Suspected myocardial necrosis in farmed Atlantic salmon, Salmo salar L.: a field case

Arteriosclerosis of the coronary artery has been described as a 'fact of life' for Pacific and Atlantic salmonids due to the high prevalence in spawning fish. The lesions are believed to be the result of overstretching of the highly distensible bulbus arteriosus whereby the endothelium of the main coronary vessel becomes mechanically damaged and a smooth muscle proliferation ensues with resultant partial occlusion of the vessel. The physiological significance for the function of the heart has yet to be demonstrated, but experimental studies show that, for example, swimming performance is compromised in fish in which the coronary artery has been ligated. This paper describes a case of myocardial necrosis in harvest-size Atlantic salmon during and after transportation to the slaughterhouse. Mortality during this process reached 10% in some of the transports and affected fish showed characteristic signs of congestive cardiac failure. Histology revealed extensive myointimal proliferation in the coronary artery and patchy necrosis of the compact ventricular myocardium. Several unfavourable factors such as high water temperature, skeletal malformations and crowding all probably contributed to extra cardiac workload. To the best of our knowledge, this is the first reported field case showing a link between coronary lesions and severe cardiac pathology.     

加味生脉补心丹对防治2型糖尿病大鼠心肌损害的影响

目的 观察加味生脉补心丹对2型糖尿病大鼠模型血糖及心肌组织结构的影响,初步探讨加味生脉补心丹对糖尿病心肌纤维化和肥大的防治作用。方法 40只SD大鼠随机分为空白组7只,实验组33只,通过高糖高脂饲料+小剂量STZ构建2型糖尿病大鼠模型。将成模后的实验组大鼠随机分为模型组、补心丹（BXD）组和罗格列酮（RSG）组各11只,BXD组以浓缩后加味生脉补心丹汤剂灌胃;RSG组按照罗格列酮钠溶液灌胃。给药8周后测各组大鼠空腹血糖,并处死取材,光镜观察心肌组织变化,Masson染色观察纤维沉积情况,免疫组化法观察Ⅰ、Ⅲ型胶原蛋白和沉默信息调节因子3（Sirt3）蛋白的表达。结果 成模时各实验组空腹血糖（FPG）均较空白组升高（P<0.05）,造模成功。治疗完成时,RSG组、BXD组FPG均较模型组下降（P<0.05）,RSG组FPG较BXD组更低（P<0.05）。模型组心肌组织破坏严重,胶原纤维含量增多,RSG组和BXD组心肌组织破坏程度较轻,胶原纤维含量较少。模型组Ⅰ、Ⅲ型胶原和Sirt3的表达明显高于其他组（P<0.05）。BXD组Ⅲ型胶原的表达明显高于空白组（P<0.05）。RSG组Sirt3的表达显著高于BXD组（P<0.05）。结论 加味生脉补心丹能够明显降低2型糖尿病大鼠的血糖,并能够明显减轻心肌纤维化、肥大的程度,延缓糖尿病所致心肌病的进程。     

脉冲微波辐照对实验动物心脏损伤的病理学研究

30只犬，180只大鼠，各随机分为6组，分别以5个功率密度（从1．004mW／cm^2至0．974kW／cm^2）脉冲微波辐照，在辐照后即刻（0h）至12个月的不同时相点，分别检测其体温、心率、心电图、心肌酶谱等指标，以研究心脏功能的变化；分别取左右房室肌（大鼠取全心）、窦房结、血管等作石蜡切片，并HE、Pollak、PTAH染色，以研究其病理组织学变化；取大鼠心室肌作超薄切片，电镜观测其超微结构的改变。结果发现，辐照后实验动物体温、心率未见明显变化；心电图波形异常，出现以S-T段压低和传导阻滞为主的变化；心肌酶谱出现以活性降低为主的紊乱性变化；辐照可对心肌纤维、窦房结、Purkinje细胞和血管壁等组织结构（包括超微结构）造成损伤。损伤累及全心，并以传导纤维的损伤更为严重。试验结果表明，高功率的脉冲微波可对实验动物心脏功能和结构造成明显损伤，心脏结构损伤和功能障碍均表现速发性、持续性和可缓慢恢复性的特点，损伤在一定范围内呈现剂量效应关系。     

Relationship between NLRP3 inflammasome-IL-1β axis and End-MT after acute myocardial infarction in rats

AIM: To investigate whether activation of NLRP3 inflammasome-IL-1β axis is consistent with endothelial-mesenchymal transition (End-MT) during the process of myocardial fibrosis after acute myocardial infarction (AMI). METHODS: Adult male SD rats (n=30) were randomly divided into sham operation group (n=15) and AMI group (n=15). After 28 d, Masson staining was used to detect the level of myocardial fibrosis. The activation of NLRP3 inflammasome including NLRP3, ASC, pro-caspase-1 and caspase-1, the endothelial cell markers CD31 and VE-cadherin, and the mesenchymal cell markers α-SMA and FSP1 were analyzed by Western blot. The expression of IL-1β was measured by ELISA. RESULTS: The levels of myocardial fibrosis and End-MT, the activation of NLRP3 inflammasome, and the expression of caspase-1 and IL-1β were significantly increased in AMI group compared with sham operation group (P<0.05). CONCLUSION: The activation of NLRP3 inflammasome-IL-1β axis is significantly consistent with End-MT process, suggesting that NLRP3 inflammasome-IL-1β, as a potential target for the activation of End-MT, will provide a novel theoretical target for the treatment of myocardial fibrosis and heart failure after AMI.     

