降钙素基因相关肽在豚鼠冠脉血流量和心脏传导系统作用的比较

本文目的在于深入研究降钙素基因相关肽（ＣＧＲＰ）对豚鼠冠状血流量以及心脏传导系统各部分的作用。采用Ｌａｎｇｅｎｄｏｒｆｆ法灌流心脏,同步记录心脏表面电图和希氏束电活动。观察应用ＣＧＲＰ前后的冠脉流量、自主心率、在相同心房周期下的房室结（ＡＨ）及希浦系传导时间（ＨＶ）、心脏出现３：２文氏传导及２：１房室传导阻滞所需的最长起搏周期（ＰＣＬ３：２,ＰＣＬ２：１）。ＣＧＲＰ（３－３０ｎｍｏｌ／Ｌ）可显著增     

三种东亚冷杉植物的核型研究

首次报道了急尖长苞冷杉ＡｂｉｅｓｇｅｏｒｇｅｉＯｒｒｖａｒ．ｓｍｉｔｈｉｉ（ＶｉｇｕｉｅｅｔＧａｕｓｓｅｎ）Ｃｈｅｎｇｅｔ．Ｌ．Ｋ．Ｆｕ,臭冷杉Ａ．ｎｅｐｈｒｏｌｅｐｉｓ（Ｔｒａｕｒｖ．）Ｍａｘｉｍ和杉松,Ａ．ｈｏｌｏｐｈｙｌｌａｍａｘｉｍ等３种东亚冷杉植物的核型,它们的核型公式分别是Ｋ（２ｎ）＝２４＝１８ｍ（２ＳＣ）＋６ｓｍ,１８ｍ（６ＳＣ）＋６ｓｍ和１４ｍ（６ＳＣ）＋１０ｓｍ,染色体相对长度组     

国产蜘蛛抱蛋属的细胞分类学研究I.四个广西特有种的核型

研究了广西特有的４种蜘蛛抱蛋属植物的核型,结果如下：巨型蜘蛛抱蛋,２ｎ＝３８＝２４ｍ（２ｓａｔ）＋２ｓｍ＋１２ｓｔ;长药蜘蛛抱蛋,２ｎ＝３６＝１８ｍ＋２ｓｍ（２ｓａｔ）＋１６ｓｔ;广西蜘蛛抱蛋,２ｎ＝３６＝１８ｍ＋４ｓｍ（２ｓａｔ）＋１４ｓｔ,隆安蜘蛛抱蛋,２ｎ＝３８＝２０ｍ＋６ｓｍ（２ｓａｔ）＋１２ｓｔ。以上核型都属２Ｃ,具有明显的二型性．     

猫冠状动脉缺血与再灌注对房室传导的影响

急性下壁心肌梗塞常引起房室传导功能障碍,然而这种障碍与心肌缺血的内在联系并不很清楚,本实验在去植物性神经传出纤维的猫上进行,通过模板匹配方法从Ｈｉｓ束电图检测Ａ,Ｈ,Ｖ波并测量两心房间期（ＡＡ）,心房波与Ｈｉｓ波间期（ＡＨ）,Ｈｉｓ波与心室波间期（ＨＶ）和心房波与心室波间期（ＡＶ）。结果如下：结扎右冠状动脉后,２０只动物的ＡＨ间期１４只出现增加（Ａ组）６只未出现增加（Ｂ组）对Ｂ组进行快速心房起博和     

3种北美冷杉的核型研究

本文首次报道３种北美冷杉Ａｂｉｅｓ ａｍａｂｉｌｉｓ、Ａ．ｇｒａｎｄｉｓ和Ａ．ｌａｓｉｏｃａｒｐａ的根尖体细胞核型、染色体参数及核型模式图。核型公式分别是Ｋ（２ｎ）＝２４＝１６ｍ（４ＳＣ）＋８ｓｍ、１４ｍ（２ＳＣ）＋１０ｓｍ和１８ｍ（４ＳＣ）＋６ｓｍ,染色体相对长度组成为２ｎ＝２４＝２Ｌ＋１２Ｍ２＋６Ｍ１＋４Ｓ、２Ｌ＋１２Ｍ２＋８Ｍ１＋２Ｓ和２Ｌ＋８Ｍ２＋１２Ｍ１＋２Ｓ。均为２Ａ核型类型。文中还讨     

