inhibiting apoptosis and endoplasmic reticulum stress via the AMPK/NRF2 pathway.

LIM‐domain proteins have been shown to be associated with heart development and diseases. Systematic studies of LIM family members at the genome‐wide level, which are crucial to further understand their functions in cardiac hypertrophy, are currently lacking. Here, 70 LIM genes were identified and characterised in mice. The expression patterns of LIM genes differ greatly during cardiac development and in the case of hypertrophy. Both Crip2 and Xirp2 are differentially expressed in cardiac hypertrophy and during heart failure. In addition, the hypertrophic state of cardiomyocytes is controlled by the relative expression levels of Crip2 and Xirp2. This study provides a foundation for further understanding of the special roles of LIM proteins in mammalian cardiac development and hypertrophy.

目的 探讨葛根素(puerarin,Pue)改善大鼠心脏缺血再灌注(ischemia reperfusion,IR)损伤和减轻线粒体氧化应激的作用.方法 采用SD大鼠离体心脏缺血再灌注模型,30只SD大鼠随机分为3组:正常对照组(control)、缺血再灌注模型组(IR)和葛根素处理缺血再灌注组(Pue+IR).TTC染色、LDH含量检测和HE染色评价心肌损伤程度.左室压力反映心脏功能.TUNEL染色法检测细胞凋亡率.ELISA检测线粒体丙二醛(MDA)和过氧化氢(H2 O2)含量、超氧化物歧化酶(SOD)活性和ATP含量.结果 与control组相比,IR组心肌梗死面积、冠脉流出液中LDH含量和细胞凋亡率明显增加(均P<0.01),而心脏功能显著降低(P<0.01),HE染色显示心肌纤维断裂明显,同时,线粒体MDA和H2 O2含量显著增加,SOD活性和ATP含量明显降低(均P<0.01).与IR组比较,Pue+IR组心肌梗死面积、冠脉流出液中LDH含量以及细胞凋亡率显著降低(P<0.01),心脏功能被改善(P<0.01),心肌纤维断裂减轻,线粒体MDA和H2O2含量降低(P<0.01),SOD活性和ATP含量增加(P<0.01).结论 Pue可以改善心肌缺血再灌注损伤,其作用机制可能与减轻线粒体氧化应激、减少细胞凋亡、提高ATP含量增强心脏功能有关.

目的 探讨葛根素(Pue)对大鼠心肌缺血再灌注损伤的保护作用及机制.方法 将32只成年雄性SD大鼠分为4组:正常对照组(Control组)、缺血再灌注模型组(IR组)、葛根素处理缺血再灌注组(Pue+IR组)和葛根素联合Sirt1抑制剂EX527处理缺血再灌注组(Pue+EX527+IR组),每组8只.采用大鼠离体心脏灌流方法模拟缺血再灌注损伤.氯化三苯基四氮唑染色观察心肌梗死面积;酶联免疫吸附法检测冠脉流出液中乳酸脱氢酶(LDH)水平;记录左室收缩压(LVSP)、左室舒张压(LVDP),评价心脏功能;蛋白免疫印迹法检测凋亡蛋白细胞色素c(cytochrome c)、凋亡诱导蛋白(Bax)和抗凋亡蛋白(Bcl2)的表达,以及沉默信息调节因子1(Sirt1)与其底物叉形头转录因子1(FOXO1)乙酰化水平.结果 与Control组比较,IR组梗死面积和LDH水平显著增加,差异有统计学意义(P<0.05);与IR组比较,Pue+IR组梗死面积和LDH水平显著减小,差异有统计学意义(P<0.05);与Pue+IR组比较,Pue+EX527+IR组梗死面积和LDH水平显著增加,差异有统计学意义(P<0.05).与Control组比较,IR组LVSP显著降低,LVDP显著升高,差异有统计学意义(P<0.05);与IR组比较,Pue+IR组LVSP显著升高,LVDP显著降低,差异有统计学意义(P<0.05);与Pue+IR组比较,Pue+EX527+IR组LVSP显著降低,LVDP显著升高,差异有统计学意义(P<0.05).与Control组比较,IR组cytochrome c和Bax表达显著增加,Bcl2表达显著降低,差异有统计学意义(P<0.05);与IR组比较,Pue+IR组cytochrome c和Bax表达显著降低,Bcl2表达显著增加,差异有统计学意义(P<0.05);与Pue+IR组比较,Pue+EX527+IR组cytochrome c和Bax表达显著增加,Bcl2表达显著降低,差异有统计学意义(P<0.05).与Control组比较,IR组Sirt1表达显著降低,FOXO1乙酰化表达增加,差异有统计学意义(P<0.05);与IR组比较,Pue+IR组Sirt1表达增加,FOXO1乙酰化表达降低,差异有统计学意义(P<0.05);与Pue+IR组比较,Pue+EX527+IR组Sirt1表达显著降低,FOXO1乙酰化表达增加,差异有统计学意义(P<0.05).结论 Pue通过上调Sirt1表达,降低FOXO1乙酰化水平,减少细胞凋亡,改善心脏功能,从而减轻心肌缺血再灌注损伤.

