心肌缺血对大鼠房室交界区的形态学影响

目的：在大鼠心肌缺血模型上研究房室交界区（房室结及房室束）的形态学变化。方法：SD大鼠20只，分为24h实验组、48h实验组、72h实验组和对照组。实验组皮下注射去甲肾上腺素5mg/Kg。取材心房室交界区，常规石蜡切片，HE或Masson三色染色，光镜下观察和照相，结果：3个缺血实验组一般心肌光镜下的形态学改变均已出现；72h实验组的房室交界区表现为传导细胞边界不清，胞浆嗜酸性增强，细胞核染色加深，传导细胞间的毛细血管扩张，而且房室束区的缺血变化比房室结区严重。结论：心肌缺血时，传导系统缺血的情况没有一般心肌严重。没有一般心肌反应快，分布也不均匀，从房室结后部到房室束逐渐加重。     

实验性心肌损伤对大鼠房室束LDH、SDH的影响

目的　观察心肌损伤时大鼠房室束乳酸脱氢酶 (LDH)、琥珀酸脱氢酶 (SDH )的变化 ,研究心肌损伤对心传导组织功能的影响。方法　SD大鼠 2 9只 ,随机分为对照组和不同时间心肌损伤 (0 5、1、3、6、12h)实验组。实验组皮下注射异丙肾上腺素 5mg/kg。NBT法染色显示LDH、SDH。将房室束分为未分叉部和分叉部 ,高倍镜 (× 40 0 )下测量各部组化反应的平均灰度值。结果　对照组和实验组房室束各部的LDH、SDH的染色均比普通心肌弱。心肌损伤时 ,房室束各部LDH的活性短时间 (0 5h)内明显增强 ,而SDH的活性则下降。从房室束的未分叉部到分叉部 ,LDH、SDH的活性减弱。结论　房室束的有氧代谢、无氧代谢均比普通心肌低 ;房室束各部的糖代谢不均衡 ;心肌损伤早期对大鼠房室束的脱氢酶有较明显的影响。     

家兔房室交界区的形态学观察及其意义

目的:观察家兔心房室结周围的纤维联系,探讨结间传导及折返机制。方法:选20只家兔心脏做房室交界区水平面及矢状面连续切片,HE染色光学显微镜下观察并拍照。结果:房间隔主要观察到3种形态的细胞,P细胞、T细胞和普通心房肌细胞。房室结由致密结和后延伸两部分组成。致密结分浅、深两层。房室结周围有3条纤维与之相连。后方为两束过渡纤维,分别源于冠状窦口及其下方,上方通过普通房肌与下房间隔相连。各肌纤维之间形成回路。结论:结间传导存在着形态学证据,肌纤维形成的回路很可能成为兴奋发生转折的部位。     

大鼠房室束的内部构筑

目的：探讨心传导系房室来形态学特征。方法：采用连续切片及图像分析的方法观察、测量了18例SD大鼠房室来的内部纤维构筑。结果：①大鼠房室束长平均1．08mm，可分为后方的未分叉部（0．42mm）和前面的分叉部（0．66mm）；②房室束主要由蒲氏细胞和T细胞构成；在结一束区P细胞与蒲氏细胞互相移行，无截然分界；③特化心肌纤维被胶原纤维分隔成细胞来，并以前后方向的纵行排列为主。结论：房室束由后向前纵行分离逐渐显著，纵行分离纤维束间的联系可能是房室束折返的解剖学基础。     

大鼠房室束的内部构筑

目的：探讨心传导系房室束形态学特征。方法：采用连续切片及图像分析的方法观察中的测量了１８例ＳＤ大鼠房室束的内部纤维构筑。结果：（１）大鼠房室束长平均１．０８ｍｍ，可分为后方的未分叉部和前面的分叉部；（２）房室束主要由蒲氏细胞和Ｔ细胞构成；在结－束区Ｐ细胞与蒲氏细胞互相移行，无截然分界；（３）特 肌纤维被胶原纤维分隔成细胞束，并以前后方面的纵行排列为主。结论；房室束由后向前纵行分离逐渐显著，纵行分离     

心脏房室交界区传导延搁的形态学基础

心脏房室交界区(Atrioventricular Junction Area,AVJ)是指心脏传导系在心房与心室之间的连接部分,形态学将其分成房室结和房室束两部分;电生理的研究将心房肌与房室结直接相连的部分也归入AVJ,称之为房室结的心房扩展部、移行区或房结区.移行区与心房肌的分界不明,大小无法确定.成人房室结的长度约7mm,房室束为10～20mm[1];成年大鼠房室结的长度约0.97mm,房室束约1.08mm[2～3].传导延搁是AVJ最主要的生理特征.     

