目的 探讨高龄冠状动脉粥样硬化性心脏病(CHD)患者血清同型半胱氨酸(HCY)水平与叶酸、维生素B12、胰岛素抵抗的相关性.方法 选择哈尔滨医科大学附属第四医院老年病科 2019 年 1 月至2020 年 12 月住院高龄CHD患者 80 例,年龄 80～98 岁,平均(89±3)岁,入选者分为HCY＜15 μmol/L组(A组)、15 μmol/L≤HCY≤20 μmol/L组(B组)、HCY＞20 μmol/L组(C组).观察入选患者年龄及血脂等临床生化指标变化,分析各组患者伴发相关疾病差异.酶联免疫吸附试验(ELISA)检测血胰岛素(FINS)、叶酸、维生素B12 水平,并计算胰岛素抵抗指数(HOMA-IR)=FINS(mU/L)×空腹血糖(FBG)(mmol/L)/22.5.结果 ①入选高龄CHD患者 80 例,A组 36 例,B组 21 例,C组 23 例,各组患者年龄、性别差异无统计学意义(P＞0.05);②C组患者肌酐、尿酸高于A、B 2 组(P＜0.05),总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白-胆固醇(LDL-C)、FBG、超敏C反应蛋白(hs-CRP)等各组间差异无统计学意义(P＞0.05);③C组患者糖尿病、慢性肾衰竭、下肢动脉硬化闭塞症的发生率高于A、B 2 组(P＜0.05),各组患者伴发高血压、感染性疾病、心力衰竭、心房纤颤差异无统计学意义(P＞0.05);④C组患者FINS、HOMA-IR水平高于A、B 2 组,其中FINS C组与A、B组之间差异有统计学意义(P＜0.05),HOMA-IR C组与A组之间差异有统计学意义(P＜0.05).叶酸、维生素B12 水平C组较A、B 2 组低,且C组与A、B组之间差异均有统计学意义(P＜0.05).结论 高龄CHD患者血清HCY水平升高,胰岛素抵抗水平增高,叶酸、维生素B12 水平降低.

Hypertension is a highly heterogeneous disease,the prevalence rate,morbidity and disability rate of hypertension are increased significantly with age.The pathogenesis of elderly hypertension is complex,and its onset is influenced by environmental and genetic factors.Besides,the hyperactivity of sympathetic nervous system and renin-angiotensin-aldosterone system and insulin are also involved in its onset.In addition,as age increases,persistence of chronic low-grade inflammation of the immune system,abnormal regulation of non-coding genes and changes in the brain-gut axis can aggravate vascular endothelial dysfunction and target organ damage,which eventually lead to the occurrence and development of hypertension.This article mainly reviews the pathogenesis of elderly hypertension from the perspectives of immune mechanism,non-coding gene regulation,and brain-gut axis regulation.

心力衰竭致心肌纤维化、心脏重塑、肾素-血管紧张素-醛固酮系统(RAAS)激活诱发心房颤动,而心房电与结构重构进一步加重心力衰竭.机体炎症反应、氧化应激、神经内分泌失衡使心力衰竭与心房颤动共存,亦涉及物质代谢、非编码核糖核酸(RNA)表达与免疫调节机制.

心脏瓣膜钙化是由多种分子机制共同参与的复杂病理过程,发病率随年龄增长而上升,瓣膜间质细胞表型分化过程是瓣膜钙化的关键环节.脂质代谢异常作为瓣膜钙化的独立危险因素,在瓣膜局部形成损伤并诱导炎症反应,产生的炎症因子可以促进瓣膜间质细胞发生表型分化.非编码RNA可以从多方面调控炎症反应和成骨分化,影响瓣膜间质细胞表型分化进程,参与心脏瓣膜钙化的发生.

瘦素是由脂肪细胞分泌的一种具有广泛生物学活性的肽类激素,瘦素不仅能调节能量代谢,还可参与炎症反应,与感染性疾病的发生密切相关,在感染性疾病易感性的调控中发挥重要作用.瘦素通过促进单核细胞活化及IL-6表达来影响感染性疾病炎症反应过程;通过调节免疫细胞的发育、增殖、成熟、激活及抗凋亡过程,调控固有免疫和适应性免疫,从而协调免疫系统,参与免疫应答;通过影响机体营养状况,干扰机体免疫系统、调控炎症反应,影响感染性疾病的病程及预后;瘦素及其受体发生基因突变可导致免疫功能缺陷,从而增加对感染的易感性.探讨瘦素对感染性疾病发生发展的调控作用及其机制,对感染性疾病的预防和诊治具有重要意义.

