人心和山羊心脏上、下腔静脉肌袖大体解剖

目的:观测人和山羊上、下腔静脉肌袖结构特点,为治疗局灶性心房颤动积累解剖学资料。方法:采用大体解剖方法观测人心(20例)和羊心(40例)的上、下腔静脉及其表面的心肌纤维。结果:人心上腔静脉肌袖的长和宽分别为(1.91±0.39)cm、(2.41±0.26)cm,下腔静脉肌袖的长和宽分别为(1.32±0.32)cm,(3.06±0.52)cm;羊心上(前)腔静脉肌袖的长和宽分别为(1.41±1.00)cm、(1.05±0.26)cm,下(后)腔静脉肌袖的长和宽分别为(0.81±0.48)cm,(1.03±0.28)cm。人和羊心脏的上腔静脉肌袖出现率均为100%;下腔静脉肌袖的出现率分别为88.89%和98%。肌纤维多数来源于右心房前后壁,也有来自于左心房或左右心房的。结论:①上腔静脉肌袖是人和羊普遍存在的解剖结构,人的下腔静脉肌袖出现率明显低于羊,可能是上腔静脉肌袖引起局灶性心房颤动多于下腔静脉肌袖的解剖学基础。②上腔静脉肌袖是构成左右房的又一重要通路。     

Prosopo-Thoracopagus Conjoined Twins and Other Cephalopagus-Thoracopagus Intermediates: Case Report and Review of the Literature

Prosopo-thoracopagus twins are united from the face down to the umbilicus, none with union in the brain but all with visceral anomalies intermediate between those of cephalopagus and thoracopagus. In a review of over 1200 cases of conjoined twins reported during the past 100 years, there were 14 that illustrate the continuum between cephalopagus and thoracopagus, including three that were united only from the cervical region to the umbilicus. Classic cephalopagus twins are joined from the top of the head to the umbilicus, sharing a single foregut as well as two relatively normal hearts, the “posterior” one often diminished. Typical thoracopagus, however, are conjoined only from the upper thorax to the umbilicus, each twin with a normal foregut but both sharing a single complex multiventricular heart. The intermediate cases shared either a single very abnormal heart or two hearts united by double aortic arches, and all except one had a single foregut. It is these cases intermediate between cephalopagus and thoracopagus which are the subject of this report. Received September 11, 1996; accepted December 16, 1996     

丹红注射液减轻DPPH所致离体心脏功能损伤的作用研究

[目的]在大鼠离体心脏灌流系统上观察丹红注射液对二苯基三硝基苯肼(DPPH)自由基所致心功能损伤的保护作用。[方法]大鼠离体心脏采用Langendorff灌流,基础平衡30 min后进行各组预给药10 min后,用含0.25μmol/L DPPH的K-H液灌流心脏10 min,造成心脏功能损伤,最后用K-H液灌流10 min进行恢复。记录灌注压(PP)、左心室舒张压(LVEDP)、左心室收缩压(LVSP)、心率(HR)、左心室内压最大上升速率(+dp/dtmax)、左心室内压最大下降速率(-dp/dtmax),并计算心率压力乘积(RPP)。[结果]丹红注射液灌注10min可以显著降低灌注压,扩张冠状动脉。DPPH自由基损伤后RPP、+dp/dtmax显著降低,-dp/dtmax显著升高。用含丹红注射液的K-H液预处理10min,丹红2.5μL/mL组、丹红5μL/mL组可以减轻DPPH自由基导致的心脏功能损伤。[结论]在离体心脏模型中丹红注射液能扩张冠状动脉,减轻外源性自由基对心脏功能的损伤。     

Possible mechanisms of mitral regurgitation in dilated hearts: A study using transesophageal echocardiography