蒿属植物的染色体数目和核型研究（一）

本文报道了我国蒿属６种的染色体核型,它们的核型公式分别为：牡蒿（ＡｒｔｅｍｉｓｉａｊａｐｏｎｉｃａＴｈｕｎｂ．）２ｎ＝１８＝１２ｍ＋６ｓｍ（２ＳＡＴ）;西南牡蒿（Ａ．ｐａｒｖｉｆｌｏｒａＢｕｃｂ．－Ｈａｍ．ｅｘＲｏｘｂ．）２ｎ＝３６＝３０ｍ＋４ｓｍ＋２ｓｔ（６ＳＡＴ）;多花蒿（Ａ．ｍｙｒｉａｎｔｈａＷａｌｌ．ｅｘＢｅｓｓ．）２ｎ＝３６＝３０ｍ＋６ｓｍ：牛尾蒿（Ａ．ｄｕｂｉａＷａｌｌ．ｅｘＢｅｓｓ．）２ｎ＝３６＝２８ｍ＋８ｓｍ（２ＳＡＴ）;野艾蒿（Ａ．ｌａｖａｎｄｕｌａｅｆｏｌｉａＤＣ．）２ｎ＝５４＝４２ｍ＋１２ｓｍ;荚毛蒿（Ａ．ｖｅｌｕｔｉｎａＰａｍｐ．）２ｎ＝５４＝３６ｍ＋１８ｓｍ．     

黑松,马尾松及其杂种的核型比较

分析了黑松、马尾松及其杂种的核型。其核型公式：黑松为Ｋ（２ｎ）＝２４－２０ｍ（６＿（ＳＡＴ）））＋４ｓｍ;杂种为Ｋ（２ｎ）＝２４＝２３ｍ＋１ｓｍ;马尾松为Ｋ（２ｎ）＝２４－２４ｍ（４＿（ＳＡＴ））。相对长度和臂比方差分析表明,两亲本和杂种差异显著。杂种在相对长度、全组染色体总长、最长与最短染色体比、臂比平均值以及染色体类型上均处于双亲之间。这些研究结果为进一步研究该天然杂种提供必要的细胞学资料。     

山东四种草本植物的核型研究

本文对山东４种草本植物进行了染色体研究。结果表明：阿尔泰狗哇花（Ｈｅｔｅｒｏｐａｐｐｕｓａｌ ｔａｉｃｕｓ（Ｗｉｌｄ）Ｎａｖｏｐｏｋｒ）的染色体数目为２ｎ＝３６,核型公式为Ｋ（２ｎ）＝３６＝３６ｍ,核型“１Ａ”型;求米草（Ｏｐｌｉｓｍｅｎｕｓｕｎｄｕｌａｔｉｆｏｌｉｕｓ（Ａｒｄｕｉｎｏ）ＲｏｅｍｅｔＳｃｈｕｌｔ）的染色体数目为２ｎ＝１２,核型公式为Ｋ（２ｎ）＝１２＝８ｍ＋４ｓｍ,核型“２Ａ”型;红秋葵（Ｈｉｂｉｓｃｕｓｃｏｃｉｎｅｕｓ（Ｍｅｄｉｃ）Ｗａｌｔ）的染色体数目为２ｎ＝３８,核型公式为Ｋ（２ｎ）＝３８＝１４ｍ＋２２ｓｍ＋２ｓｔ,核型“２Ｂ”型;蟋蟀草（Ｅｌｅｕｓｉｎｅｉｎｄｉｃａ（Ｌ）Ｇａｅｒｔｎ）的染色体数目为２ｎ＝１８,核型公式为ｋ（２ｎ）＝１８＝１６ｍ＋２ｓｍ,核型“２Ａ”型。     