目的 探讨葛根素(Pue)在小鼠压力负荷诱导的心肌肥厚中的作用及机制.方法 采用小鼠主动脉弓缩窄术(TAC)制备心肌肥厚模型.将48只C57/bl小鼠随机分为假手术组(Sham组)、TAC组、Pue干预TAC组(Pue+TAC组)和Pue联合EX527干预TAC组(Pue+EX527+TAC组),每组12只.Pue+TAC组术后给予65 mg/kg Pue饮用,Pue+EX527+TAC组给予腹腔注射EX527,持续4周,模型组有2只死亡.小动物超声检测左心室射血分数(LVEF)和左心室短轴缩短率(LVFS),RT-PCR检测钠尿肽(ANP)、脑钠肽(BNP)和β-肌球蛋白重链(β-MHC)的mRNA水平,ELISA检测血清中肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)的含量,测量4组心脏质量与体质量比值(HW/BW),HE染色和Masson染色分别观察4组心肌细胞横截面积和纤维化程度,Western blot检测CollagenⅠ、α-SMA、沉默信息转录调节因子1(Sirt1)和Ac-FOXO1蛋白的表达.结果 与Sham组比较,术后4周,TAC组LVEF和LVFS值显著降低,ANP、BNP和β-MHC的mRNA水平及血清TNF-α和IL-1β含量增加,心肌细胞横截面积明显增大,纤维化加重,CollagenⅠ和α-SMA蛋白表达增加,Sirt1蛋白水平显著降低,Ac-FOXO1水平增加(P<0.01);与TAC组比较,用Pue处理后,可显著提高心脏LVEF和LVFS,降低ANP、BNP和β-MHC的mRNA水平以及血清中TNF-α和IL-1β含量,减小心肌细胞横截面积和纤维化程度,增高Sirt1蛋白水平,降低Ac-FOXO1水平(P<0.01).结论 Pue可通过抑制心脏炎症反应和纤维化,减轻压力负荷诱导的病理性心肌肥厚.

Aims: The purpose of this study was to investigate the protective effects of puerarin and elucidate the underlying mechanisms of puerarin in myocardial ischemia/reperfusion (MI/R) injury. Main methods: C57BL/6 mice were exposed to puerarin (100 mg/kg) with or without the SIRT1 inhibitor nicotinamide (500 mg/kg) and then subjected to MI/R operation. Myocardial infarct size, serum creatine kinaseMB (CK-MB) activity, apoptotic cell death, and cardiac structure and function were examined to evaluate MI/R injury. RT-PCR and western blotting were used to determine the inflammatory response and inflammasome activation, as well as activation of SIRT1/NF-kappa B pathway. Results: Puerarin significantly reduced myocardial infarct size, serum CK-MB activity, and apoptotic cell death, and improved cardiac structural damage and dysfunction. Moreover, puerarin notably decreased the mRNA and protein levels of TNF-alpha, IL-6, and IL-113, indicating that puerarin attenuated MI/R-induced inflammation. Furthermore, puerarin markedly decreased the protein levels of Ac-NF-kappa B, NLRP3, cleaved caspase-1, cleaved IL 113, and cleaved IL-18 and increased the protein level of SIRT1. More importantly, the SIRT1 inhibitor nicotinamide prevented these puerarin-induced cardioprotective effects and regulation of the SIRT1/NF-kappa B pathway, as well as the NLRP3 inflammasome activation. Conclusion: Puerarin protected against MI/R injury by inhibiting inflammatory responses probably via the SIRT1/NF-kappa B pathway, and inhibition of the NLRP3 inflammasome was also involved in puerarin-induced cardioprotective effects. These results suggest that puerarin may be a novel candidate for the treatment of ischemic heart disease.

