Adult T cell leukemia/lymphoma with massive involvement of cardiac muscle and valves

An autopsy case of a 58-year-old woman with massive cardiac Involvement of adult T cell leukemia/lymphoma (ATLL) is reported. She developed cardiac failure due to aortic and mitral regurgitation with cardiac infiltration of ATLL cells, and underwent replacement of both aortic and mitral valves. Studies of the cut-surfaces revealed diffuse thickening of the subendocardial wall of the left chamber with widespread whitish-brown tumor infiltrates. In the regions surrounding the replaced aortic and mitral valves there was also massive tumor cell infiltration. The tumor cells infiltrating the cardiac muscle wall were T cell in origin and exhibited Leu-3a (CD4)-positive immunoreaction. Ultrastructurally, tumor cells contained markedly indented nuclei and some were attached directly to the muscle cells. These findings suggest that this was an unusual form of ATLL with widespread involvement of the heart.     

Demonstration of Ri-type adenosine receptors in bovine myocardium by radioligand binding

Summary Adenosine has been shown to have negative inotropic, chronotropic and dromotropic effects on the heart. The pharmacological profiles of these effects suggest that they are mediated via R_i (A₁) adenosine receptors, but a direct demonstration of these receptors is still missing. In the present study we report direct labelling of these receptors with (-)N⁶-[¹²⁵I]-p-hydroxyphenylisopropyladenosine ([¹²⁵I]HPIA). The radioligand bound in a saturable and reversible manner to a crude membrane preparation, the B _max-value was 30.5 fmol/mg protein and the K _D-value 1.1 nmol/l. A similar affinity of the ligand was obtained in kinetic and competition experiments. Competition experiments with a variety of adenosine analogues gave a pharmacological profile characteristic of R_i adenosine receptors with high affinities of N⁶-substituted derivatives and a marked stereospecificity for N⁶-phenylisopropyladenosine (PIA). Purification of the membrane preparation by density gradient centrifugation resulted in a 30-fold increase in the number of binding sites which was paralleled by a similar increase in the number of binding sites for [³H]ouabain. Guanine nucleotides decreased binding of [¹²⁵I]HPIA in a dose-dependent manner, but the IC₅₀-values were considerably higher than those reported in other tissues. Finally, binding of [¹²⁵I]HPIA appeared to be entropy-driven which has been shown to be characteristic of agonist binding to R_i adenosine receptors. These results suggest the presence of R_i adenosine receptors in ventricular myocardium which may be responsible for the mediation of the effects of adenosine and its analogues.Abbreviations [¹²⁵I]HPIA (-)N⁶-[¹²⁵I]-p-hydroxyphenylisopropyladenosine - (-)IHPIA (-)N⁶-iodo-p-hydroxyphenylisopropyladenosine - (+)/(-)PIA (+)/(-)N⁶-phenylisopropyladenosine - CHA N⁶-cyclohexyladenosine - NECA 5-N-ethylcarboxamidoadenosine - App(NH)p 5-adenylylimidodiphosphate - Gpp(NH)p 5-guanylylimidodiphosphate     

Coronary Reperfusion Following Experimental Myocardial Infarction

Numerous studies have shown that early coronary reperfusion is feasible in the setting of evolving acute myocardial infarction in man. While early reperfusion reduces myocardial infarct size, there are potentially deleterious consequences of reperfusion. The concept of "reperfusion injury", oxygen-free radical damage, no reflow phenomenon, and stunned myocardium are discussed.     

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。     

心肌细胞β_1和β_2 肾上腺素能信号传导系统的区别(英文)

尽管 β1和β2 亚型肾上腺素能受体在结构和功能上十分相似 ,作者最近的研究显示这两种受体亚型在心肌细胞上的信号传递机制有很大的不同。β1受体激活后 ,启动经典的刺激性G蛋白 -腺苷酸环化酶 -环磷酸腺苷 -蛋白激酶A的线性信号传导途径 ;而 β2 受体除与刺激性G蛋白耦联外 ,还与抑制性G蛋白 ,Gi2 和Gi3 ,耦联。β2 受体与抑制性G蛋白的耦联在很大程度上决定了 β受体亚型在心脏钙调控、收缩力、环磷酸腺苷水平和蛋白磷酸化上的不同作用。β2 受体激活所引起的细胞内钙和收缩力的增加与细胞内环磷酸腺苷的增加和胞浆蛋白磷酸化有明显的脱节。这主要由于抑制性G蛋白激活的蛋白脱磷酸酶可以使 β2 受体诱导的环磷酸腺苷 -蛋白激酶A的作用局限于细胞质膜上。这种格局化作用 ,使公用的第二信使 ,环磷酸腺苷 ,在不同的 β受体亚型激活时 ,选择性地执行不同的功能。新的证据表明 ,β受体亚型不仅在激动剂激活时表现不同 ,而且自发激活的能力也不同。另外 ,自发激活的 β2 受体和激动剂激活的 β2 受体在细胞内信号传递和靶蛋白的特异性上都不同。这些发现不仅进一步揭示了 β受体亚型在信号传递上的多样性和特异性 ,而且为理解 β受体亚型在健康和疾病状态下的调节和功能提供了新的线索。     

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.