目的 探讨高龄男性冠心病(CHD)患者血清睾酮与同型半胱氨酸(Hcy)水平的相关性.方法 选择高龄男性CHD患者120例,依据血浆Hcy水平,将入选患者分为Hcy<15μmol/L组(A组)、15μmol/L≤Hcy≤20μmol/L组(B组)、Hcy>20μmol/L组(C组),观察各组年龄、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、肌酐(Cr)、尿酸(UA)、空腹血糖(FPG)、D-二聚体、纤维蛋白原(Fbg)、总胆红素、血小板计数(PLT)等基线资料变化,分析各组伴发高血压、糖尿病、感染性疾病、心力衰竭、心房颤动、慢性肾功能不全、下肢动脉硬化闭塞症等疾病差异,酶联免疫吸附试验(ELISA)检测各组血清睾酮、超敏C反应蛋白(hs-CRP)水平变化.结果 C组UA、Cr水平显著高于A组、B组(P<0.05).C组发生慢性肾功能不全、下肢动脉硬化闭塞症概率显著高于A组、B组(P<0.05).C组Hcy水平显著高于A、B组,而睾酮水平显著低于A组、B组(P<0.05).结论 高龄男性CHD患者中血清睾酮水平与Hcy呈负相关,低水平睾酮使心血管事件发病风险增加.

伴随人口老龄化加速,高龄老年人口比重增加,动脉粥样硬化性疾病致死致残率逐年增高.动脉粥样硬化是各种动脉粥样硬化性疾病的共同病理基础,发病机制复杂,涉及慢性炎症、内皮损伤、血脂代谢紊乱等过程,目前研究发现遗传、血流动力学和免疫等因素亦参与动脉粥样硬化形成.

investigate the effect of pathways of insulin-like growth factor-1 (IGF-1) and insulin-like growth factor-1 receptor (IGF-1R) in myocardial infarction and influence of irbesartan on them through observing the changes of myocardial IGF-1 mRNA and protein and IGF-1R mRNA and protein. Methods The anterior descending branch of left coronary artery was ligatured in rats, and after 24 h the survived rats were randomly divided into medicinal group and control group (each n=9). A sham-operation group was established (n=9) and did not given ligation. The medicinal group was treated with irbesartan (50 mg·kg/d) and control group and sham-operation group were orally given normal saline (NS) in the same volume once a day. After 4 weeks all rats were sacrificed. The myocardial pathological changes were observed after HE staining, and levels of IGF-1 mRNA and protein and IGF-1R mRNA and protein were detected by using real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) and Western blotting assay. Results The results of HE staining showed aligned cardiomyocytes in sham-operation group, and swelling cardiomyocytes and infiltration of inflammatory cells in medicinal group and control group. These changes were more significantly in control group than those in medicinal group. The weight of left ventricle was lower in medicinal group than that in control group (P<0.05). The IGF-1 mRNA and protein and IGF-1R mRNA and protein were detected in all groups, and they were higher in medicinal group and control group than those in sham-operation group (all P<0.05). The levels of IGF-1 mRNA and protein and IGF-1R mRNA and protein were lower in medicinal group than those in control group (all P<0.05). Conclusion The expressions of myocardial IGF-1 mRNA and protein and IGF-1R mRNA and protein can be detected in rat myocardial tissue. The levels of IGF-1 mRNA and protein and IGF-1R mRNA and protein will increase after myocardial infarction. Irbesartan can significantly reduced the levels of myocardial IGF-1 mRNA and protein and IGF-1R mRNA and protein in myocardial tissue and relieve myocardial damage in rats with myocardial infarction after applied for 4 weeks.

