小儿癫痫持续状态心肌损伤的初步研究

目的　探讨小儿癫痫持续状态是否存在心肌损伤。方法　测定 2 4例全身性惊厥性癫痫持续状态患儿 (试验组 )血清心肌酶谱 (包括AST、CK MB、CK、LDH1、LDH)、心肌肌钙蛋白T(cTnT)、心电图 (ECG) ,并与 2 7例非惊厥持续状态的惊厥儿 (对照组 )进行比较。结果　试验组各心肌酶值 (u/L)为AST 2 77.9± 766.8,CK 1615 .8± 70 2 .3 ,CK MB 70 .3±70 .2 ,LDH1180 .0± 162 .0 ,LDH 619.8± 3 91.9;对照组为AST 83 .6± 163 .7,CK 13 4.6± 12 6.8,CK MB 2 5 .4± 13 .4,LDH171.9± 3 8.8,LDH 3 3 9.2± 2 14 .3 ,两组均值进行比较 ,CK ,CK MB ,LDH ,LDH1差异有统计学意义 ,AST差异无统计学意义 ;cTnT试验组测 13例 ,阳性 6例 ,对照组测 8例均阴性 ,两组比较差异有统计学意义 ;ECG试验组查 2 3例异常 15例 ,对照组查 2 4例异常 4例 ,两组比较差异有统计学意义。结论　小儿全身性惊厥性癫痫持续状态可引起心肌损伤     

兔心肌梗塞模型制备方法的改进及其在MRI中的应用

目的　对兔心肌缺血的模型制备方法进行改进 ,并探讨其在 MRI诊断研究中的价值。方法　分别采用高位结扎左冠状动脉前降支 (L AD)和同时低位结扎 L AD及左冠状动脉旋支 (L Cx)建立兔心肌梗塞模型 ,并在术后行 MRI检查 ,对取材后心肌标本行氯化三苯四氮唑 (TTC)及病理检查。结果　 1L AD组 2 0 % (5 / 2 5 )发生心室颤动导致死亡 ,L AD +L Cx组无一例发生室颤死亡。 2 L AD组 EKG改变明显者占 5 6 % (14 / 2 5 ) ,其中 2 1.4 3% (3/14 )在即刻就有 EKG明显改变 ,并在 30分钟后恢复正常 ;EKG改变不明显者占 4 4 % (11/ 2 5 ) ;L AD +L Cx组 10 0 %有 EKG明显改变 ,且 30分钟后亦无明显恢复。 3L AD组心肌梗塞范围较小 ,并均限于左室前壁 ,室间隔前部损害 ;而 L AD+L Cx组心肌梗塞范围较大 ,且累及左室前壁及侧壁 ,无一例有室间隔前部损害。4 L AD组中有 30 % (6 / 2 0 )不能显示小灶缺血局部心肌运动降低 ,16 .6 7% (3/ 18)无法分辨早期小梗塞灶的 MRI信号变化 ;而 L AD+L Cx组均能显示缺血局部心肌运动降低及梗塞灶早期的 MRI信号变化。结论　低位结扎兔心 L AD+L Cx,手术死亡率低 ,EKG改变明显 ,梗塞面积较大 ,是 MRI研究中一种较理想的心肌缺血动物模型制备方法。     

Combined evaluation of first pass radionuclide angiography and equilibrium radionuclide ventriculography in the diagnosis of coronary artery disease

Results of 203 patients who underwent first pass radionuclide angiography (FP) and quantitative equilibrium radionuclide ventriculography (qERNV) were stored in a data base system and evaluated statistically. Eighty eight of these patients also underwent exercise equilibrium radionuclide ventriculography (E-qERNV). In patients with coronary artery disease (CAD) without previous myocardial infarction (MI), evaluation of global and regional ejection fraction (gEF, rEF) at rest revealed a poor sensitivity of 64%, the specificity was about 71% (qERNV). FP at rest revealed similar values of sensitivity (69%) and specificity (83%). Additional assessment of stress induced changes of gEF, significantly (P<0.05) improved sensitivity of qERNV in CAD patients without a history of previous MI to 84% (specificity 86%). In patients with one previous MI, however, similar values of sensitivity were found (RFP: 87%, R-qERNV: 84%, E-qERNV: 93%). In patients with several MI's, sensitivity was above 90% at rest and during exercise (R-FP: 96%, R-qERNV: 93%, E-qERNV: 100%).     