High-magnesium exposure to bullfrog heart causes ST segment elevation

Hypermagnesemia occurs in elderly people or patients with renal insufficiency after excessive ingestion of magnesium-containing laxatives. In addition to typical electrocardiogram (ECG) findings caused by conduction defects, changes in the ST segments and T waves are also observed in patients with severe hypermagnesemia. This suggested the involvement of similar pathophysiology to acute myocardial infarction, as we previously demonstrated using burn-induced subepicardial injury model in frog hearts. In the present study, by exposing the bullfrog heart to high-magnesium solution, we reproduced prominent ST segment changes in ECG as actually observed in patients with severe hypermagnesemia. In addition to the great increase in the T waves, the ECG showed a marked elevation of the ST segments and the cardiac action potential demonstrated a marked shift of the resting membrane potential to the depolarized side. High-magnesium exposure did not affect the abundance of Na⁺/K⁺-ATPase proteins. However, the pharmacological stimulation of Na⁺/K⁺-ATPase activity by insulin quickly retrieved the elevated ST segments in ECG. From these results, the functional blockade of Na⁺/K⁺-ATPase activity by magnesium ions was thought to be responsible for generating the potassium concentration gradient and the subsequent ST segment changes.     

Rho激酶抑制剂治疗急性心肌梗死血清炎症因子的变化及疗效观察

目的给予急性心肌梗死患者早期应用Rho激酶抑制剂,测查其血清炎症因子IL-6,TNF-a,NO的变化情况,并以此为依据,观察Rho激酶抑制剂临床治疗效果.方法选择同期收治的未接受冠脉介入治疗的急性心肌梗死患者50例.随机分为治疗组和常规组,各25例.两组均给予硝酸甘油、硫酸氢氯吡格雷、辛伐他丁等常规治疗.治疗组在常规治疗的基础上静脉滴注盐酸法舒地尔30 mg,2次/d,10 d为1个疗程,观察患者血清炎症因子IL-6,TNF-a,NO浓度变化.结果加用法舒地尔的治疗组患者血清炎症因子IL-6,TNF-a浓度下降,NO浓度增高,均比常规组明显,且患者心功能检测治疗组改善更明显.结论 Rho激酶抑制剂治疗急性心肌梗死能够更有效地保护心肌细胞,降低炎症因子对心肌细胞的损伤,对改善患者心功能有显著效果.     

主动脉内球囊反搏术治疗急性心肌梗死的疗效和安全性观察

目的观察主动脉内球囊反搏术（IABP）治疗急性心肌梗死（AMI）的疗效和安全性。方法 80例AMI患者随机分为IABP组和对照组,每组40例。两组均给予WHO规定的标准基础治疗方案及PCI治疗,IABP组在PCI前使用IABP治疗。观察治疗前后两组脑利钠肽水平、肌钙蛋白I水平、左心室舒张末期容积（LVEDV）、左心室收缩末期容积（LVESV）和射血分数变化、治疗后30d内主要心血管事件。结果与对照组比较,IABP的使用显著降低心肌梗死后1周脑利钠肽及肌钙蛋白I水平（P〈0.01）,缩小LVEDV和LVESV（P〈0.01或0.05）,提高LVEF（P〈0.01）,降低30d内主要心血管事件的发生率（P〈0.01）。结论 IABP的使用能改善梗死后心肌缺血程度、心室压力、容量负荷和心室重构,从而改善AMI患者的预后。     

Intra-city Differences in Cardiac Expression of Inflammatory Genes and Inflammasomes in Young Urbanites: A Pilot Study

Southwest Mexico City (SWMC) air pollution is characterized by high concentrations of ozone and particulate matter < 10 μm (PM(10)) containing lipopolysaccharides while in the North PM(2.5) is high. These intra-city differences are likely accounting for higher CD14 and IL-1β in SWMC v NMC mice myocardial expression. This pilot study was designed to investigate whether similar intra-city differences exist in the levels of myocardial inflammatory genes in young people. Inflammatory mediator genes and inflammasome arrays were measured in right and left autopsy ventricles of 6 southwest/15 north (18.5 ± 2.6 years) MC residents after fatal sudden accidental deaths. There was a significant S v N right ventricle up-regulation of IL-1β (p=0.008), TNF-α (p=0.001), IL-10 (p=0.001), and CD14 (p=0.002), and a left ventricle difference in TNF-α (p=0.007), and IL-10 (p=0.02). SW right ventricles had significant up-regulation of NLRC1, NLRP3 and of 29/84 inflammasome genes, including NOD factors and caspases. There was significant degranulation of mast cells both in myocardium and epicardial nerve fibers. Differential expression of key inflammatory myocardial genes and inflammasomes are influenced by the location of residence. Myocardial inflammation and inflammasome activation in young hearts is a plausible pathway of heart injury in urbanites and adverse effects on the cardiovascular system are expected.     

生脉注射液对大鼠实验性心肌梗死的保护作用

采用大鼠结扎左冠状动脉前降支制备急性心肌梗死模型,观察生脉注射液对实验性心肌梗死的保护作用。结果表明,生脉注射液中、大剂量组可使急性心肌梗死24小时大鼠的心肌梗死面积明显缩小,血清AST、LDH、CK活性及MDA含量明显降低,SOD及GSH-Px活性明显升高,血液粘度及血浆粘度明显下降。表明生脉注射液对大鼠实验性心肌梗死具有明显保护作用,可能与其增强抗氧化酶活性,减少自由基对心肌的氧化损伤以及降低血液粘度等机制有关。     

糖尿病并发急性心肌梗塞的临床研究

对１７例糖尿病并发急性心肌梗塞１７例非糖尿病的急性心肌塞患者作了配对比较研究。结果表明：糖尿病患者的无痛型心梗发生较多，心室晚电位检出阳性率明显和蔼同，超声心动图测定左室功能受损严重。提示糖尿病并发急性心肌梗塞有其临床特殊性，并作了讨论。