Hypothesis: This study was undertaken to clarify the mechanisms of mitral regurgitation (MR) in dilated hearts. Methods: in all, 68 patients with dilated heart and MR, including 26 patients with dilated cardiomyopathy (DCM), 24 with prior anterior myocardial infarction (A-MI), and 18 with prior posteroinferior myocardial infarction (I-MI), as well as 25 normal subjects were examined by transesophageal two-dimensional and color Doppler echocardiography. Results: The maximum area of the MR signal in the DCM group correlated positively with the anteroposterior diameter of the mitral annulus at late systole. Although the coaptation edge length of the anterior and posterior mitral leaflets appeared shorter in dilated hearts than in the hearts of controls, a significant difference did not exist. The length of the coaptation edge correlated negatively with the maximum area of the MR signal in all dilated hearts, and characteristic systolic displacement of the coaptation point of both mitral leaflets occurred. The MI groups demonstrated anterior and posterior displacement in the direction of the short axis of the left ventricle in the A-MI and I-MI groups, respectively. However, the DCM group demonstrated inferior displacement toward the long axis of the left ventricle; its magnitude correlated positively with the maximum area of the MR signal. Conclusion: A major cause of MR in dilated hearts is mitral malcoaptation due to displacement of the coaptation point of the mitral leaflets along the long or short axis of the left ventricle. This is caused by left ventricular enlargement and/or asynergy of the left ventricular wall, rather than by a decrease in mitral coaptation edge length due to mitral annular dilation.     

Intracoronary superoxide dismutase for the treatment of “reperfusion injury” A blind randomized placebo-controlled trial in ischemic,reperfused porcine hearts

Summary The effect of recombinant human superoxide dismutase (rh-SOD) on infarct size was investigated in porcine hearts. The left anterior descending coronary artery was occluded in each of 24 anesthetized pigs for 45 min and reperfused for 24 h. The animals were randomly assigned to either rh-SOD (n=12) or placebo treatment (n=12). 2 min before reperfusion, an intracoronary (i.c.) infusion of rh-SOD (total dose: 2000 U/kg) or placebo was started which lasted for up to 45 min reperfusion. At the end of the experiment, the infarcted myocardium was assessed using a tetrazolium stain (NBT) and related to the risk region which was determined with a fluorescent dye. Two pigs of the SOD group and one of the control group died before the end of the experiments. Except for a lower calculated myocardial oxygen consumption and a lower dp/dt_max in the SOD group during ischemia, hemodynamic parameters of the two groups did not differ significantly. rh-SOD i.c. treatment during reperfusion did not reduce infarct size significantly. Infarct size amounted to 74±13% in the control group and to 66±19% in the treated group. The incidence of reperfusion arrhythmias was not affected by rh-SOD treatment. It is concluded that i.c. rh-SOD treatment at the beginning of reperfusion neither significantly reduces infarct size nor diminishes the incidence of reperfusion arrhythmias in this preparation.This study was supported by a grant from Deutsche Forschungsgemeinschaft, SFB-330 Organprotektion Göttingen, F.R.G.This paper includes parts of the Habilitationsschrift of Dr. H. H. Klein     

Sodium channel haploinsufficiency and structural change in ventricular arrhythmogenesis

Normal cardiac excitation involves orderly conduction of electrical activation and recovery dependent upon surface membrane, voltage‐gated, sodium (Na⁺) channel α‐subunits (Na_v1.5). We summarize experimental studies of physiological and clinical consequences of loss‐of‐function Na⁺ channel mutations. Of these conditions, Brugada syndrome (BrS) and progressive cardiac conduction defect (PCCD) are associated with sudden, often fatal, ventricular tachycardia (VT) or fibrillation. Mouse Scn5a^+/? hearts replicate important clinical phenotypes modelling these human conditions. The arrhythmic phenotype is associated not only with the primary biophysical change but also with additional, anatomical abnormalities, in turn dependent upon age and sex, each themselves exerting arrhythmic effects. Available evidence suggests a unified binary scheme for the development of arrhythmia in both BrS and PCCD. Previous biophysical studies suggested that Na_v1.5 deficiency produces a background electrophysiological defect compromising conduction, thereby producing an arrhythmic substrate unmasked by flecainide or ajmaline challenge. More recent reports further suggest a progressive decline in conduction velocity and increase in its dispersion particularly in ageing male Na_v1.5 haploinsufficient compared to WT hearts. This appears to involve a selective appearance of slow conduction at the expense of rapidly conducting pathways with changes in their frequency distributions. These changes were related to increased cardiac fibrosis. It is thus the combination of the structural and biophysical changes both accentuating arrhythmic substrate that may produce arrhythmic tendency. This binary scheme explains the combined requirement for separate, biophysical and structural changes, particularly occurring in ageing Na_v1.5 haploinsufficient males in producing clinical arrhythmia.     

