冷血停搏液中加入磷酸肌酸在体外循环手术中的心肌保护效果

摘要目的认识冷血停搏液中加入磷酸肌酸在体外循环手术中的心肌保护效果。方法50例病人随机分为实验组（磷酸肌酸组）和对照组,实验组在升主动脉阻断后于主动脉根部顺行灌注含磷酸肌酸（10mmol／L）的冷血停搏液,对照组冷血停搏液不含磷酸肌酸。分别观察两组体外循环、心肌阻断时间,心脏复跳情况及两组正性肌力药物应用剂量,并检测术前、后24h两个时点两组动脉血肌酸激酶（CK）、肌酸激酶同功酶（CK—MB）、乳酸脱氢酶（LDH）值。结果两组体外循环及心肌阻断时间无差异,心脏自动复跳率无差异;正性肌力药物使用剂量实验组低于对照组,48％的对照组患者需盐酸肾上腺素辅助心功能,高于实验组12％（P〈0．01）;术后两组心肌酶均升高（P〈0．01）,实验组较对照组低（P〈0．05）。结论含磷酸肌酸的冷血停搏液对心肌细胞损害轻,心律失常发生率降低,心肌细胞功能恢复快,县有较好的心肌保护效果。     

缺血预适应对心肌保护效应的临床研究

为观察缺血预适应对心肌缺血的保护作用，将ＡＭＩ１０６例分为缺血预适应组（Ａ组）７７例和无缺血预适应组（Ｂ组）２９例。根据血清肌酸激酶及同工酶、丙酮酸激酶活性－时间变化曲线定量计算其心肌梗塞范围，Ａ组分别为３４．２±２２．５ＣＫ－ＭＢ－ｇ，３５．２±２４．４ＣＫ－ｇ，３２．８±２２．７ＰＫ－ｇ；Ｂ组分别为４４．９±２１．７ＣＫ－ＭＢ－ｇ，４６．６±２３．６ＣＫ－ｇ，４３．６±２０．７ＰＫ－ｇ，Ａ组心肌梗塞量明显小于Ｂ组（Ｐ＜０．０５）。提示缺血预适应对心肌具有保护效应     

CK-MB在儿童支气管肺炎辅助检查中的临床意义

目的 探讨血清磷酸肌酸同工酶(CK-MB)检测在儿童轻症支气管肺炎辅助检查中的临床意义,以期指导临床诊治.方法 收集2015年1~8月85例本院收治的轻症支气管肺炎患儿,分为学龄期组(7~14岁) 6例、学龄前期组(4~6岁) 22例和婴幼儿期组(0~3岁) 57例,入院时常规检测患儿CK-MB的数值,分析其在不同年龄组中的变化情况.结果 85例住院患儿中男性49例,女性36例,婴幼儿组11例患儿CK-MB升高(19%),学龄前期患儿组1例升高(5%),学龄期组患儿无一例CK-MB升高.男性患儿CK-MB数值为(2.40±1.76) ng/ml,女性患儿为(2.93±1.96) ng/ml,两者比较差异无统计学意义(P>0.05).婴幼儿组患儿CK-MB为(3.23±1.84) ng/ml,学龄前期组为(1.58±1.27) ng/ml,学龄期组为(0.75±0.57) ng/ml,婴幼儿组支气管肺炎患儿血液CK-MB数值较学龄前期和学龄期患儿显著升高,差异均有统计学意义(P<0.05).结论 CK-MB是目前临床判断患儿心肌受损的经典检测指标,婴幼儿支气管肺炎轻症合并心肌受损的发生概率相对较高,血清CK-MB的检测应作为婴幼儿支气管肺炎的常规检查,可以使患儿得到更好的诊治.对于学龄前期和学龄期轻症支气管肺炎患儿,血清CK-MB可不作为临床常规的辅助检查.     

急性心肌梗死溶栓后检测肌红蛋白、肌钙蛋白I、肌酸激酶同工酶对冠脉再通的诊断价值

目的探讨血清肌红蛋白(Mb)、肌钙蛋白I(cTnI)和肌酸激酶同工酶(CK-MB)对急性心肌梗死溶栓冠脉再通的早期诊断价值。方法应用酶联免疫分析法测定106例急性心肌梗死患者溶栓治疗后Mb、cTnI、CK-MB浓度的变化,分析急性心肌梗死患者溶栓再通组(73例)和溶栓未通组(33例)上述指标的变化。结果急性心肌梗死溶栓再通组Mb、cTnI和CK-MB达到峰值浓度的时间较未通组明显提前(P<0.05),其中Mb较cTnI、CK-MB峰值出现更早,分别为(5.9±2.5)h、(14.5±3.2)h和(14.8±3.9)h(P<0.01);Mb、cTnI和CK-MB对判断冠脉再通的敏感性、特异性、预测值无显著性差异(P>0.05)。结论血清Mb、cTnI和CK-MB可以较好地预测急性心肌梗死患者溶栓再通,其中Mb较cTnI、CK-MB能更早的判定冠状动脉是否再灌注。     