安徽黄精属的细胞分类学研究

本文首次报道黄精属ＰｏｌｙｇｏｎａｔｕｍＭｉｌｌ我国三种特有植物的染色体数目和核型,结果如下：安徽黄精Ｐ．ａｎｈｕｉｅｎｓｅ发现两个细胞型：（１）２ｎ＝２４＝４ｍ＋６ｓｍ＋１４ｓｔ;（２）２ｎ＝２０＝４ｍ十６ｓｍ＋１０ｓｔ;　　黄精Ｐ．ｌａｎｇｙａｅｎｓｙ２ｎ＝１８＝６ｍ＋８ｓｍ＋４ｔ;距药黄精Ｐ．ｆｒａｎｃｈｅｔｉｉ有三个细胞型：（１）２ｎ＝２２＝８ｍ＋８ｓｍ（２ｓｃ）＋６ｓｔ;（２）２ｎ＝２０＝２ｍ＋１４ｓｍ＋４ｓｔ;（３）２ｎ＝１８＝４ｍ＋８ｓｍ＋４ｓｔ＋２Ｔ,全部属３Ｂ核型。黄精属植物安徽共有１０种,本文对９种黄精的染色体数目、核型进行了比较研究,发现它们可划分成三个类群,与中国植物志（第十五卷）的形态分类基本相符。     

中国樟科5属9种植物的核型研究

报道了我国樟科（Ｌａｕｒａｃｅａｅ）５属９种植物核型研究结果,其中７种染色体数目为首次报道,核型结果为：樟（Ｃｉｎｎａｍｏｕｍｃａｍｐｈｏｒａ）２０ｍ＋４ｓｍ油樟（Ｓｉｎｎａｍｏｕｍｌｏｎｇｅｐａｎｉｃｕｌａｔｕｍ）２０ｍ＋４ｓｍ;黑壳楠（Ｌｉｎｄｅｒａｍｅｇａｐｈｙｌｌａ）１８ｍ（２ＳＡＴ）＋６ｓｍ,山苍子（Ｌｉｎｄｅｒａｃｕｂｅｂａ）１６ｍ＋８ｓｍ,香叶树（Ｌｉｎｄｅｒａｍｅｇａｐｈｙｌｌａ）     

Electrophysiological effects of ethmozine in perfused rabbit hearts

His-bundle electrocardiography was used to evaluate the effects of ethmozine on cardiac conduction in isolated perfused rabbit hearts electrically driven at cycle lengths of 320 and 250 ms. There was no significant change in conduction until high concentrations of ethmozine were reached. His-Purkinje and atrioventricular (AV) nodal conduction were slowed significantly at 0.1 microgram/mL and atrial conduction at 1.0 microgram/mL. Conduction block occurred at 10.0 micrograms/mL in all the hearts treated. Effects of the drug (0.1 and 0.01 microgram/mL) on conduction of extrasystoles were also studied in hearts driven at a basic cycle length of 270 ms. No significant change was observed in atrial conduction of extrasystoles throughout the coupling intervals tested at both concentrations. Ethmozine (0.01 and 0.1 microgram/mL) caused slowing of His-Purkinje conduction of extrasystoles but the effect of the drug did not change as a function of the coupling interval. An interval-dependent increase in AV-nodal conduction time was observed, with the maximum slowing of conduction occurring at coupling intervals close to the effective refractory period of the AV node. AV-nodal functional refractory period was increased significantly by ethmozine (0.01 and 0.1 microgram/mL). The effective refractory period was significantly increased only at the higher concentration.     

Functional mathematical model of dual pathway AV nodal conduction

Dual atrioventricular (AV) nodal pathway physiology is described as two different wave fronts that propagate from the atria to the His bundle: one with a longer effective refractory period [fast pathway (FP)] and a second with a shorter effective refractory period [slow pathway (SP)]. By using His electrogram alternance, we have developed a mathematical model of AV conduction that incorporates dual AV nodal pathway physiology. Experiments were performed on five rabbit atrial-AV nodal preparations to develop and test the presented model. His electrogram alternances from the inferior margin of the His bundle were used to identify fast and slow wave front propagations. The ability to predict AV conduction time and the interaction between FP and SP wave fronts have been analyzed during regular and irregular atrial rhythms (e.g., atrial fibrillation). In addition, the role of dual AV nodal pathway wave fronts in the generation of Wenckebach periodicities has been illustrated. Finally, AV node ablative modifications have been evaluated. The model accurately reproduced interactions between FP and SP during regular and irregular atrial pacing protocols. In all experiments, specificity and sensitivity higher than 85% were obtained in the prediction of the pathway responsible for conduction. It has been shown that, during atrial fibrillation, the SP ablation significantly increased the mean HH interval (204 ± 39 vs. 274 ± 50 ms, P < 0.05), whereas FP ablation did not produce significant slowing of ventricular rate. The presented mathematical model can help in understanding some of the intriguing AV node mechanisms and should be considered as a step forward in the studies of AV nodal conduction.     

