再灌注损伤大鼠心肌细胞核3H-Ryanodine结合特性的变化

目的观察缺血-再灌注损伤(IRI)心肌细胞核兰尼定受体(RyR)结合特性改变.方法雄性Wistar大鼠随机分为IRI组和假手术(Sham)组,结扎冠状动脉左主干建立IRI模型,3H-Ryanodine饱和结合法分析分离的心肌细胞核上RyR最大结合容量(Bmax)和解离常数(Kd).结果大鼠心肌细胞核存在高亲和力的RyR,IRI组较Sham组Bmax降低29%(P<0.01),Kd差异无显著性(P>0.05).IRI组和Sham组心肌细胞核经佛波酯(PMA)+磷脂酰丝氨酸(PS)处理后,Bmax均显著增加(P均<0.01),但IRI组的增加幅度较小(P<0.01);IRI组和Sham组心肌细胞核经Ca2+-钙调素(CaM)处理后,Bmax均降低(P均<0.05),但IRI组降低幅度较小(P<0.01);上述处理对两组Kd均无显著影响(P均>0.05).结论 IRI心肌细胞核RyR的Bmax呈降低趋势;经PMA+PS和Ca2+CaM处理后,Bmax的改变削弱,而Kd无改变.     

渗透压对大鼠心室肌细胞L型Ca2+电流的影响

目的 :观察细胞胞外渗透压的改变对大鼠心室肌 L型 Ca2 +（ICa,L）电流的影响。方法 :采用全细胞膜片钳技术记录大鼠心室肌细胞 ICa,L。结果 :细胞外的渗透压由 3 10 m Osm / kg H2 O降低至 2 2 0 m Osm/ kg H2 O可使 ICa,L的 rundown明显变慢 ,电流大小无统计学意义上的差异 ;而当其中细胞外的渗透压由 3 10 m Osm/ kg H2 O升高至 410m Osm/ kg H2 O时可使 ICa,L减小 （5 1.4± 7.9） % （n=4,P<0 .0 1）。结论 :细胞外渗透压变化对大鼠心室肌基础 ICa,L有明显影响     

AngⅡ对心肌细胞Kv4．2钾通道蛋白表达的影响及机制

【目的】体外培养新生大鼠心肌细胞,观察AngⅡ在诱导细胞肥厚过程中对Kv4．2蛋白表达的影响,及钙离子在其细胞内信号传导通路中的作用。【方法】AngⅡ心肌细胞肥大模型,用激光共聚焦显微镜检测AngⅡ对心肌细胞胞浆钙离子浓度的影响,用流式细胞仪检测AngⅡ诱导心肌细胞肥厚过程中细胞Kv4．2表达的变化。【结果】AngⅡ明显增加细胞的蛋白总量,诱导心肌细胞肥大,AngⅡ能增加心肌细胞胞浆钙离字浓度,下调Kv4.2编码的通道蛋白的表达含量。【结论】AngⅡ在诱导心肌细胞肥大过程中,可能通过细胞内钙离子以外的信号通路下调Ito通道蛋白Kv4．2。     

干细胞对心力衰竭保护作用的研究进展

干细胞不仅丰富了移植技术领域,而且是生物工程中理想的种子细胞,干细胞移植对心肌损伤及心力衰竭保护作用的可能机制为干细胞的定向分化作用、细胞间相互连接形成的"绑定"作用、干细胞的自/旁分泌功能等。近期研究干细胞移植机制偏向于旁分泌作用,主要通过分泌生物活性因子促进心脏内源性心肌前体细胞增殖,调控血管内皮细胞及平滑肌细胞增殖,抑制心肌纤维化来发挥阻止心室重构,改善心功能的作用。     

诃子提取物含药血清对乳鼠心肌细胞损伤的保护作用

目的:研究诃子提取物含药血清对H2O2所致心肌细胞损伤的保护作用.方法:采用H2O2处理培养心肌细胞,造成氧化应激模型,通过检测细胞培养液中LDH、CK漏出量、MDA含量和SOD活性反映诃子提取物含药血清对H2O2氧化模型的影响.结果:与模型组比较,诃子提取物含药血清能显著减少LDH、CK漏出量(P＜0.05,P＜0.01);降低培养液中MDA含量(P＜0.05,P＜0.01),升高SOD活性(P＜0.01).结论:诃子提取物含药血清可减轻H2O2对心肌细胞的损伤程度,对心肌细胞具有保护作用,其机制可能与稳定细胞膜和抗氧化有关.     