大鼠房室结区的特化心肌纤维构筑

目的：为探讨心传导系房室结区双（多）径路传导、折返等复杂电生理的形态学基础。方法：本文采用连续切片的方法观察了18例SD大鼠房室结区的特化心肌纤维构筑。结果：①大鼠房室结位置较恒定贴于中心纤维体的右侧,大小约为0.97mm×0.51mm×0.13mm,后份薄而宽,中份厚,前份窄。③房室结可分为浅、深两层.浅层包裹深层.为上下方向的特化纤维;深层由上、下两部前后走向的细胞束组成.下部较粗大并延伸为房室柬。③房室结可明确区分出四种细胞：P细胞、T细胞、浦氏细胞及普通心肌细胞.④房室结的覆盖层为心房肌与房室结之间的特化过渡区,与房室结有较多联系,部分可穿房室环联系心室肌。⑤房室结与心房肌之间有多条路径相连.有的还与心室肌直接联系。结论：房室结内部的分层、分部及其周围与心房或心室肌的联系可能与多路径传导和折返有关。     

间隔部房室交界区解剖

正间隔部房室交界区主要包括Koch三角(内含房室结)、膜部室间隔、希氏束、左右束支等重要解剖结构。希氏束-浦肯野纤维传导系统的最重要解剖结构是:被分割成两部分的希氏束(包括希氏束的穿越部分和希氏束的分支部分)。房室交界区是心房与心室之间唯一的电通路,从组织学的角度上讲,它是指连接心房工作肌与希氏束之间的3种不同的特化组织:(1)心房肌和致密结之间的过渡细胞区;     

大鼠房室结区的特化心肌纤维构筑

目的：为探讨心传导系房室结区双（多）径路传导、折返等复杂电生理的开矿学基础。方法：本文采用连续切片的方法观察了１８例ＳＤ大鼠房室结区的特化心肌纤维构筑。结果：①大鼠房室结位置较恒定巾于中心纤维体的右侧，大小约为０．９７ｍｍ×０．５１ｍｍ×０．１３ｍｍ，后份薄而宽，中份厚，前份窄。②房室结可分为浅、深两层，浅层包裹深层，为上下方向的特化纤维；深层由上、下两部前后走向的细胞束组成，下部较粗大并延伸为房     

肢端缺血预处理对缺血性脑损伤保护作用的初探

[目的]通过观察肢端缺血预处理(LIP)对大鼠脑缺血性损伤后炎症反应及海马区神经元细胞的影响,探讨LIP对脑缺血的保护作用.[方法]选取36只SD大鼠,实验组(LIP组)15只、缺血组15只和对照组6只.实验组和缺血组设立5个时间点:6h、12h、24h、48h和72h,每点3只.通过线栓法建立大鼠大脑中动脉阻塞(MCAO)的局灶性脑缺血模型及LIP法建立脑缺血耐受模型,观察并计算每组大鼠的神经功能缺损评分(NSS)、脑组织形态学与组织学改变、炎性细胞计数以及神经元密度的变化.[结果]缺血组和实验组在各时间点的NSS均无统计学差异.实验组脑组织学病理改变程度明显轻于缺血组;在24h、48 h和72h时间点,实验组炎性细胞计数明显少于缺血组,海马CA1区正常神经元细胞明显多于缺血组,且两组相比均有统计学差异(P＜0.05).[结论]LIP诱导脑缺血耐受,可以减轻脑部炎症反应和延迟海马区神经元死亡,从而减轻缺血后脑组织损伤,对缺血性脑损伤有一定的保护作用.     