心脏跳动下修补小儿室间隔缺损的临床研究

目的　探讨在浅低温体外循环心脏跳动下完成小儿室间隔缺损修补术的可行性。方法　 18例小儿室间隔缺损随机分为观察组和对照组 ,观察组在浅低温体外循环心跳下修补室间隔缺损 ,对照组为常规心脏停跳下修补室间缺损。测定心肌同功酶释放和三磷酸腺苷 ,观察左室压力 ,评价术野显露及气栓预防效果等。结果　观察组心肌同功酶释放明显低于对照组 ,三磷酸腺苷含量明显高于对照组 ,心肌超微结构基本正常 ,术中左室压力低于主动脉压力 ,术后无气栓发生。结论　浅低温体外循环心脏跳动下行小儿室间隔缺损修补术能更好地保护心肌。术野显露技术和防气栓的方法简便可行。     

骨髓间充质细胞与速固化磷酸钙支架共培养的实验研究

[目的]观察人骨髓间充质干细胞在速固化磷酸钙骨水泥支架中的增殖和生长情况。[方法]将速固化壳聚糖-磷酸钙骨水泥支架材料预先成形。采用全骨髓法分离人骨髓间充质细胞并在体外对细胞进行培养和扩增。72h首次换液,细胞融合80%传代,取第3代细胞用于实验。将细胞与磷酸钙骨水泥支架复合培养,分别利用四甲基偶氮唑蓝MTT法及扫描电镜等检测细胞在材料中的增殖和生长情况。[结果]用酶标仪检测OD值提示共培养后,支架内的细胞数量逐渐增加。扫描电镜结果显示支架材料内部为多孔结构,孔内见有细胞生长,细胞表面可见分泌颗粒。[结论]速固化壳聚糖-磷酸钙骨水泥对人骨髓间充质干细胞有较好的细胞相容性,细胞可在材料内黏附和增殖,是理想的骨组织工程支架材料。     

冠心病患者血栓前状态分子标志物的变化

观察冠心病患者凝血、纤溶指标的变化 ,以探讨凝血系统的变化与冠心病发病的关系。采用酶联免疫吸附双抗体夹心法检测 10 0例冠心病患者血浆D 二聚体、血小板α颗粒膜蛋白 14 0及血管性血友病因子含量 ,并与4 4例健康人比较。结果发现 ,冠心病患者血浆D 二聚体、血小板α颗粒膜蛋白 14 0和血管性血友病因子明显升高 ,与对照组比较差异显著 (P <0 .0 1) ,且急性心肌梗死患者各指标变化明显高于陈旧性心肌梗死、不稳定型心绞痛和稳定型心绞痛患者 (P <0 .0 1) ,其中不稳定型心绞痛患者血浆血小板α颗粒膜蛋白 14 0明显高于稳定型心绞痛患者 (P <0 .0 5 )。冠心病患者血小板α颗粒膜蛋白 14 0、血管性血友病因子及D 二聚体水平之间呈明显的正相关性(P <0 .0 5 )。结果提示 ,冠心病患者存在明显的高凝状态 ,表现为继发性纤溶亢进 ,血小板活性增加及血管内皮细胞损伤 ,且与冠心病患者的病情变化有一定关系。     

大鼠骨髓间充质干细胞与多孔双相磷酸钙陶瓷支架体外黏附的实验研究

目的研究大鼠骨髓间充质干细胞(marrowmesenchymalstemcells,MSCs)诱导培养后在多孔双相磷酸钙(biphasiccalciumphosphate,BCP)陶瓷支架材料上的黏附和生长。方法SD大鼠MSCs经矿化诱导培养、扩增,具有成骨细胞表型后,与多孔BCP陶瓷支架及普通多孔羟基磷灰石(hydroxyapatite,HA)陶瓷支架体外复合培养,扫描电镜观察比较MSCs在两种材料支架表面的黏附数量和形态;同时以0.5、1.0、2.0、3.0和4.0×106/ml浓度细胞悬液接种于多孔BCP支架材料,检测适宜的接种浓度及单位体积支架材料可黏附MSCs数量。结果大鼠MSCs经诱导培养14d后,行矿化沉积茜素红染色、型胶原免疫细胞化学染色及碱性磷酸酶细胞化学染色,结果均为阳性。大鼠MSCs黏附于多孔BCP陶瓷上的细胞数(88.00±6.58)明显高于HA陶瓷组(39.00±3.65),两组比较差异有统计学意义(P<0.01)。当接种浓度为2.0×106/ml时,单位体积的陶瓷支架材料最多可黏附MSCs数量为1.28×107个/cm3,为细胞适宜接种浓度。结论大鼠MSCs在体外经矿化诱导培养可表达成骨细胞表型,细胞浓度为2.0×106/ml时与多孔BCP陶瓷支架材料具有良好的黏附能力。     

Toxic effects of Fusarium mycotoxin butenolide on rat myocardium and primary culture of cardiac myocytes.