促红细胞生成素对乳鼠缺氧心肌细胞的保护作用及机制

目的：探讨促红细胞生成素（EPO）发挥心肌细胞保护作用的可能分子机制。方法：采用流式细胞仪检测各组心肌细胞的存活率、凋亡率和坏死率。将心肌细胞分为正常对照组、缺氧组、缺氧＋EPO组。采用North-ern-blot方法检测各组心肌细胞中的Bcl-2、Bax、Caspase-3mRNA的表达,采用Western-blot方法检测各组心肌细胞中的CytC、STAT-3、Caspase-3蛋白的表达。结果：3组心肌细胞的存活率,凋亡率和坏死率差异显著（92．1％w70．9％vs89．0％,2．3％vs18．73％Fs6．0％,3．5％US8．0％傩3．5％,P〈0．01）。IU／mL EPO开始发挥对缺氧心肌细胞的保护作用,5U／mL、25U／mL和125U／mL的保护作用相似。与缺氧组相比：EPO组Bcl-2mRNA和STAT-3蛋白表达增加（P〈0．01）,Bax、Caspase-3mRNA和Caspase-3蛋白表达减少（P〈0．01）。结论：5U／mL的EPO是其发挥心肌细胞保护作用的最佳浓度。缺氧心肌细胞中,EPO可能通过JAK-STAT途径发挥抗凋亡的作用。     

Effects of remifentanil on intracellular Ca2+ and its transients induced by electrical stimulation and caffeine in rat ventricular myocytes

Background Preconditioning with remifentanil confers cardioprotection. Since Ca^2＋ overload is a precipitating factor of injury, we determined the effects of remefentanil on intracellular Ca^2＋ （[Ca^2＋]i） and its transients induced by electrical stimulation and caffeine, which reflects Ca^2＋ handling by Ca^2＋ handling proteins, in rat ventricular myocytes. Methods Freshly isolated adult male Sprague-Dawley rat myocytes were loaded with Fura-2/AM and [Ca]i was determined by spectrofluorometry. Remifentanil at 0.1-1000 μg/L was administered. Ten minutes after administration, either 0.2 Hz electrical stimulation was applied or 10 mmol/L caffeine was added. The [Ca^2＋]i, and the amplitude, time resting and 50% decay （t50） of both transients induced by electrical stimulation （E[Ca^2＋]i） and caffeine （C[Ca^2＋]i） were determined. Results Remifentanil （0.1-1000.0 μg/L） decreased the [Ca^2＋]i in a dose-dependent manner. It also decreased the amplitude of both transients dose-dependently. Furthermore, it increased the time to peak and tso of both transients dose-dependently. Conclusion Remifentanil reduced the [Ca^2＋]i and suppressed the transients induced by electrical stimulation and caffeine in rat ventricular myocytes.     

Impaired contractile reserve in severe mitral valve regurgitation with a preserved ejection fraction

BACKGROUND: Impaired contractile reserve in chronic MR results from load-independent, myocyte contractile abnormalities. AIMS: Investigate the mechanisms of contractile dysfunction in chronic mitral valve regurgitation (MR). METHODS: Mild MR was produced in eight dogs followed by pacing induced left ventricular (LV) dilatation over eight months. In-vivo LV dP/dt was measured at several pacing rates. Contractile function was measured in isolated LV trabeculae and myocytes at several stimulation rates and during changes in extracellular [Ca2+]. Identical studies were performed with six control dogs. RESULTS: Chronic MR resulted in a preserved ejection fraction with decreased dP/dt (p<0.01). LV trabeculae demonstrated significantly lower developed force and a negative force-frequency relation with chronic MR (p<0.05). Myocytes exhibited a negative shortening-frequency relationship in both groups with a greater decline with chronic MR (p<0.001) paralleled by decreases in peak [Ca2+](i) transients. Increases in extracellular [Ca2+] abrogated the defects in force generation in trabeculae from animals with chronic MR. CONCLUSION: Even with a preserved EF, chronic severe MR results in a significant reduction in intrinsic contractile function and reserve. Functional impairment was load-independent reflecting a predominant defect in calcium cycling rather than impaired peak force generating capacity due to myofibrillar attenuation.