心力衰竭(heart failure,HF)是心室充盈和(或)射血功能受损的一组复杂临床综合征.导致HF的疾病复杂多样,有学者观察到引起HF的各种疾病中冠心病占49.4％,高血压占54.6％,慢性肾脏病占29.7％,LVEF＜ 40％的患者占37.5％[1].HF是各种心脏病的终末阶段,尽管近年来HF的治疗取得了长足的进步,但其发病率及病死率仍较高.HF时由致命性心律失常引起的猝死是普通人群的6～9倍,占HF患者死亡的50％[2].

目的 观察厄贝沙坦对心肌梗死大鼠血清肝细胞生长因子(HGF)水平的影响.方法 通过结扎左冠状动脉前降支建立大鼠心肌梗死模型,将术后24 h存活大鼠随机分为厄贝沙坦组(n=11)、对照组(n=9),另设假手术组(n=6).厄贝沙坦组给予厄贝沙坦50mg/(kg·d),对照组及假手术组予以等体积生理盐水灌胃,1次/d,于术后24 h、1、2、4周经眶后静脉丛采血,采用ELISA法检测大鼠血清HGF水平,4周后处死大鼠,采用HE染色法观察大鼠缺血心肌病理改变.结果 HE染色可见假手术组大鼠心肌细胞排列整齐,少量炎性细胞浸润;对照组与厄贝沙坦组心肌细胞溶解断裂,心肌结构紊乱,厄贝沙坦组病变较对照组减轻.术后24 h,各组大鼠血清中均检测到HGF水平,组间差异无统计学意义(P＞0.05);假手术组1周时的HGF水平低于术后24 h(P＜0.01),2、4周时的HGF水平升高但仍低于术后24h(P＜0.01);对照组及厄贝沙坦组1周时的HGF水平均高于术后24h,4周时的HGF水平明显下降且低于1周时(P＜0.01);1、2周时对照组及厄贝沙坦组的HGF水平均高于假手术组(P＜0.01),而2、4周时厄贝沙坦组的HGF水平较对照组明显降低(P＜0.01);对照组1、2周时的HGF水平较术后24 h增高(P＜0.01),2、4周时的HGF水平高于1周时(P＜0.05,P＜0.01),而厄贝沙坦组4周时的HGF水平较术后24h、1周时降低(P＜0.05,P＜0.01).结论 厄贝沙坦应用4周,心肌梗死大鼠心肌缺血得到改善;心肌梗死大鼠血清中的HGF水平升高,1周时达到高峰,厄贝沙坦应用4周能够明显降低大鼠血清HGF水平.

The present study aimed to investigate the mechanisms underlying the cardioprotective effect of Astragaloside against myocardial injury following myocardial infarction (MI) in a rat model. Male Wistar rats were subjected to left anterior descending branch ligation. The rats that survived 24 h (n=18) were randomly and equally assigned to three groups: MI model group, and 2.5 and 10 mg/kg/day Astragaloside group. A further six rats underwent identical surgical procedures without artery ligation, serving as sham controls. Following 28 days of treatment, the left ventricle was harvested for morphological analysis, and mRNA and protein expression levels of hypoxia inducible factor-1 alpha (HIF-1 alpha), Notch1 and Jagged1 were measured. Treatment with Astragaloside attenuated pathological changes in the myocardium. Compared with untreated MI rats, rats treated with Astragaloside exhibited significantly increased mRNA expression levels of HIF-1 alpha, Notch1 and Jagged1 (all P<0.01). HIF-1 alpha demonstrated a dose-dependent effect (P<0.05). Astragaloside (10 mg/kg/day) significantly increased HIF-1 alpha (P<0.05), Notch1 (P<0.01) and Jagged1 (P<0.01) protein expression levels. Additionally, 2.5 mg/kg Astragaloside significantly increased Jagged1 protein expression levels compared with untreated MI rats. Furthermore, there was a dose-dependent effect of Astragaloside treatment (P<0.01). These findings suggested that the cardioprotective effects of Astragaloside against myocardial injury following MI may involve upregulation of HIF-alpha, Notch1 and Jagged1 signaling, implicating these molecules as therapeutic targets for the treatment of MI.