Mycotoxin toxicosis has been implicated in the etiopathogenesis of Keshan disease (KD), an endemic cardiomyopathy prevailing in some regions of China. Butenolide (4-acetamido-4-hydroxy-2-butenoic acid gamma-lactone, CAS No. 16275-44-8), a mycotoxin produced by several Fusarium species such as Fusarium tricinctum and Fusarium graminearum, is frequently detected from the cereals in the endemic areas of KD. The present study is undertaken to investigate whether this mycotoxin can induce myocardial damage. Exposure of primary culture of cardiac myocytes to butenolide resulted in significant cytotoxicity, manifested by changes in cell morphology and decreases in cell viability. Consistent with the in vitro findings, distinct myocardial toxicity in vivo was observed after administration of rats by gavage with butenolide (10 and 20 mg/kg/day) for 2 months, and the myocardial injuries were characterized by focal necrosis of myocardium and fragmentation of myofiber. Butenolide also induced significant oxidative damage to the myocardium in vitro evidenced by a concentration-dependent lipid peroxidation in the myocardial homogenates, whereas antioxidants superoxide dismutase (SOD), N-acetylcysteine (NAC) and glutathione (GSH) provided significant protections against this oxidative effect. Taken together, these results clearly reveal that butenolide possesses the potential to induce myocardial toxicity. The present findings may reinforce the hypothesis that toxicosis by mycotoxins is one of the etiological factors for KD.     

Scintigraphic evaluation of myocardial uptake of thallium 201 and technetium 99m pyrophosphate utilizing a rat model of chronic doxorubicin cardiotoxicity

To evaluate the usefulness of myocardial scintigraphy as a monitoring tool for chronic doxorubicin (DXR) cardiotoxicity, a rat model was used to investigate the relationship between the myocardial uptake of thallium 201 (Tl) or rechnetium 99m pyrophosphate (^99mTc-PPi) and histological changes of the heart. Although there was no significant difference in myocardial Tl uptake between control and DXR-treated rats at an early phase after Tl injection, late-phase Tl uptake was significantly higher in the DXR-treated rats than in the control rats, indicating a slow wash-out of Tl from the myocardium. The wash-out rate calculated from scintigraphic examination of DXR-treated rats was significantly decreased with increasing degree of cardiomyopathy. Since the Tl wash-out rate was sharply decreased even in animals with minimal histological changes, it may be a possible monitoring tool for the early detection of chronic DXR cardiotoxicity. On the other hand, myocardial^99mTc-PPi images could be obtained only in rats with severe myocardial changes and hence would not useful for early detection.     

The effects of altering time delays of coupled pacing during acute atrial fibrillation

BACKGROUND: Coupled pacing (CP), which consists of delivering a premature electrical stimulation to the heart after the effective refractory period of ventricular activation, is a novel method for controlling ventricular rate during atrial fibrillation (AF). It also has been established that CP improves pump function by enhancing external cardiac work and myocardial efficiency. OBJECTIVE: The purpose of the present study was to determine if two time delays for CP (short and long) would result in similar improvements in ventricular function. METHODS: In a canine model, we applied CP at two time delays (CP-S and CP-L) during two stages: sinus rhythm (SR) and acute AF. The cardiac responses to CP during SR served as the nontachycardic and nondepressed control. During both rhythms, we shortened the coupling interval until we obtained maximal contractility, designated CP-S. Next, we increased the delay until we started to see a measurable secondary contraction (left ventricular pressure development of approximately 20 mmHg). These longer delays were designated CP-L. RESULTS: Our results showed that the ventricular rate of intrinsic activation (VRIA) remained decreased despite prolongation of the time delay of CP during both AF and SR. Also, both delays of CP increased left ventricular systolic pressure (LVSP) and dLVP/dt, which are indices of myocardial contractility. In contrast, CP increased external cardiac work only during AF. Prolonging this time delay did not markedly decrease the improvement in external cardiac work. Myocardial O(2) consumption (MVO(2)) did not significantly change as the result of CP during either SR or AF. Finally, myocardial efficiency improved during AF as the result of CP at both time delays. CONCLUSIONS: In conclusion, shorter time delays for CP increased contractile strength during both SR and AF. However, extending the time delay of CP had minimal effects on diminishing the improved ventricular pump function and energetics that resulted from CP during AF. Thus, the maximal enhancement of myocardial contractility via CP-S was not needed to maintain the improved ventricular function during acute AF when CP is applied.