人心肌肌凝蛋白重链的制备研究

目的：探讨制备人心肌肌凝蛋白重链（MHC）的方法,为制备其抗体提供抗原。方法：采用改良性制备人心肌MHC,通过SDS-PAGE及Western印迹分析其纯度及抗原特性。结果：①SDS-PAGE显示,纯化的人心肌MHC呈现只有一分子量较大的代表人心肌MHC带的典型图像;②Western印迹显示,200ku处有一典型的感光带。结论：所用的改良法能有效地提取纯化人心肌MHC,可满足制备其抗体的需要。     

普鲁卡因对缺氧心肌细胞的影响

目的 探讨普鲁卡因对心肌细胞缺氧损伤的影响。方法 将原代培养成活48h的大鼠乳鼠心肌细胞分为三组：A组为对照组（氰化钠造成心肌细胞内缺氧模型）,B组为Prol组（缺氧＋7．4mg／L普鲁卡因）,C组为Pro2组（缺氧＋14．8mg／L普鲁卡因）。比较三组心肌细胞形态学（倒置相差显微镜、透射电镜观察）的变化及吸光度A值的改变。结果 缺氧12h后,对照组细胞搏动功能变化明显,呈散在细胞搏动,而实验组搏动频率减慢。随着时间的延长,细胞形态学变化逐渐明显,对照组较实验组变化更显著。结论 普鲁卡因对培养心肌细胞缺氧损伤有一定的保护作用。     

外源性磷酸肌酸对开心手术病人的心肌保护作用

20例需行瓣膜置换手术的风湿性心脏瓣膜病患者 ,随机等分为 2组。实验组 (CP组 )于术前 2d静脉滴注护心通 ,总量为 4g ;对照组 (C组 )用 5 %G S滴注。结果示实验组的心脏自动复跳率明显高于对照组 ,而对正性肌力药物的需求、缺血再灌后的MDA活性增高及心肌超微结构的改变则较对照组明显减轻 ,两组间的心肌酶活性和心肌ATP含量差异无显著性。提示护心通是一有效的心肌保护药物     

益气通络丹抗缺氧再给氧心肌细胞凋亡的实验研究

目的观察含益气通络丹的大鼠血清对缺氧24h再给氧4h后新生乳鼠心肌细胞凋亡的抑制作用及其对心肌细胞乳酸脱氢酶(LDH)释放、一氧化氮(NO)生成和硫代巴比妥酸反应物质(TBARS)的影响。方法采用AnnexinV-PI双标记方法以流式细胞仪和ELISA法检测细胞凋亡,以紫外分光光度法测定LDH释放水平,采用改良Yu方法测定NO浓度,用Ohkawa法测定TBARS含量。结果心肌细胞缺氧再给氧后NO、TBARS水平升高,LDH释放增加。含益气通络丹的血清能显著抑制心肌细胞凋亡,抑制LDH释放,降低培养细胞上清液中NO和TBARS水平,其效应呈剂量依赖关系。结论益气通络丹具有抗缺氧再给氧心肌细胞凋亡作用,其机制与清除氧自由基和NO特性有关。     

腺苷脱氨酶抑制剂对氧反常大鼠心脏的保护作用

本文观察到腺苷脱氨酶抑制剂EHNA对离体灌流大鼠心脏氧反常性损伤有明显的作用,此外还发现在缺氧期(无氧灌流30分钟)EHNA也表现出明显的保护作用,心脏收缩幅度的降低和静息张力的升高均显著低于对照组。表明在缺氧期也可能有自由基的产生。     

Changes in myocardial metabolism and ultrastructure of myocardial microvessels during pharmacological and cold cardioplegia under hypothermic conditions without perfusion

A combination of pharmacological and cold cardioplegia in with hypothermia without perfusion in open-heart surgery guarantee the reversible character of shifts in energy and free radical balance in the myocardium. However, this procedure can impair coronary micricirculation due to structural and functional changes in microvessel endothelium. Our results demonstrate that new cytoprotective approaches are extremely needed for cardiac protection during surgery.     

Effects of 4-aminopyridine on contractile response and action potential of rabbit papillary muscle

The effects of 4-aminopyridine (4-AP) were studied on isolated papillary muscles from the heart of reserpinized rabbits (at 37°C). The preparations were paced to contract at 0.67 Hz under isometric conditions and the muscle length was adjusted to 95 % of the length for optimum force production. Simultaneous recordings of isometric force and membrane potentials were performed. 4-AP (50 μM) increased peak force by approximately 20% of the control and prolonged the action potential by 20%. Higher concentrations of 4-AP (800 μ.M) resulted in further increments of force and action potential duration (60 and 70% of controls, respectively). Prolongation of the action potential and potentiation of the isometric force was still present one hour after withdrawal of the drug from the perfusate. The results are consistent with the view that 4-AP prolongs the action potential by inhibiting the late repolarizing potassium current. It is suggested that the calcium uptake by the ventricular cell during the prolonged action potential is increased and that this leads to the positive inotropic effect.     

The preferential inhibition of α1- over β-adrenoceptor-mediated positive inotropic effect by organic calcium antagonists in the rabbit papillary muscle

Summary Experiments were carried out to elucidate the mechanism that the positive inotropic effect mediated by ₁-adrenoceptors is more susceptible to organic calcium antagonists than the -adrenoceptor-mediated effect. Verapamil and diltiazem displaced the specific binding of [³H]prazosin to the membrane fraction derived from the rabbit ventricular myocardium, verapamil being about 70 times more potent than diltiazem. Nifedipine did not displace the binding. While these compounds suppressed the positive inotropic effect mediated via _l-adrenoceptors in ₁- concentration-dependent manner, there was no correlation between the potency of the compounds to displace the [³H]prazosin binding and to inhibit the -mediated positive inotropic effect. The relative potency of three calcium antagonists to decrease the basal force of contraction and the al-mediated effect (of the same extent as compared to basal force of contraction) was consistent to each other. The positive inotropic effect mediated by -adrenoceptors was inhibited much less, and was enhanced by low concentrations of organic calcium antagonists. The differential action of calcium antagonists on the - and -mediated positive inotropic effect was mimicked by lowering the extracellular calcium concentration to 1/2, 1/4 and 1/8 of that in normal Krebs-Henseleit solution (2.5 mmol/l). These results indicate that the ₁-adrenoceptor blocking activity does not play an essential role for the preferential inhibition of -mediated positive inotropic effect by organic calcium antagonists. Difference in the subcellular mechanism involved in mobilization of intracellular Ca²⁺ subsequent to ₁-and -adrenoceptor activation may be responsible for the differential inhibitory action of calcium antagonists in the rabbit heart. Send offprint requests to M. Endoh at the above address