Post-ischemic release of nucleosides and oxypurines in isolated rat hearts. Possible involvement of ventricular fibrillation

Summary In isolated perfused rat hearts global ischemia for 2, 5, and 15 min was produced. Depending on the duration of the ischemia, postischemic reperfusion led to the release of adenosine and its catabolites, and to more or less severe ventricular tachyarrhythmias. When ventricular fibrillation occurred, a highly significant increase in the purine release was observed compared with non-fibrillating hearts. Prevention of fibrillation by antiarrhythmic drugs decreased the purine release in a highly significant way. After only 2 min of ischemia, reperfusion did not lead to ventricular fibrillation. Electrical induction of fibrillation during the reperfusion in these hearts provoked the release of very high amounts of the purine compounds. A similar effect of electrically-induced fibrillation was also obtained in hearts without a previous ischemic period. The findings suggest that ventricular fibrillation is able to induce the release of purine derivatives from the heart.     

高血压患者左室舒张功能与左室肥厚的关系及随龄改变

为探讨原发性高血压 (以下简称高血压 )患者的左室舒张功能和左室肥厚的关系及其随龄改变 ,抽取 1995年 2月至 2 0 0 2年 7月间门诊高血压患者 4 81例为高血压组 ,以同期体检健康者 2 54 3例为对照组 ,年龄 10～ 80岁 ,并将原发性高血压患者分为 3级 ,每级中按性别分 2组。采用惠普 2 50 0彩色多普勒超声诊断系统检测 2组的室间隔厚度、左室后壁厚度、E/A等指标。使用SPSS软件进行统计学处理分析。结果 :高血压和正常对照组相比E/A显著下降 ,室间隔和左室后壁显著增厚 (P <0 .0 1)。 2个组的E/A均随年龄下降 ,而室间隔厚度随年龄增厚 ,且室间隔厚度和E/A呈显著负偏相关 (P <0 .0 1)。在高血压分级组中 ,Ⅰ～Ⅲ级高血压组中男性的室间隔厚度均厚于女性 (均P <0 .0 1) ,Ⅰ、Ⅱ级高血压组中男性的左室后壁厚度厚于女性 (P <0 .0 5,P <0 .0 1) ,Ⅰ级高血压组中女性的E/A低于男性 (P <0 .0 5)。提示 :左室舒张功能随着年龄的增加而降低 ,而且和高血压左室肥厚呈负偏相关关系 ,性别对其也有一定的影响     

The Effects of Na~+/Ca~(2+) exchange (NCX) on the Repolarization of Canine Ventricular Myocyte-Potential Arrhythmogenic Effect of NCX during a Mis-matched Repolarization and Relaxation Xiamen Zhongshan Hospital, Xiamen Medical College, Xiamen University

The Effects of Na~+/Ca~(2+) exchange (NCX) on the Repolarization of Canine Ventricular Myocyte-Potential Arrhythmogenic Effect of NCX during a Mis-matched Repolarization and Relaxation Xiamen Zhongshan Hospital, Xiamen Medical College, Xiamen University@巩燕$Visiting scholar of cardiac arrhythmia research institute,university hospital of Oklahoma!U.S.A @王焱 @BELA Szabo$Basic cardiac research laboratory,cardiac arrhythmia research institute,university hospital of Oklahoma!…     

右室心内膜流入道永久性起搏电极植入的体会

目的 :探讨右室心内膜永久性起搏电极植入术中 ,心尖部起搏与流入道起搏二者在术中起搏参数比较 ,以及流入道起搏电极植入方法。方法 :选择本院行永久性心脏起搏器安置术的 67例患者为研究对象 ,在右室心尖部起搏电极不易固定或测试起搏参数不理想时 ,改为右室流入道起搏 (12例 )。结果 :①右室心尖部及流入道两种位置起搏阈值、R波振幅、心肌阻抗比较无显著性差异 ;②术后随访 2～ 14个月两组病例均未发生电极脱位、感知异常、膈肌收缩。结论 :①右室流入道起搏与心尖部起搏一样是电极植入的有效部位 ;②右室流入道起搏与心尖部起搏一样心室电极植入技术简单易行     

比索洛尔对冠心病心力衰竭患者心室重塑和心功能的影响

目的 :探讨比索洛尔对冠心病心力衰竭患者心室重塑及心功能的影响。方法 :冠心病心力衰竭患者 12 0例 ,左室射血分数≤ 45 % ,心功能 (NYHA)Ⅱ -Ⅳ级 ,常规治疗基础上随机分为比索洛尔治疗组和对照组。治疗 6个月 ,观察比索洛尔对心室重塑、心功能的影响。应用心脏彩色超声仪测定基线值及 1个月、3个月、6个月左室结构及功能指标变化。结果 :比索洛尔平均用量为 (7 5 0± 2 5 0 )mg/d ,经过 6个月治疗 ,比索洛尔治疗组症状和心功能改善 ,与对照组比较左室射血分数上升 [(4 9 2± 2 8) %VS(3 9 6± 3 6) % ,P <0 0 5 ] ,左室收缩末容积下降[(15 7 7± 42 6)mlVS(180 9± 3 9 6)ml] ;与基线比较左室舒张末容积下降 (P <0 0 5 )。结论 :在强心、利尿、血管紧张素转化酶抑制剂基础上 ,应用比索洛尔能显著改善冠心病心力衰竭患者的心功能 ,改善心室重塑。长期应用可改善衰竭心脏心肌细胞的生物学效应 ,这种有益的作用在不同心功能级别间无显著性差异     