CLU4A is identified as a proto-oncogene in various human cancers. CLU4A was reported to be up-regulated in myocardial ischemia/reperfusion injury, but the precise role of CLU4A played in myocardial ischemia/reperfusion injury remains unknown; and the underlying mechanism of CLU4A in myocardial ischemia/reperfusion injury needs to be investigated. CLU4A expression was measured after myocardial ischemia/reperfusion in mice and in H9C2 cells with hypoxia/reoxygenation treatment by q-PCR and western blotting. The cardioprotective effect of CLU4A inhibition was detected by monitoring the cell viability, cell apoptosis, and LDH activity in vitro and in vivo, and examining the infarct size and cardiac function in vivo. The molecular mechanism was further determined by examining the effects of PD98059, a specific inhibitor of the ERK signaling pathways in H9C2 cells with hypoxia/reoxygenation treatment. CLU4A expression was up-regulated after myocardial ischemia/reperfusion in mice and in H9C2 cells with hypoxia/reoxygenation treatment. Inhibition of CLU4A improved the cell viability, restrained the cell apoptosis, and suppressed LDH activity in vitro. Consistently, knockdown of CLU4A reduced the myocardial infarct size and improved cardiac function in vivo. si-CLU4A treatment increased phosphorylated ERK (p-ERK) in vitro, but the protection role of si-CLU4A was abolished by the ERK inhibitor, PD98059. In conclusion, CLU4A expression was up-regulated in myocardial ischemia/reperfusion. Inhibition of CLU4A exhibited a cardioprotective role by an ERK-dependent pathway.

Background/Aims: Myocardial apoptosis plays an important role in doxorubicin (Dox) cardiotoxicity. MicroRNA-29 (miR-29) is suggested to function as an anti-fibrotic factor with potential therapeutic effects on cardiac fibrosis. However, it has not been shown whether there is an association between miR-29b and myocardial apoptosis. Methods: Male Wistar rats were transfected with miR-29b agomir by local delivery to the myocardium prior to Dox treatment. Rat cardiomyocytes were pretreated with miR-29b mimics or inhibitor followed by Dox incubation in vitro. Cardiac function and underlying mechanisms were evaluated by echocardiography, immunofluorescence, flow cytometry, real-time PCR, and western blotting. Results: Our results revealed that miR-29b is the only member of the miR-29 family that was significantly downregulated in myocardium from Dox-treated rats. Delivery of miR-29b agomir to myocardium resulted in a marked improvement of cardiac function. Terminal deoxynucleotidyl transferase dUTP nick end labeling staining showed that rescue of miR-29b expression inhibited Dox-induced myocardial apoptosis, concomitantly with increased Bcl-2 expression and decreased Bax expression and caspase-3 activity. In vitro, miR-29b overexpression mitigated, whereas inhibition of miR-29b promoted, Dox-induced cardiomyocyte apoptosis. Mechanistically, miR-29b negatively regulated Bax expression by directly targeting the 3′ untranslated region of Bax. In Dox-treated cardiomyocytes, upregulation of miR-29b resulted in a significant decrease in Bax expression, with an increase in Bcl-2 expression, accompanied by inhibition of mitochondrial membrane depolarization, cytochrome c release, and caspase activation. However, inhibition of miR-29b produced the opposite effects by further augmenting the effects of Dox. Conclusions: These data demonstrate that miR-29b prevents Dox-induced myocardial apoptosis through inhibition of the mitochondria-dependent pathway by directly targeting Bax, suggesting that miR-29b is a potential novel therapeutic target for the treatment of Dox cardiotoxicity.

Objective To investigate the expression of endoplasmic reticulum stress( ERS)-related GRP78 and caspase-12 in myocar-dial tissues of diabetic rats, and explore the effect of ERS on cardiac structure and function. Methods Fifteen diabetic rat models were induced by streptozotocin( STZ) and then randomly divided into 0 week group, 8 weeks group, and 16 weeks group. Blood pres-sure, heart rate and myocardial function were measured by carotid artery intubation indicator. Heart weight to body weight ratio ( HWI) , left ventricular weight to whole heart weight( LVWI) were calculated, and collagenous fiber was observed by Masson staining. The expression levels of GRP78, caspase-12 and cleaved caspase-3 in rat myocardial tissues were measured. Results Compared with 0 week group, left ventricular end-diastolic pressure(LVEDP) and-dp/dtmax were increased in 8 weeks group(P<0. 05) and 16 weeks group(P<0. 01). Compared with 0 week group, HWI and LVWI were increased in 16 weeks group(P<0. 05). Collagenous fi-ber was slight, whereas it was increased in 8 weeks group. Compared with 0 week group, the expression of GRP78 significantly up-reg-ulated in 8 weeks group(P<0. 01), but down-regulated in 16 weeks group(P<0. 05). The expression of caspase-12 and cleaved caspase-3 were markedly increased in 8 weeks and 16 weeks group(P <0. 05). Conclusion Hyperglycemia could exert a direct effect on heart in rats. In the early stage of hyperglycemia, the expression of GRP78 protein is up-regulated, and the expression of caspase-12 and cleaved caspase-3 is also significantly up-regulated as the stress is enlarged. The ERS of myocardial tissues could be one of the reasons of the changes of cardiac structure and function in diabetic rats.