AIM:To investigate the effects of irbesartan on the expression of hepatocyte growth factor (HGF) at mRNA and protein levels in rats with myocardial infarction (MI), and to explore the mechanisms of irbesartan attenuating myocardial fibrosis.METHODS:The male Wistar rat model of MI was successfully established.The surviving rats 24 h after the operation were randomly divided into 3 groups:model group,irbesartan group and sham group, with 9 rats in each group.The rats in irbesartan group were treated with the solution of irbesartan (50 mg·kg-1·d-1) by intragastric administration, while the rats in model group and sham group received the equal volume of saline by the same way.The body weight and left ventricle mass (LVM) of the rats were measured at the 4th week after operation, and the pathological changes of the ischemic myocardium were observed with HE staining.Meanwhile, the expression of HGF at mRNA and protein levels was detected by RT-qPCR and Western blot.RESULTS:HE staining showed that the myocardial cells in sham group were in neat arrangement, while the cardiac structure in model group and irbesartan group was in disorder.The pathological changes in irbesartan group were less than that in model group.No difference in the body weight at the 4th week after operation was observed, while the LVM was significantly different among the 3 groups (P<0.01).The LVM in model group was higher than that in sham group (P<0.01), and that in irbesartan group was higher than that in sham group (P<0.05).The LVM in irbesartan group was lower than that in model group (P<0.05).The expression of HGF at mRNA and protein levels was detected in each group.The expression of HGF at mRNA and protein levels in irbesartan group was higher than that in sham group (P<0.05), and that in model group was higher than that in sham group (P<0.01).Moreover, the mRNA and protein levels of HGF in irbesartan group were lower than those in model group (P<0.05).CONCLUSION:The LVM of MI rats with the treatment of irbesartan was reduced obviously at the 4th week after operation, and the pathological changes were also improved.At the 4th week after the operation, the treatment of irbesartan inhibited the expression of HGF at mRNA and protein levels.

Myocardial fibrosis after myocardial infarction is a self-repair process of myocardium.The pathophysiogical basis of myocardial fibrosis is similar to diversified cardiovascular diseases,which is an important reason for the irreversible and sustained development of ventricular remodeling.The mechanism of myocardial fibrosis is complicated,which includes not only the occurrence and development of renin-angiotensin-aldosterone system,cytokines,gas signal molecules,but also autophagy and microRNAs.Myocardial fibrosis can lead to heart failure and sudden cardiac death,so it is of great significance to improve the prognosis of patients by discussing the molecular mechanism of myocardial fibrosis after myocardial infarction.

心脏瓣膜钙化( CVC)主要病理改变为黏液样变性及脂质聚集、钙盐沉积,以异位钙化和瓣膜纤维增厚为特点. CVC的发生随年龄增长而增加,有文献报道主动脉瓣钙化( AVC)在西方国家整体人群中发病率达2.5%,75 岁以上人群达13%,85岁以上人群高达48%〔1 ,2〕,已发现瓣膜钙化是终末期肾病患者动脉粥样硬化和动脉钙化的标志〔3〕. 有证据表明老年人晕厥、猝死的重要病因与CVC相关〔4〕,已证实瓣膜钙化对早期诊断冠心病有预测价值,因此探讨老年冠心病患者CVC相关机制尤为重要.

随着年龄增长,老人舌头上的味蕾会逐渐退化,舌头感知食物的反应减弱,消化功能下降,都会导致老人食欲不振.偶尔吃得少问题不大,但如果长期食欲不振,则可能导致身体机能下降,甚至患病.那么如何改善老人食欲不振呢?

通过对老年医学的特点的分析,论述了医患沟通在老年医学研究中的重要性,并针对其提出了加强研究生医患沟通能力培养的措施:加强人文教育与导师的导向作用,增强医学生的自我提升能力,培养共情能力,注重倾听的方式与技巧,加强循证医学实践,注重文化背景对沟通的影响.