磷酸肌酸钠对冠心病并慢性心力衰竭患者B型利钠肽及心功能的影响

目的探讨注射用磷酸肌酸钠对冠心病并慢性心力衰竭患者B型利钠肽及心功能的影响。方法选择冠心病慢性心力衰竭患者80例,随机分为对照组（n=40）以及磷酸肌酸钠治疗组（n=40）,应用超声心动图检测患者左心室收缩末直径（LVESD）,左心室舒张末直径（LVEDD）及左室射血分数（LVEF）;实验室检测B型利钠肽水平。用药治疗2周,观察治疗前后的指标变化。结果治疗后磷酸肌酸钠治疗组LVESD、LVEDD与对照组比较均明显下降（P〈0.05）,LVEF明显增加（P〈0.05）。治疗2周后两组患者B型利钠肽均较治疗前降低,磷酸肌酸钠治疗组与对照组比较下降更显著（P〈0.05）。结论磷酸肌酸钠可以改善冠心病并慢性心力衰竭患者的心功能,提高活动耐受。     

Prednisone can protect against exercise-induced muscle damage

In an experimental animal exercise model we tested whether daily administration of prednisone prevents the development of mechanically induced muscle fibre damage. Six-week-old rats were treated with different doses of prednisone ranging from 1 to 50 mg/kg body weight per day or with placebo, for 8 days. On day 6 of treatment the rats were forced to run for 2 h on a level treadmill. Two days after exercise morphological damage in the soleus muscles was quantified using light microscopy and a semi-automatic image analysis system. Creatine kinase (CK) activity was measured before exercise (day 5) and directly after exercise (day 6). The expression of dystrophin in a placebo group and in a group that received 5 mg prednisone/kg body weight per day with and without performing exercise was studied with Western blotting. The effect of prednisone on fibre type distribution was determined with an antibody against fast myosin and the effect of prednisone on the proliferative activity of muscle satellite cells was studied using bromodeoxyuridine (BrdU) immunohistochemistry. Exercise-induced muscle fibre damage varied in a dose-dependent way. In the placebo group the mean (SEM) damaged muscle fibre area was 4% (1%). The groups that received low doses of prednisone, 1 or 2.5 mg/kg per day, showed a similar level of muscle damage. However, with 5 mg prednisone/kg per day the amount of muscle fibre damage [mean (SEM)] was significantly reduced to 1.4% (0.5%) (P 0.05, Student'st-test). High doses of prednisone had no protective effect. Directly after exercise the CK activity was increased two-fold, except in the group that received 50 mg prednisone/kg body weight per day. No changes in the amount of dystrophin were found after densitometric analysis of the Western blots. Prednisone did not affect the fibre distribution or the labelling index of satellite cells. We conclude that prednisone, given in an appropriate dose, protects muscle fibres against the development of mechanically induced damage, possibly by stabilizing the muscle fibre membranes. This action may explain the beneficial effect of prednisone observed in Duchenne muscular dystrophy patients.     

脑梗死患者心电图与血浆肌酸激酶-同工酶活性变化

目的探讨不同部位大脑半球脑梗死患者心电图与血浆肌酸激酶-同工酶(CK-MB)活性的变化.方法检测156例首发急性大脑半球脑梗死患者的心电图和血浆CK-MB活性,分析比较不同部位大脑半球梗死患者的心电图和血浆CK-MB活性变化.结果右侧岛叶脑梗死患者快速心律失常和QTc延长发生率显著增加,左侧岛叶脑梗死患者ST段上升或下降显著增加,其他各种心电图改变各组间无明显区别.血浆CK-MB活性升高亦主要见于岛叶梗死患者,血浆CK-MB活性升高者心电图异常发生率明显增加,预后更差.结论造成心电图异常和血浆CK-MB活性升高的大脑半球脑梗死部位主要是岛叶,对影响到岛叶的脑硬死患者应加强心肌保护和心脏监护.     

Cardioprotective effects of sinomenine in myocardial ischemia/reperfusion injury in a rat model

BackgroundIschemia reperfusion (I/R) play an imperative role in the expansion of cardiovascular disease. Sinomenine (SM) has been exhibited to possess antioxidant, anticancer, anti-inflammatory, antiviral and anticarcinogenic properties. The aim of the study was scrutinized the cardioprotective effect of SM against I/R injury in rat.MethodsRat were randomly divided into normal control (NC), I/R control and I/R + SM (5, 10 and 20 mg/kg), respectively. Ventricular arrhythmias, body weight and heart weight were estimated. Antioxidant, inflammatory cytokines, inflammatory mediators and plasmin system indicator were accessed.ResultsPre-treated SM group rats exhibited the reduction in the duration and incidence of ventricular fibrillation, ventricular ectopic beat (VEB) and ventricular tachycardia along with suppression of arrhythmia score during the ischemia (30 and 120 min). SM treated rats significantly (P < 0.001) altered the level of antioxidant parameters. SM treatment significantly (P < 0.001) repressed the level of creatine kinase MB (CK-MB), creatine kinase (CK) and troponin I (Tnl). SM treated rats significantly (P < 0.001) repressed the tissue factor (TF), thromboxane B2 (TXB2), plasminogen activator inhibitor 1 (PAI-1) and plasma fibrinogen (Fbg) and inflammatory cytokines and inflammatory mediators.ConclusionOur result clearly indicated that SM plays anti-arrhythmia effect in I/R injury in the rats via alteration of oxidative stress and inflammatory reaction.     

他汀类与核苷类药物所致横纹肌溶解症及其防治

本文列举了他汀类和核苷类药物中可诱发药源性横纹肌溶解症的相关药物,介绍药源性横纹肌溶解症的防治措施.通过对横纹肌溶解症的发生机制及诱发该不良反应的药物应用进行分析,并结合临床诊断及治疗进行阐述.认为临床上应该慎用可能诱发药源性横纹肌溶解症的药物,观察到横纹肌溶解症出现的初始症状及时停用相关药物,避免横纹肌溶解症的发生,促进临床合理用药.