目的 观察马来酸依那普利对高血压大鼠心肌细胞内质网应激相关因子GRP78和CHOP表达的影响,并探讨其与左室肥厚的关系. 方法 将30只大鼠均行腹主动脉缩窄术,术后2周采用大鼠尾动脉测压系统测大鼠动脉收缩压(SBP),择取SBP＞ 140 mmHg大鼠24只,随机分为对照组和药物干预组.对照组给予生理盐水灌胃,药物干预组给予马来酸依那普利粉剂10 mg/(kg ·d)灌胃.根据喂养时间的不同,将各组再分成4周亚组和8周亚组,每亚组6只.无创大鼠尾动脉测压仪检测大鼠SBP,称取体质量、全心质量及左心室质量计算大鼠心肌肥厚指数HWI及LVWI,免疫组化及Western blot检测大鼠心肌细胞中GRP78及CHOP表达水平. 结果 ①药物干预组4周、8周亚组大鼠SBP显著低于相应对照组(P＜0.01).②药物干预组4周、8周亚组大鼠左室肥厚指数HWI及LVWI明显低于相应对照组(P＜0.05).③药物干预组4周及8周亚组GRP78及CHOP表达均明显低于相应对照组亚组(均P＜0.05). 结论 马来酸依那普利可显著降低高血压大鼠血压水平,且可以抑制高血压所致的心肌细胞内质网应激(endoplasmic reticulum stress,ERS),降低应激相关因子GRP78及CHOP表达水平,使心肌细胞受损减轻,有效缓解或逆转高血压大鼠左室肥厚.

目的 比较氨氯地平+复方盐酸阿米洛利(氨+阿)与氨氯地平+复方盐酸阿米洛利联合应用辛伐他汀(氨+阿+辛)治疗高血压伴有左室肥厚(LVH)患者的血压及左室肥厚的效果. 方法 将确诊的59例LVH高血压患者随机分为氨+阿组(41例)和氨+阿+辛组(18例).治疗18月后,观察两组患者心脏形态、功能及血压水平的变化. 结果 氨+阿组及氨+阿+辛组患者经过治疗后,收缩压(SBP)、舒张压(DBP)、室间隔厚度(IVST)、左室后壁厚度(LVPW)、左室质量(LVM)、左室质量指数(MI)与治疗前比较,均有显著降低(P ＜0.01);E/A比值及EF值与治疗前比较均有显著增高(P＜0.05);两组治疗后收缩压、舒张压差异无统计学意义(P＞0.05),但氨+阿组与氨+阿+辛组两组治疗后的IVST、LVPWT、LVM、LVMI比较差异均有统计学意义(P＜0.05),氨+阿+辛组作用更明显. 结论 氨+阿组具有逆转高血压左室肥厚的作用,而加用辛伐他汀后有更好的逆转LVH的作用,提示辛伐他汀具有增强氨氯地平+复方盐酸阿米洛利逆转高血压左室肥厚的作用.