Sunao Tawara: a father of modern cardiology

Knowledge of the conduction system of the heart was greatly advanced by Tawara's work carried out in Aschoff's laboratory in Marburg at the beginning of this century. In his monograph, The Conduction System of the Mammalian Heart, published in 1906, Tawara indicated that the treelike structure of specific muscle fibers comprising the atrioventricular node, His bundle, bundle branches, and Purkinje fibers served as the pathway for atrioventricular conduction of excitation in the mammalian heart. From his own anatomic and histological findings of the conduction system, he assumed precisely that the conduction velocity of excitation in the system, except in the atrioventricular node, would be fast and that contraction as the result of excitation would take place at the various sites of the ventricles almost simultaneously. According to Tawara, a long pathway to each contracting unit and a fast conduction velocity of excitation would be a prerequisite for the effective contraction of the ventricles. Tawara's findings and assumptions provided Einthoven the theoretical basis for interpreting the electrocardiogram, resulting in rapid popularization of electrocardiography. This century has witnessed the rapid progress of cardiology, including cardiac pacing and its related sciences. This progress has its roots in the discovery of the conduction system and the development of electrocardiography that took place almost in the same period at the beginning of this century. Tawara's pioneering work on the conduction system still serves as an invaluable reference for basic and clinical research.     

Concealed Paroxysmal Atrioventricular Block: Diffuse Congenital Atrioventricular Conduction System Disorder with Nonpropagated His Bundle Depolarizations

A 2 1/2-year-old girl with bradycardia and left bundle branch block at birth began to experience "night cries" when deeply asleep. Electrophysiological study demonstrated congenital diffuse atrioventricular conduction disease with concealed paroxysmal atrioventricular block, nonpropagated His bundle depolarizations, severe sinus node abnormality, and a low atrioventricular junctional escape rhythm with probable reciprocation. After pacemaker implant, the "night cries" ceased.     

Familial Congenital Sinus Rhythm Anomalies: Clinical and Pathological Correlations

We describe pathological abnormalities in a 72-year-old male member of a family with a congenital absence of sinus rhythm and a tendency to develop atrial fibrillation at an early age, and in a 54-year-old female member of a family with cardiomyopathy and progressive conduction system disease manifested by first-degree atrioventricular (AV) block, left bundle branch block, and atrial arrhythmias. Both patients died suddenly. The absence of sinus rhythm in case 1 could be explained by marked atrophy, degeneration, and isolation of the sinoatrial (SA) node. The SA node was also diseased in the member of the other family with atrial arrhythmias. Additional common features in both cases included: fatty metamorphosis and degenerative changes of the approaches to the SA node, the atrial preferential fibers, and the approaches to the AV node, a small AV node, degenerative changes of the bundle branches, and floppy AV valves. These findings show that the pathological substrate of familial supraventricular arrhythmias consists of a diffuse involvement of the entire conduction system, bearing resemblance to pathological findings in elderly subjects with acquired sick sinus syndrome.     

Wide QRS Supraventricular Tachycardia Due to Coexisting Mahaim and Kent Pathways

In two patients with Wolff-Parkinson-White syndrome, we observed the unusual coexistence of functional Mahaim and accessory atrioventricular pathways. In the first patient, three types of reciprocating tachycardia were demonstrable: (1) anterograde conduction over the atrioventricular (AV) node with right bundle branch block (RBBB) and retrograde conduction via a right-sided atrioventricular accessory pathway; (2) anterograde conduction through the AV node with RBBB and retrograde conduction via two (right-sided and septal) anomalous pathways; and (3) anterograde conduction through nodoventricular fibers and retrograde conduction over a right-sided accessory pathway. In the second patient the reentry circuit was comprised of AV node fasciculoventricular fiber in an anterograde direction and a right-sided accessory pathway in a retrograde direction. We believe this to be the first report of triple accessory pathways, consisting of two atrioventricular and one nodoventricular connection, demonstrated by intracardiac electrophysiologic study.     