右心室不同部位起搏血液动力学改变的研究

目的：根据右心室不同部位起搏时血液动力学改变，研究选择置入右心室双部位起搏器辅助治疗心脏扩大合并充血性心力衰竭(CHF)，观察临床效果及心脏功能；方法：对13例在心内科住院的扩张型心肌病、缺血性心肌病、心动过速性心肌病所致心力衰竭的患者，男9侈4，女4侈4，年龄36岁～75岁(平均58．61岁)，心功能均在Ⅲ级～Ⅳ级(NYHA)，均有置入起搏器的适应证。术中通过Swan—ganz漂浮导管对右心室内不同部位起搏10分钟后测各部位的急性血液动力学改变，然后置入右心室双部位起搏器(右室流出道应用主动固定电极)。术后应用心电图、超声心动图观察右心室双部位起搏的血液动力学效果；结果：全组13例患者术中检查及置入右心室双部位起搏器均获成功。测得右心室流出道起搏(RV—OT)和右室心尖部(RVA) 右室流出道(RVOT)起搏时各参数均较单纯右室心尖部(RVA)为好。置入心脏起搏器后观察射血分数从0．31提高至0．39，左室充盈时间延长，二尖瓣返流量减少，心脏缩小，心脏功能平均提高Ⅱ级。其中一例心功能由Ⅳ级提高至I级～Ⅱ级；结论：初步血液动力学观察提示，右心室双部位起搏能改善充血性心力衰竭患者的心功能。     

Electrophysiologic mechanisms of ventricular arrhythmias

In this work the electrophysiologic mechanisms of ventricular arrhythmias have been briefly summarized. Ventricular arrhytmias can be caused either by pacemaker activity or by reentrant excitation. Enhancement of normal automaticy can generate a parasystolic rhythm in normal fibers. Abnormal automaticity may arise fom fibers in which maximum diastolic potential has been reduced by a variety of interventions. Triggered activity is caused by either an early (EAD) or delayed (DAD) afterdepolarization and requires a prior normal action potential for initiation. While there is growing evidence that EAD-induced triggered activity plays a significant role in the Long QTU syndrome and Torsade de Pointes, no clinical arrhythmias has definitely been ascribed to DADs, although DADs have been recorded in man after acute digoxin intoxication.Ventricular arrhytmias can be also caused by reentrant excitation, which can be subdivided into reflection or circus movement reentry (CMR). In the reflection model impulses in both directions are transmitted over the same pathway. In the CMR three models can be differentiated: the ring model, which requires a fixed anatomical obstacle; the figure-eight model and the leading circle model, where functional rather than fixed anatomical obstacles are involved.Abbreviations AV atrio-ventricular - CMR circus movement reentry - DAD delayed afterdepolarization - EAD early afterdepolarization - ECG electrocardiogram - LV left ventricle - MAP monophasic action potential - MF muscle fiber - PF Purkinje fiber - RV right ventricle - TdP Torsade de Pointes     

An uncommon cause of acute right ventricular failure and high mixed venous oxygen saturation

Ruptured sinus of Valsalva aneurysms are rare. We report a case in which the usual clinical manifestations were not present and the patient was initially treated as an acute pulmonary embolus. Despite three negative echocardiograms an intra-cardiac shunt was suspected because of a persistently elevated mixed venous oxygen saturation. Cardiac catheterisation confirmed the diagnosis. Surgical repair was performed and post operative recovery was uneventful.     

Termination Of Sustained Tachycardia By External Noninvasive Pacing

Invasive cardiac pacing has proved useful in the induction and termination of reentrant sustained tachycardias. In one of our two cases, programmed ventricular extra-stimulation was used to induce sustained ventricular tachycardia from the endocardial surface of the right ventricle. Induced ventricular tachycardia was terminated by burst ventricular pacing with an external cardiac pacemaker. In our second patient, external pacing was effective at inducing and terminating sustained supraventricular tachycardia. These patients illustrate that the principles of terminating sustained reentrant tachycardia with invasive pacing may also apply to noninvasive external pacing. The usefulness of this approach in treating reentrant tachycardias needs further evaluation.     

Evaluation of left ventricular contractile performance from baseline stress-shortening data in humans: comparison with pharmacological afterload challenge

The purpose of this study was to evaluate whether the baseline stress-shortening data reflect the contractile state adequately and give results comparable to the evaluation of the end-systolic stress-shortening relationships using pharmacological manipulation of afterload. Five groups were studied (total 152 patients): a control group of 30 healthy volunteers, 32 patients after surgical correction of infantile tetralogy of Fallot, 50 patients treated for childhood malignancies with doxorubicin, 17 patients with left ventricular hypertrophy due to systemic hypertension, and 23 patients with congestive cardiomyopathy. In all patients except those with congestive cardiomyopathy, afterload was altered pharmacologically to evaluate the individual stress-shortening relationship. In all patients the baseline stress-shortening data were evaluated, as well as their relative positions to two predefined normal ranges for the relationship between end-systolic stress and shortening. Additionally, a slope value was calculated from the baseline data of the five groups studied and compared with the data obtained by pharmacological afterload increment. Our data show that the comparison of individual baseline data of end-systolic wall stress and fractional shortening with predefined normal ranges for the relationship between end-systolic stress and shortening is inadequate. The appropriate normal range to compare with is the 95% confidence interval of baseline stress-shortening data in normal subjects. Also the calculation of a slope value from the baseline stress-shortening data of a group of patients seems to be inappropriate. Such a slope value does not necessarily reflect the contractile state, as the specific conditions leading to variations of end-systolic wall stress are undefined and not standardized, and the correlation between baseline stress-shortening data depends largely on the influence of the end-systolic dimension on both parameters.