Objective To evaluate the influence of Safflow Yellow (SY) on hs-CRP/HCY/UA and LVEDD/LVEF with eldly NSTEMI patients, explore the mechanism in myocardial protection. Methods 60 patients were chosen into the experiment, who in hospital during october 2013 to december 2014 with eldly NSTEMI, the average age is 80.57±8.13, the patients were divided into control group(n=30) and treatment group(n=30). Control group received conventional therapy (Nitrates, Beta-receptor blocker, lipid regulation, antiplatelet, anticoagulation etc), treatment group received extra SY injection (100mg,QD). All the treatment lasted for 2 weeks.The level of serum hs-CRP/HCY and UA were analyzed respectively and LVEDD/LVEF also were tested before and after the treatment. Results 1 There is no difference in the age, gender, diabetes, hypertension with the two groups ( >0.05);2 The level of hs-CRP/HCY in two groups after the treatment were lower than before, there was a significantly lower in the treatment group ( <0.05);The level of UA after the treatment was lower than before, but there was no statistical difference between the two groups ( >0.05). 3 At the end of 2nd week LVEDD was decreaser than before treatment in two groups and the trend is obvious in the treatment group( <0.05). the same as LVEF is increaser than before treatment in two groups, and more obvious in the treatment group ( <0.05). Conclusion 1 The level of hs-CRP/HCY were reduced by SY in the elderly patients with NSTEMI who received the treatment for two weeks. 2 There was an effect of SY that can decline LVEDD, improve LVEF and make the left ventricular systolic function of heart better.

心肌纤维化(myocardial fibrosis,MF)是多种心血管疾病发展到终末阶段的必然过程,也是决定心血管疾病预后的关键性因素,其不仅是心肌重构的主要表现之一,还可使心肌顺应性下降、心脏舒张及收缩功能受损.心肌纤维化是高血压、心肌梗死、心肌炎、动脉粥样硬化、糖尿病等多种疾病的共同病理变化,是心力衰竭、心律失常等发生发展的基础[1].

目的:探讨厄贝沙坦对老年非ST抬高型心肌梗死(NSTEMI)患者血清转化生长因子-β1 (TGF-βl)与结缔组织生长因子(CTGF)水平的影响.方法:选择我院2013年10月-2014年05收治的诊断明确为NSTEMI的患者38例,将因各种原因不能服用厄贝沙坦者作为对照组(n=17),余为药物组(n=21).入院后,两组患者均给予常规治疗(抗血小板、抗凝、调脂、单硝酸异山梨酯注射液等),药物组加服厄贝沙坦150mg,1次/日,应用2周.分别于治疗前、治疗后第7、14天抽取患者空腹静脉血,采用ELISA法检测患者血清TGF-β1、CTGF水平.结果:治疗第7天时,两组患者血清TGF-β1、CTGF水平均高于治疗前(P＜0.05,p＜0.01),但两组间比较差异无统计学意义(P＞0.05);治疗14天时,两组患者血清TGF-β1、CTGF水平均较第7天降低(P＜0.01),且药物组血清TGF-β1、CTGF水平低于治疗前(P＜0.05,p＜0.01),对照组血清TGF-β1水平高于治疗前(P＜0.05),药物组TGF-β1水平低于对照组(P＜0.05),差异均有统计学意义,而两组之间血清CTGF水平比较差异无统计学意义(P＞0.05).结论:厄贝沙坦可使NSTEMI患者血浆中TGF-β1水平受到抑制,虽能使CTGF水平下降,但作用不明显.

The aim of the present study was to evaluate the effect of astragalosides (ASTs) on angiogenesis, as well as the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) following myocardial infarction (MI). MI was induced in rats by ligation of the left coronary artery. Twenty-four hours after surgery, the rats were divided into low-dose, high-dose, control and sham surgery groups (n=8 per group). The low- and high-dose groups were treated with ASTs (2.5 and 10 mg/kg/day, respectively, via intraperitoneal injection), while, the control and sham surgery group rats received saline. Serum levels, and mRNA and protein expression levels of VEGF and bFGF, as well as the microvessel density (MVD) were determined four weeks post-treatment. Twenty-four hours post-surgery, VEGF and bFGF serum levels were observed to be comparable between the groups; while at four weeks, the VEGF and bFGF levels were higher in the AST-treated rats (P<0.01). Similarly, VEGF and bFGF mRNA and protein expression levels were higher following AST treatment (P<0.05). No difference in VEGF mRNA expression between the low- and high-dose groups was noted, however, an increase in the bFGF expression levels was detected in the high-dose group. Newly generated blood vessels were observed following MI, with a significant increase in MVD observed in the AST-treated groups (P<0.05). AST promotes angiogenesis of the heart and increases VEGF and bFGF expression levels. Thus, it is hypothesized that increased VEGF and bFGF levels may contribute to the AST-induced increase in angiogenesis in rat models of MI.