Organ-cultured chick embryonic hearts of various ages. I. Electrophysiology

Tetrodotoxin (TTX)-insensitive slow Na⁺ channels are converted or replaced by TTX-sensitive fast Na⁺ channels during normal embryonic development of the chick heart, and rapid reversion occurs in monolayer cell culture (denervated). Fast Na⁺ channels first appear at 4 to 5 days, which is about the time of innervation. Studies were done to determine whether changes in cation channels will occur while hearts are in organ culture. To test whether fast Na⁺ channels will develop in the absence of innervation, hearts from chick embryos 2 to 3 days old were placed into culture for 6 to 8 days. Although the resting potentials of the ventricular cells were about the same as those obtained from fresh 8 to 10 day old hearts, the maximum rate of rise of the action potentials ($\text{+}\text{V}\text{?}{}_{\mathrm{<mtext>max</mtext>}}$) did not reach the high value (about 80 V/s) expected from the calendar age. Instead $\text{+}\text{V}\text{?}{}_{\mathrm{<mtext>max</mtext>}}$ remained at about the same value (12 V/s) that the hearts had when placed into culture. The action potentials were completely insensitive to TTX. The slow channels admit primarily Na⁺ and not Ca²⁺ because Mn²⁺ (1 mm) and lowering [Ca²⁺]₀ to nearly zero by EGTA did not diminish $\text{+}\text{V}\text{?}{}_{\mathrm{<mtext>max</mtext>}}$. To test whether the fast Na⁺ channels disappear in organ culture, hearts from embryos 15 to 19 days old were cultured as whole hearts or minced hearts. The whole hearts survived well for 1 to 6 days; the $\text{+}\text{V}\text{?}{}_{\mathrm{<mtext>max</mtext>}}$ values remained high (～ 100 V/s), and TTX completely blocked the action potentials. The minced hearts had variable $\text{+}\text{V}\text{?}{}_{\mathrm{<mtext>max</mtext>}}$ values, depending on the piece. Those pieces which had a low $\text{+}\text{V}\text{?}{}_{\mathrm{<mtext>max</mtext>}}$ were insensitive to TTX, and those which had a high or intermediate $\text{+}\text{V}\text{?}{}_{\mathrm{<mtext>max</mtext>}}$, were reduced to 5 to 20 V/s by TTX; these persisting responses in TTX were not blocked by Mn²⁺ or zero [Ca²⁺]₀. The results suggest that, while in organ culture, young hearts do not gain fast Na⁺ channels or lose the slow Na⁺ channels that would normally occur in situ. Organ-cultured old hearts left intact do not lose their fast Na⁺ channels. Thus, young or old hearts retain the channels that they originally possessed when placed into culture. Mincing initiates a gain of slow Na⁺ channels, and in some pieces, a partial loss of fast Na⁺ channels.     

