Museum preparations of the conducting system of the heart.

A technique of dissection of the sinuatrial node and of the atrioventricular node and main conducting bundles of the ox heart, without injection, is described. Museum specimens prepared in this way are illustrated.     

Penetrating knife injury to the heart.

A 39-year-old man attempted to kill himself using a small knife to penetrate the left anterior chest wall because of trouble at work and with his girlfriend. On arrival at the emergency room, his consciousness was not clear and vital signs were unstable. The knife remained vertically located in the left anterior chest wall. A large left hemothorax was identified by chest X-ray, and moderate cardiac tamponade was detected by echocardiography. Left-sided chest drainage was performed by inserting a chest drainage tube, and about 2500 ml of hemorrhagic effusion was drained. An emergency operation was performed to relieve the cardiac tamponade and repair the penetrating cardiac injury. About an hour after arrival at the emergency room, a median sternotomy was performed in the operating room. The knife had injured the surface of the right ventricular outflow tract, the left lung, and the 3rd intercostal artery and vein. Cardiopulmonary bypass was immediately prepared for the repair of the cardiac injury. The wounds were successfully repaired with pledgeted sutures under cardiac beating. The postoperative course was uneventful with no sign of infection. The patient was discharged at 9 days after the operation. Here we have reported a case of successful surgical repair of a penetrating knife injury to the heart, which was managed by immediate resuscitation and emergency surgery.     

缺血后处理对大鼠离体心脏缺血再灌注损伤的作用

目的探讨缺血后处理对大鼠离体心脏缺血再灌注损伤的作用。方法24只Wistar大鼠,随机分为3组(n=8):正常对照组(C组)、缺血再灌注组(I/R组)、缺血后处理组(IPC组)。采用大鼠离体心脏Langendorff灌流模型,C组用K-H液灌注160min;I/R组全心缺血40 min,再灌注120 min; IPC组全心缺血40 min后,再灌注10 s,缺血10 s,反复6次,然后持续再灌注118 min。测定再灌注15、30、120 min时冠脉流量(CF)及冠脉流出液心肌肌钙蛋白I(cTnI)浓度,再灌注120 min时,取心肌组织,测定丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性,电镜下观察心肌细胞超微结构。结果缺血再灌注可导致CF降低,冠脉流出液cTnI浓度升高,心肌SOD活性下降,MDA含量升高,心肌细胞超微结构产生病理学改变,缺血后处理可减弱上述改变。结论缺血后处理减轻脂质过氧化反应,对大鼠离体缺血再灌注心脏产生保护作用。     

麻醉药物对心肌缺血再灌注损伤的保护研究进展

心肌缺血再灌注损伤(MIRI)是临床上一类非常常见而严重的并发症,被麻醉学界广泛关注.实际上,自从1985年Freedman首次报道安氟醚能改善缺血后心功能以来,如何找到防治MIRI经济有效的方法,已经成为这个领域多年来研究的方向.大量实验证明,多种麻醉药物对MIRI具有不同方面的保护作用.此文综述了国内外关于麻醉药物以及具有中国特色和优势的中药复方制剂对MIRI保护研究的进展,其中重点综述几种代表性药物,如瑞芬太尼、丙泊酚、咪达唑仑、参附注射液等,并总结了近年来这一方向的研究成果.     

丙酮酸乙酯预先给药对大鼠离体心脏缺血再灌注损伤的影响

目的 探讨丙酮酸乙酯预先给药对大鼠离体心脏缺血再灌注损伤的影响.方法 雄性SD大鼠24只,体重250～320 g,3月龄,制备Langendorff主动脉逆行灌注模型.随机分为3组(n=8),对照组(C组):改良的K-H缓冲液持续灌流120 min;缺血再灌注组(IR组)改良的K-H缓冲液平衡灌注30 min后,全心停灌30 min,再灌注60 min;丙酮酸乙酯组(EP组)改良的K-H缓冲液平衡灌注15 min后,再用含2 mmol/L丙酮酸乙酯的改良K-H缓冲液平衡灌注15 min,全心停灌30 min,最后用含2 mmol/L丙酮酸乙酯的改良K-H缓冲液再灌注60 min.记录各组平衡灌注15 min(基础值)、再灌注10、30、60 min的左室收缩峰压(LVSP)、左心室内压上升/下降最大速率(±dp/dtmax )、冠脉流量(CF),再灌注60 min时测定心肌ATP含量、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性及冠状动脉流出液中乳酸脱氢酶(LDH)活性、肌酸激酶(CK)的活性.结果 与C组比较,IR组CF、LVSP、±dp/dtmax、SOD活性、ATP含量降低,MDA含量、CK活性、LDH活性升高(P＜0.05),EP组差异无统计学意义(P＞0.05);与IR组比较,EP组CF、LVSP、±dp/dtmax、SOD活性、ATP含量升高,MDA含量、CK活性、LDH活性降低(P＜0.05).结论 丙酮酸乙酯2 mmol/L预先给药通过提高心肌ATP含量,降低氧化应激反应,可减轻大鼠离体心脏缺血再灌注损伤.     