Effect of Ibutilide on the Canine Cardiac Conduction System

The objective of the study was to evaluate the effect of ibutilide on canine cardiac sinoatrial and atrioventricular nodes (AVNs). For this purpose, 18 mongrel dogs were injected intravenously with ibutilide and the changes in heart rate, sinus node recovery time, and AVN were measured. Our data show that ibutilide administration caused significant suppression of the sinus atrial node, the peak response time was 20?C30?min, and the heart rate was restored to pre-drug administration level. After receiving ibutilide, 1 animal had a 5?s sinus pause, and after 5?min of ibutilide administration, 1 dog showed 2:1 atrioventricular conduction. Therefore, it was concluded that ibutilide had a suppressive effect on the sinoatrial node and AVN.     

One-Dimensional Mathematical Model of the Atrioventricular Node Including Atrio-Nodal, Nodal, and Nodal-His Cells

Mathematical models are a repository of knowledge as well as research and teaching tools. Although action potential models have been developed for most regions of the heart, there is no model for the atrioventricular node (AVN). We have developed action potential models for single atrio-nodal, nodal, and nodal-His cells. The models have the same action potential shapes and refractoriness as observed in experiments. Using these models, together with models for the sinoatrial node (SAN) and atrial muscle, we have developed a one-dimensional (1D) multicellular model including the SAN and AVN. The multicellular model has slow and fast pathways into the AVN and using it we have analyzed the rich behavior of the AVN. Under normal conditions, action potentials were initiated in the SAN center and then propagated through the atrium and AVN. The relationship between the AVN conduction time and the timing of a premature stimulus (conduction curve) is consistent with experimental data. After premature stimulation, atrioventricular nodal reentry could occur. After slow pathway ablation or block of the L-type Ca²⁺ current, atrioventricular nodal reentry was abolished. During atrial fibrillation, the AVN limited the number of action potentials transmitted to the ventricle. In the absence of SAN pacemaking, the inferior nodal extension acted as the pacemaker. In conclusion, we have developed what we believe is the first detailed mathematical model of the AVN and it shows the typical physiological and pathophysiological characteristics of the tissue. The model can be used as a tool to analyze the complex structure and behavior of the AVN.     

Interesting response to ventricular overdrive pacing during regular narrow QRS tachycardia. What is the mechanism?

33 year old gentleman has undergone an electrophysiology study for recurrent paroxysmal palpitation. During one of the episodes of palpitation a regular narrow QRS tachycardia was documented which has terminated with intravenous adenosine. Baseline electrocardiogram did not show any pre-excitation. Atrial-His (AH) and His-Ventricular (HV) intervals were normal at baseline. There was no evidence of dual atrioventricular (AV) nodal physiology. Earliest atrial electrogram during ventricular pacing was recorded at coronary sinus (CS) 9,10 dipoles placed at CS OS region. Narrow QRS tachycardia with cycle length (TCL) of 400 ms and earliest retrograde atrial activation at CS 9,10 dipoles was induced with programmed ventricular stimulation. Ventricular overdrive (VOD) pacing was performed at 30 ms shorter than TCL during the tachycardia (Fig: 1). What is the mechanism of tachycardia?     

The development of the conduction system in the mouse embryo heart: IV. Differentiation of the atrioventricular conduction system

The development of the atrioventricular conduction system in the mouse heart has been studied by light and electron microscopy from the time of the completion of ventricular septation to fetal stage II, 13–16 days postcoitum. At the beginning of this period the already established atrioventricular node (AVN) enlarges rapidly into the dorsal AV cushion from the primitive AV tract, reaching almost its full fetal size when septation is complete. The development of the atrionodal interconnections is a slow and complex process. The dorsal atrial myocardium develops on both sides of the node, establishing a muscular overlay over its proximal aspect, and also incorporating the former AV tract. At this time also, the developing muscular interatrial septum grows downward to establish contact with the node, the sinus venosus, and the myocardium of the right and left atrial walls. The distally proceeding differentiation of the ab initio continuous conduction pathway along the AVN, His bundle, and bundle branches demonstrates a progressive and sequential development of high cellular glycogen content. Progressive isolation of the atrioventricular conduction system leading to (still incomplete) insulation by connective tissue, has been observed.     