雷米普利预适应对大鼠心脏延迟性的保护作用

目的探讨雷米普利预适应对大鼠离体心脏缺血-再灌注损伤的延迟性保护作用及机制。方法离体大鼠心脏采用Langendoff灌流法建立心肌缺血再灌注损伤模型。35只大鼠随机分为5组：（1）对照组；（2）缺血-再灌组（I／R组）；（3）雷米普利预处理组（Ramipril 0．05mg／kg）；（4）雷米普利预处理组（Ramipril 0．1mg／kg）：（5）HOE140＋雷米普利预处理组（HOE1400．1mg／kg＋Ramipril 0．1mg／kg）。每组7只。记录左室内压（LVP）、左室内压最大上升速率（＋dp／dtmax）、左室舒张末压（LVEDP）、心率（HR），定时收集冠脉流出液测量冠脉流量（CF）和肌酸激酶（CK）活性。再灌注结束后采用分光光度法测定心肌组织中丙二醛（MDA）含量。结果（1）与对照组比较，I／R组缺血-再灌注后10、20、30min可显著降低LVP和＋dp／dt max（P〈0.01），升高LVEDP（P〈0．01），降低CF（P〈0．01），缺血-再灌注后10、20min显著降低HR（P〈0．01）；（2）与I／R组比较，Ramipril 0．05mg／kg组缺血-再灌注后20、30min可显著升高LVP（P〈0．01）及增加CF（P〈0．05）；缺血-再灌注后10、20、30min可显著升高＋dp／dtmax（P〈0.01），降低LVEDP（P〈0.01）；（3）与I／R组比较，Ramipril 0．1mg／kg组缺血-再灌注后10、20、30min可显著升高LVP（P〈0．01），升高＋dp／dtmax（P〈0.01），降低LVEDP（P〈0.01）；增加CF（P〈0.05）；（4）与Ramipril 0．1mg／kg组比较，HOE1400．1mg／kg＋Ramipril 0．1mg／kg组缺血-再灌注后10、20、30min可显著降低LVP（P〈0.05）；降低＋dp／dtmax（P〈0．05）；升高LVEDP（P〈0.05）；降低CF（P〈0．05）；（5）I／R组缺血-再灌注后10、20、30minCK与对照组比较，均有显著性差异（P均〈0.01）；Ramipril 0．05mg／kg组及Ramipril 0．1mg／kg组缺血-再灌注后10、20、30minCK与I／R组比较，均有显著性差异（P均〈0.01）；HOE1400．1mg／kg＋Ramipril 0．1mg／kg组缺血-再灌注后10、20、30minCK与Ramipril 0．05mg／kg组及Ramipril 0．1mg／kg组比较，均有显著性差异（P均〈0.01）；（6）实验前24h舌下静脉注射雷米普利0．05mg／kg或0．1mg／kg均可显著降低缺血-再灌注心肌组织中MDA含量。结论雷米普利对缺血再灌注诱导离体大鼠心肌损伤具有延迟性保护作用，其机制可能是与激活缓激肽B2受体，减少缓激肽降解有关。     

Lack of a role for blood platelets in the uptake of 5-hydroxytryptamine by the rabbit heart

Perfused rabbit hearts removed 5-hydroxytryptamine (5-HT) from a perfusion solution of 1.0 × 10^?8 g ml^?1 and at the same time their endogenous 5-HT concentrations increased. Pretreatment of animals with heparin did not affect either the removal of 5-HT from the perfusion fluid or its accumulation in the heart. The proportion of 5-HT removed from the perfusion fluid which was subsequently found in the heart was small in both the heparinised and the non-heparinised groups. The results suggest that platelets trapped within heart tissue are unimportant for cardiac 5-HT uptake.     

Scanning Electron Microscopic Evaluation of the Surfaces of Artificial Hearts

This Report summarizes the surface changes seen in artificial hearts implanted in calves for periods up to four months. Fabrication defects as well as degradation resulting from wear are identified. SEM evaluation of the blood contacting surface as well as the surface of the diaphragm associated with the drive mechanism has revealed potential problems with current heart designs and methods of fabrication. Materials evaluation of implanted hearts is crucial for a clinically useful system to evolve.