Studies of myocardial protection in the immature heart. III. Models of ischemic and hypoxic/ischemic injury in the immature puppy heart

This study compares the metabolic and functional effects of three different models of ischemia in the immature heart. The intent was (1) to develop a model of energy-depleted and functionally depressed heart to be used in subsequent studies of myocardial protection and (2) to characterize the biochemical changes following different interventions. Forty-five minutes of normothermic global ischemia produced severe depletion of adenosine triphosphate and creatine phosphate (greater than 70%) but was associated with 85% +/- 10% recovery of left ventricular function. Postischemic functional depression (less than 30% recovery) could be produced by either (1) extending the ischemic duration to 60 minutes or (2) preceding 45 minutes of ischemia by 60 minutes of hypoxic stress (oxygen tension 25 to 30 mm Hg). Neither of these more severe interventions caused more profound depletion of adenosine triphosphate or creatine phosphate, but hypoxic stress produced marked tissue depletion of glutamate (52%) and aspartate (48%) before aortic clamping. Longer ischemia or preceding hypoxia led to greater myocardial accumulation of lactate (greater than 250 versus 104 mumol/gm dry weight) and succinate (18 versus 11 mumol/gm dry weight) during aortic clamping, p less than 0.05 versus 45 minutes of ischemia) and greater postischemic depression and amino acid (greater than 65% aspartate depletion) and carbohydrate (greater than 50% glycogen depletion) metabolism, p less than 0.05 versus simple ischemia. These findings suggest that more severe ischemic/hypoxic models are needed in immature hearts to produce functional depression, and the biochemical analyses suggest the characteristics of metabolic defects that must be corrected to resuscitate these hearts during surgical correction of congenital defects.     

Effect of halothane on myocardial reoxygenation injury in the isolated rat heart

Several studies have reported a protective effect of halothane on myocardial injury in an ischaemia-reperfusion situation. It is unclear if the protection is a result of the haemodynamic effects of halothane or if halothane has a specific action on ischaemia or reperfusion pathomechanisms. To examine this question, we have used an isolated rat heart model where heart rate (300 beat min-1), ventricular volume and coronary flow are constant. Left ventricular developed pressure (LVDP) and release of creatine kinase (CK) were measured as variables of myocardial performance and cellular injury, respectively. Five control hearts were subjected to 35 min of low-flow (2 ml min-1) anoxic and substrate-free perfusion and were then perfused for 1 h with the oxygenated buffer. In the treatment groups, halothane 0.4 mmol litre-1 was added during the first 30 min of anoxic perfusion (n = 5) or during the first 30 min of reoxygenation (n = 5). In five additional hearts, the effect of halothane 0.4 mmol litre-1 was tested under normoxic conditions. Mean basal CK release was 0.29 (SEM 0.13) iu g-1 min-1 and LVDP was 105.5 (4.0) mm Hg. Under normoxic conditions, halothane reduced LVDP to 52.0 (2.6) mm Hg. In control hearts, the major cell injury occurred at the onset of reoxygenation (CK release increased to 149.1 (9.1) iu g-1 min-1) and functional recovery after 1 h of reoxygenation was poor (control LVDP, 14.2(2.)% of baseline). Halothane during anoxia attenuated myocardial injury only moderately (CK release 50.2(5.7) iu g-1 min-1) and LVDP recovered to 30.8(3.0)% (each P < 0.05 vs control). When halothane was administered at reoxygenation, CK release was reduced to 10.1 (0.9) iu g-1 min-1 and LVDP recovered to 69.4(4.9)% (each P < .05 vs control). We conclude that halothane not only attenuated ischaemic injury but had a specific protective action against reoxygenation injury.      