Objective To compare the therapeutic effect of amlodipine +compound amiloride hydrochloride and am-lodipine +compound amiloride +Tongxinluo capsule for treating of hypertension associated with left ventricular hypertrophy . Methods Eighty-two patients with LVH were divided into conventional group ( 48 cases) , and Tongxinluo group ( 34 ca-ses), they were given routine amlodipine +compound amiloride;Tongxinluo capsule group based on the conventional thera-py, also added Tongxinluo capsule(1.14g once ,three times a day).After 6 months of treatment, cardiac structure and heart function and changes in blood pressure levels in the two groups were observed .Resutl s After treatment , conventional group and Tongxinluo group patients’ systolic blood pressure (SBP), diastolic blood pressure (DBP), inter-ventricular septum thickness ( IVST ) , left ventricular wall thickness ( LVPWT ) , left ventricular weight ( LVM ) , left ventricular mass index (LVMI) were significantly decreased compared with before treatment ( P <0.01);E /A ratio and LVEF values?were sig-nificantly increased than before treatment ( P <0.05);after treatment, between the two groups, systolic blood pressure, di-astolic blood pressure’s difference were not statistically significant ( P >0.05), but IVST [(9.60 ±2.48) min vs.(8.80 ± 1.23) min],LVPWT [(9.39 ±1.20) min vs.(8.07 ±1.40) min],LVM [(275.11 ±14.77) g vs.(271.02 ±16.25) g],LVMI[( 1509.9 ±7 .35) g /m2 vs.(147.02 ±8.88) g/m2 ],E/A (0.75 ±0.18 vs.0.78 ±0.24), LVEF [(65.28 ± 3.15)%vs .(66.32 ±3.12)%]’ s differences in the 2 groups were statistically significant ( P <0.05 ), the Tongxinluo group improved more obviously .Conclusion Tongxinl uo capsule combined with amlodipine +compound amiloride hydro-chloride can increase left ventricular ejection fraction , improving heart function , so as to delay ando/r reverse left ventricular hypertrophy .

Objective:To study the effect of captopril to the expression of glucose-regulated protein of 78 kd(GRP78) and CAAT/enhancer binding protein homologous protein(CHOP) the correlation factors of endoplasmic reticulum in the vascular smooth muscle cells of early hypertension rats.Methods:Eighteen Sprague-Dawley(SD) rats were divided randomly into three groups:the control group(n=6)、the model group(n=6) and the captopril group(n=6).The rats in the model group and the captopril group received abdominal transverse aortic constriction(TAC).Four weeks later,blood pressure was measured,expression of GRP78 and CHOP in the vascular smooth muscle cells of each group was detected by immunohistochemistry,apoptosis was detected by TdT-mediated dUTP nick end labeling(TUNEL).Results:①Mean arterial blood pressure(MAP) of the model group increased significantly(P<0.05),compared with that of the control group.MAP of the captopril group was higher than the control group,and lower than the model group,and the difference was significant(P<0.05).② The expression of GRP78 and CHOP of the model group increased significantly(P<0.01),compared with that of the control group.The expression of GRP78 and CHOP of the captopril group was higher than the control group,and lower than the model group,and the difference was significant(P<0.01).③Apoptosis rate of the vascular smooth muscle cells in the model group decreased significantly(P<0.01),compared with that of the control group.That of the captopril group was lower than the control group,and higher than the model group,and the difference was significant(P<0.01).Conclusions:Captopril reduced the the expression of GRP78 and CHOP in the vascular smooth muscle cells of hypertensive rats,increased apoptosis.That might relate to captopril's weakening the endoplasmic reticulum response which induced by hypertension,and maitaining of vascular smooth muscle cell proliferation /apoptosis balance.

目的:研究成年大鼠心脏成纤维细胞（cardiac fibroblasts,CFs）在血管紧张素Ⅱ刺激下单核细胞趋化蛋白-1（monocyte chemotaxia protein-1,MCP-1）表达情况,探讨高血压合并心脏损害的可能机制。 方法:成年大鼠CFs体外培养,在不同浓度血管紧张素Ⅱ不同作用时间刺激下,应用免疫蛋白印迹法和ELISA法分别测定细胞中和培养上清中MCP-1的含量。 结果:①在细胞内和培养上清中均有MCP-1表达。②随着血管紧张素Ⅱ、刺激浓度的增加和刺激时间的延长,细胞内和上清中MCP-1的表达量也逐渐增加。在1×10 -11 ,1×10 -9 ,1×10 -8 ,1×10 -7 ,1×10 -6 mol/L的血管紧张素Ⅱ作用下,上清中MCP-1的含量分别为（1.60±0.21）,（3.18±0.15）,（4.70±0.22）,（9.18±0.52）,（8.75±0.42）μg/L,与对照组（1.13±0.09）μg/L比较,除1×10 -11 mol/L组外,差异均有显著性意义（t=26.21～39.67,P＜均0.05）。③在1×10 -7 mol/L的血管紧张素Ⅱ作用下,3,6,12和24h MCP-1的表达量分别为（2.13±0.31）,（3.25±0.20）,（5.28±0.50）和（9.18±0.52）μg/L,与空白对照组（1.13±0.09）μg/L比较差异均有显著性意义（t=6.93～34.11,P均＜0.05）。 结论:成年大鼠CFs的MCP-1的表达对血管紧张素Ⅱ的刺激有浓度和时间依赖性。CFs的MCP-1的表达可能参与高血压时?