Effects of pituitary adenylate cyclase-activating polypeptide on canine atrial electrophysiology

We hypothesized that pituitary adenylate cyclase-activating polypeptide (PACAP) activates intracardiac postganglionic parasympathetic nerves and has a different effect than cervical vagal stimulation. We measured effective refractory period (ERP) and conduction velocity at four atrial sites [high right atrium (HRA), low right atrium (LRA), high left atrium (HLA), and low left atrium (LLA)] and minimum atrial fibrillation (AF) cycle length at 12 atrial sites during cervical vagal stimulation and after PACAP in 26 autonomically decentralized, open-chest, anesthetized dogs. PACAP shortened ERP to a similar extent at all four sites (HRA, 58 +/- 2.0 ms; LRA, 60 +/- 6.3 ms; HLA, 68 +/- 11.5 ms; and LLA, 60 +/- 8.3 ms). Low- and high-intensity vagal stimulation shortened ERP at the HRA, but not in the other atrial sites (low-intensity stimulation: HRA, 64 +/- 4.0 ms; LRA, 126 +/- 5.1 ms; HLA, 110 +/- 9.5 ms; and LLA, 102 +/- 11.5 ms; high-intensity stimulation: HRA, 58 +/- 4.2 ms; and HLA, 101 +/- 4.0 ms). Conduction velocity was not altered by any intervention. Minimum AF cycle length after PACAP was similar in both atria but was shorter in the right atrium than in the left atrium during vagal stimulation. After atropine administration, no interventions changed ERP. These results suggest that PACAP shortens atrial refractoriness uniformly in both atria through activation of intrinsic cardiac nerves, not all of which are activated by cervical vagal stimulation.     

Atrial natriuretic factor attenuates sympathetic neuroeffector responses in hindlimb vasculature of rabbits

To determine whether atrial natriuretic factor (ANF) affects vasoconstrictor responses to electrical stimulation of sympathetic nerves or intra-arterial norepinephrine (NE), changes in perfusion pressure were measured during lumbar sympathetic nerve stimulation (LSNS, 1-8 Hz), or administration of NE (50-200 ng), in an isolated constant flow-perfused hindlimb of chloralose-anesthetized rabbit before and after intra-arterial infusion of ANF (0.5 ng.mL-1.min-1). ANF significantly attenuated responses to LSNS (relative potency, RP = 0.65) and to NE (RP = 0.47). We conclude that ANF attenuates vasoconstrictor responses to both LSNS and NE. Thus ANF alters sympathetic nervous system mediated changes in vascular resistance possibly at the neuroeffector site.     

Phasic influences of vagal stimulation on atrioventricular conduction

The beat-by-beat changes in atrioventricular (AV) conduction evoked by constant frequency and phase-coupled vagal stimulation were examined both qualitatively and quantitatively in 13 anesthetized dogs. The effects of pacing cycle length and sympathetic activity on the vagally induced phasic changes in AV conduction were also characterized. When the vagal stimulus interval was nearly equal to the pacing cycle length and the vagal stimulus moved progressively through the cardiac cycle, AV interval oscillated in a rhythmic fashion. The rhythmicity of the vagally induced AV interval oscillations was altered substantially by changes in either the vagal stimulus interval or the pacing cycle length. The vagally induced AV interval oscillations were abolished during phase-coupled vagal stimulation; however, the magnitude of the resultant steady-state AV interval depended on the time relative to the phase of the cardiac cycle that the vagal stimulus was delivered. In the presence or absence of sympathetic stimulation, a vagal stimulus falling approximately 200 ms prior to atrial depolarization evoked the greatest prolongation in AV interval, regardless of the pacing cycle length. Additionally, the effects of combined sympathetic and phase-dependent vagal stimulation on the AV interval were additive. These data confirm that the influence of a vagal stimulus on AV interval can be predicted from the phase in the cardiac cycle that the vagal stimulus is delivered. Moreover, this phase dependency of vagal effects evokes marked qualitative variations in AV interval response patterns when either the vagal stimulus interval or the pacing cycle length is altered.