Ischemic injury before heart transplantation does not cause coronary arteriopathy in experimental isografts

In this study we investigated whether the duration of ischemia before heart transplantation was related to coronary arteriopathy. Heterotopic cardiac isografts were done in 24 Lewis rats. Group 1 hearts (n = 4) were transplanted immediately after harvesting. Hearts in groups 2 (n = 8), 3 (n = 6), and 4 (n = 6) were implanted after preservation at 4 degrees C for 1, 2, or 3 hours, respectively. No immunosuppressive drugs were given. After 120 days, grafts were removed and evaluated by means of light microscopy for coronary artery intimal proliferation. Minimal intimal thickening was noted throughout, and no differences among the groups were found. Pretransplant ischemia in the absence of other factors does not cause coronary arteriopathy after heart transplantation.     

Autologous heart cell transplantation improves cardiac function after myocardial injury

Background. Fetal ventricular cardiomyocyte transplantation into a cardiac scar improved ventricular function, but these cells were eventually eliminated by rejection. We therefore examined the feasibility of autologous adult heart cell transplantation.

Methods. A transmural scar was produced in the left ventricular free wall of adult rats by cryoinjury. The left atrial appendage was harvested, and the atrial heart cells were cultured and their number expanded ex vivo. Three weeks after cryoinjury, either a cell suspension (2 × 10⁶ cells, n = 12 rats, transplant group) or culture medium (n = 10 rats, control group) was injected into the scar. Rats having a sham operation (n = 5) did not undergo cryoinjury or transplantation with cells or culture medium.

Results. Five weeks after injection, ventricular function was evaluated in a Langendorff preparation, measuring systolic, diastolic, and developed pressures over a range of intraventricular balloon volumes. Systolic and developed pressures were greater in the transplant group than in the control group (p = 0.0001). Rats with a sham operation had the greatest systolic, diastolic, and developed pressures (p = 0.0001). Histologic studies demonstrated survival of the transplanted heart cells within the scar. The area of the scar was smaller (p = 0.0003) and its thickness greater (p = 0.0003) in rats in the transplant group. Left ventricular chamber volume was smaller in the transplant group (p = 0.043).

Conclusions. Transplantation of autologous cultured adult atrial heart cells limited scar thinning and dilatation and improved myocardial function compared with results in control hearts. This technique may lead to a novel therapy to prevent scar expansion after a myocardial infarction and prevent the development of congestive heart failure.     

Failure of standard cardioplegic techniques to protect the conducting system

To determine the site of persistent electrical activity during cardioplegic arrest, microelectrodes that were also capable of recording temperature were placed along the conducting system in dogs undergoing one hour of cardioplegic arrest. Electrical activity was highest in the atrioventricular (AV) junction area (AV node and proximal bundle of His), and the temperature in this area could not be lowered to the level of the temperature in the left ventricular apex by routine cardioplegic technique. Neither changing K+ concentration (16 to 20 mEq/L) nor adding procaine hydrochloride abolished the activity of the conducting system during cardioplegia, and only 2 of 15 dogs were in sinus rhythm 30 minutes after reperfusion. When the conducting system temperatures were lowered to less than 15 degrees C by right AV lavage with iced saline solution, electrical activity was abolished during arrest and all 4 of 4 animals were in sinus rhythm 30 minutes after reperfusion. This study localizes the site of persistent conducting system activity during cardioplegic arrest, confirms it can be abolished with local cooling, and establishes the relationship between conducting system activity during cardioplegia and the incidence of conduction block and junctional rhythm following reperfusion.     