房室结双径路消融中特殊电生理现象分析与处理

目的 :分析房室结折返性心动过速 (AVNRT)慢径路消融中特殊电生理现象及处理体会。方法 :慢径路消融前常规行心内电生理检查。结果 :有特殊电生理现象者 8例 ,其中 3例患者AVNRT开始时表现为房室 2 :1传导 ,阻滞点在希氏束以上部位 ;3例患者房室结功能曲线呈连续性 ;1例为慢 -慢型AVNRT ;1例心内电生理检查未能诱发出AVNRT。所有患者慢径消融均成功。结论 :术前应行详细的心内电生理检查和仔细鉴别 ,其消融方法与典型AVNRT相同     

Complete Atrioventricular Block Associated with Non-penetrating Cardiac Trauma in a 40-year-old Man

Background

Myocardial contusion is a rare complication of blunt chest trauma. Transient conduction and rhythm problems, right ventricular dysfunction, or pulmonary embolism may occur after chest trauma, but these complications almost always occur early in the post-operative period.

Objectives

The objective is to describe a case illustrating that trauma may induce high-grade atrioventricular block.

Case Report

We report the case of a patient who developed delayed onset of complete atrioventricular block after transient complete atrioventricular block and alternating bundle branch block secondary to blunt chest trauma.

Conclusion

Even with an injury that does not seem to be caused by direct penetrating trauma to the heart, maybe every trauma patient needs an electrocardiographic evaluation. It is important to note that myocardial healing is a continuous process after trauma, and additional pathology may be revealed later in the course of healing from myocardial contusion.     

The Effect of Fascicular Block on Ventriculoatrial Conduction During AV Reentrant Tachycardia

Two patients with Wolff-Parkinson-White syndrome and surgically mapped anterior left free wall atrioventricular bypass tracts had orthodromic atrioventricular reentry tachycardia conducted with complete left bundle branch block (CLBBB), complete right bundle branch block (CRBBB), left anterior fascicular block (LAFB), and a narrow QRS. Ventriculoatrial conduction increased by 35 and 85 ms with CLBBB compatible with the left free wall location of the bypass tracts. In one patient, resolution of CLBBB occurred in two stages. Initially, left posterior fascicular block (LPFB) resolved, decreasing VA conduction by 20 ms. With resolution of the remaining LAFB, there was a further 15 ms decrease in VA conduction. In the other patient, the isolated occurrence of LAFB increased ventriculoatrial conduction by 30 ms. These changes confirmed the location of the bypass tracts in the anterior portion of the left ventricular free wall. Changes in VA conduction with fascicular block can help localize the ventricular insertion of atrioventricuiar bypass tracts.     

Double Atrial Responses to a Single Ventricular Impulse in Long RP' Tachycardia

Double atrial responses (DARs) to a single ventricular impulse have been described in patients with long RP' tachycardia. To define the determinants for the occurrence of DARs. 8 cases with long RP' tachycardia were examined. The mechanism of long RP' tachycardia was the orthodromic atrioventricular reciprocating tachycardia (AVRT) involving a slow conducting concealed accessory pathway in 4 cases and uncommon (fast-slow) type of atrioventricular nodal reentrant tachycardia (AVNRT) in the other 4 cases. Programmed and rapid ventricular pacing was performed during sinus rhythm and also rapid ventricular pacing during tachycardia (i.e., entrainment). The retrograde effective refractory period (ERP) and the retrograde maximal 1:1 conduction rate of the fast and slow conducting pathways were examined. In 1 of the 4 cases with AVRT, DARs were observed during programmed and rapid ventricular pacing, performed during sinus rhythm and also during entrainment. In 1 of the 4 cases with AVNRT, DARs were observed only during entrainment. The determinants of DARs in cases with long RP' tachycardia were: (1) presence of two different retrogradely conducting pathways; (2) short ERP of the retrograde fast and slow conducting pathways and a short minimal pacing cycle length at which 1:1 ventriculoatrial conduction occurs via these pathways; (3) crucial conduction delay in the slow conducting pathway: and (4) preexisting antegrade unidirectional block in the slow conducting pathway or the antegrade block in the slow conducting pathway produced by collision with a previous retrograde impulse during entrainment.