心肌肌钙蛋白Ⅰ在体外循环心内直视手术中对心肌损伤的监测作用

目的　探讨心肌肌钙蛋白Ⅰ (cTnⅠ )对先心病心内直视手术围体外循环期心肌缺血再灌注损伤的监测价值。方法　选择 2 0例拟行房或室间隔缺损修补术的先心病病人 ,随机分为对照组 (C组 )与乌司他丁组 (U组 ) ,每组 10例。分别于围术期多个时点采取桡动脉血 ,测定血浆肌钙蛋白Ⅰ (cTnⅠ )、肌酸激酶 (CK)及同工酶 (CK MB)浓度。结果　两组病人术前血浆cTnⅠ、CK和CK MB浓度均在正常范围内 ,且组间比较无差异。C组血浆cTnⅠ浓度在T3 、T4和T5时点都有显著升高 (P <0 0 0 1) ,于T4时点达峰值 ,T5时点开始下降。U组血浆cTnⅠ浓度在T3 、T4时点明显升高(P <0 0 0 1) ,于T5时点已下降至正常水平 ;在T3 、T4及T5时点U组cTnⅠ明显低于C组 (P <0 0 5 )。C组与U组血浆CK和CK MB浓度 ,在T2 、T3 、T4和T5时点都明显升高 (P <0 0 0 1) ,T2 、T3 及T4时点两组比较无显著性差异 ,至T5时点U组显著低于C组 (P <0 0 5 )。结论　cTnⅠ作为心肌损伤标志物 ,与CK、CK MB比较敏感性和特异性更高 ,是心内直视手术围术期检测心肌损伤的可靠指标。     

Ischemic heart disease associated with protein C deficiency.

Three patients of ischemic heart disease associated with protein C deficiency are reported. Although delayed diagnosis of protein C deficiency resulted in the failure of repeated interventions, coronary artery bypass grafting performed after making the correct diagnosis has led to satisfactory mid-term results under strict anticoagulation therapy. The level of protein C should be measured more frequently in the field of ischemic heart disease and earlier diagnosis of its deficiency should be made, because measurement of protein C does not cost much.     

Biochemical markers of myocardial injury in the pericardial fluid of patients undergoing heart surgery

The purpose of this study was to compare cardiac markers in the pericardial fluid and serum in order to evaluate preoperative myocardial injury. Thirty patients were divided into three groups. The first group (AVR; n=10) received an aortic valve replacement. The second group (SA; n=10) included patients with stable angina who underwent elective coronary artery bypass grafting (CABG). The third group (ACS; n=10) included patients with acute coronary syndrome who underwent urgent CABG. Pericardial fluid and venous samples were taken after opening the pericardium and 24 h postoperatively. Serum and pericardial concentration of troponin I (cTnI), creatine kinase (CK), its MB isoenzyme (CK-MB) and myoglobin were determined. Preoperative pericardial cTnI was significantly (P<0.01) higher than in serum in all groups. Preoperative pericardial CK, CK-MB and myoglobin were significantly (P<0.01) lower than in serum in groups AVR and SA. Preoperative pericardial and serum cTnI were significantly higher in the ACS than in AVR and SA groups (P<0.01). Postoperative pericardial concentration of all markers was significantly higher (P<0.01) than in serum in all groups. We conclude that preoperative pericardial accumulation of cTnI may reflect subclinical injury which may not be demonstrated by the usual laboratory tests.     

前列地尔乳剂对缺血再灌注心肌的保护作用

目的　研究前列地尔脂肪乳剂 (Lipo PGE1)对大鼠心肌缺血再灌注损伤 (MIRI)的影响。方法　应用Langendorff鼠心脏灌注模型 ,将 3 0只SD大鼠随机分成空白对照组 (A组 )、再灌注时K H液加Lipo PGE1组 (B组 )、停跳液中加Lipo PGE1组 (C组 ) ,各组分别平衡灌注 2 0min后灌注冷晶体停搏液 ,2 5℃缺血 5 0min ,再灌注 60min ,观察比较各组心肌I/R前后心率 (HR )、左室发展压 (LVDP)、左室压力变化速率 (△dp/dt)、冠脉流量 (CF)、冠脉流出液中磷酸肌酸激酶 (CPK)、乳酸脱氢酶 (LDH)含量及再灌注后心肌超氧化物歧化酶 (SOD)活性、丙二醛 (MDA)和ATP含量的变化、心肌细胞超微结构的变化。结果　Lipo PGE1改善心肌I/R后的收缩功能、增加冠脉流量和心肌ATP含量 ,促进SOD活性恢复 ,减少心肌细胞CPK和LDH的漏出及MDA的生成 ,减轻了心肌细胞超微结构的损伤。结论　Lipo PGE1通过其抗氧化和扩张冠脉作用可减轻MIRI。