新生猪缺氧缺血性脑病时的心肌损伤和环磷腺苷葡甲胺的预防作用

目的研究新生猪缺氧缺血性脑病时心肌损伤情况以及环磷腺苷葡甲胺对这种损伤的预防作用。方法选生后3-7天的新生猪22头,随机分成假手术组(Sham)、缺氧缺血组(HIE)和环磷腺苷葡甲胺组(MCA)。Sham组4头猪,只游离双侧颈动脉;HIE组9头,阻断双侧颈总动脉同时控制呼吸吸入6%氧气;MCA组9头,在缺血缺氧前静脉注射环磷腺苷葡甲胺(2mg/kg)。每头新生猪在缺氧前和缺氧后10h,采用化学发光法测定肌钙蛋白I含量,缺氧后12h进行脑磁共振扫描,处死后做心肌组织HE染色。结果缺氧缺血10h,HIE组肌钙蛋白值显著高于Sham组或MCA组(0.01)。Sham组MR未见信号异常改变,HIE组和MCA组可见信号增强。Sham组心肌细胞结构完好,HIE组心肌细胞损伤严重,MCA组心肌细胞结构只有轻微改变。结论新生猪缺氧缺血性脑病引起心肌损伤,环磷腺苷葡甲胺对损伤有一定预防作用。     

运动与ATP-敏感型钾离子通道

背景：在运动生理状态下，KATP 在调节冠状动脉张力、运动诱导心肌保护效应和延缓骨骼肌疲劳等多个方面具有重要作用。目的：对KATP在运动中的作用进行了综述和探讨，以期为深入了解运动调节机体代谢提供理论参考。方法：检索1991年1月至2014年6月 PubMed数据库及维普中文科技数据库文献。英文检索词为“KATP Channels；Adenosine Triphosphate；Sports；Myocardium；Ion Channels”，中文检索词为“KATP通道；三磷酸腺苷；运动；心肌；离子通道”。选择与KATP分子结构、生物学功能及调控相关，以及KATP与冠状动脉、心肌、骨骼肌疲劳及运动能力相关的文献42篇文献进行探讨。结果与结论：ATP敏感性钾离子通道可以偶联细胞内能量代谢和细胞膜兴奋性，在应对各种生理和病理应激时是保护心肌的效应器之一。长期的耐力训练则会增加骨骼肌和心肌KATP的表达，可能是心肌和骨骼肌对运动应激产生的一种适应性表现。KATP 可能参与冠状动脉血流量的调节。在运动诱导的减轻心肌缺血再灌注损伤的保护效应中，心肌KATP具有重要作用。当骨骼肌疲劳发生时，KATP的激活有利于防止ATP的过度消耗而造成肌纤维损伤和细胞死亡，有利于疲劳的快速恢复。关于KATP与运动能力的关系仍需进一步的研究。     

小儿肺炎支原体肺炎合并心肌损害的临床分析

目的 探讨肺炎支原体肺炎（MPP）合并心肌损害的临床特点.方法 选择我院2012年1月至2013年6月确诊为MPP的患儿共478例,按年龄进行分组,分别比较不同年龄组间心肌损害的发生率.结果 0～1岁患儿中合并心肌损害的有75例,占0～1岁患儿的28.4％;2～3岁患儿中有27例,占20.5％;4～5岁患儿中有9例,占16.4％;大于6岁患儿中有4人,占14.8％.MMP患儿合并心肌损害的发生率与年龄呈负相关（r=-0.722,P＜0.001）.结论 MPP在婴幼儿中并不少见,且更易合并心肌损害.     

Echocardiographic Hypertrabeculated/Non-compacted Right Ventricle Accompanied by Atrial Septal Defect and Anomalous Pulmonary Vein Connection

Myocardial noncompaction (NC) is a disorder of the embryonic endomyocardial morphogenesis frequently associated with congenital cardiac abnormalities. NC predominantly affects the left ventricle (LV). Right ventricle (RV) NC may occur in association with LV involvement or in isolation. A 47-year-old woman was admitted for atrial septal defect closure. Transthoracic echocardiography revealed hypertrabeculation of the RV apex, consisting of multiple deep recesses with the entrance of blood flow in color Doppler imaging, suggestive of isolated RV hypertrabeculation/NC. The RV and right atrium (RA) were enlarged, and systolic pulmonary arterial pressure was slightly increased. Our patient''s associated abnormalities were atrial septal defect (superior sinus venosus type), anomalous connection of the right upper pulmonary vein to the junction of the superior vena cava and the RA, and large patent foramen ovale. Association between atrial septal defect and partial anomalous pulmonary vein connection and isolated hypertrabeculated/noncompacted RV should be considered by cardiologists.     

Apoptosis in heart failure and the senescent heart

The progressive loss of cardiac myocytes by apoptotic cell death has been discussed as an important pathogenic component in the failing myocardium as well in the aging heart. The degree to which apoptosis contributes to myocyte loss in these conditions, however, is a controversial issue. This review focuses on the regulation of apoptosis, evidence implicating apoptosis as a mechanism for the progression and development of heart failure, the role of apoptotic death in senescent cardiac dysfunction, as well as on the problems of detection of apoptosis.     

Cardiac electrolytes and water in thyroparathyroidectomized rat

The effect of thyroparathyroidectomy (TPTX) on myocardial extracellular space (ECS), water and electrolytes was studied in young, female, Sprague-Dawley rats. Eight weeks after TPTX the ventricular ECS, measured in vivo with [³⁵S]sulfate, was found to be 0.219 ± 0.004 (g H₂O/g tissue as compared to 0.177 ± 0.006 in euthyroid control rats. Measurement of ECS in the same ventricular tissue of TPTX rat by a morphometric procedure confirmed the increase: 0.209 ± 0.004 (cm³/cm³). This increase in ECS was only relative to the size of the cellular compartment, for the absolute volume of the ECS in the ventricular myocardium fell. Thus, the relative expansion of the ECS at the expense of the cellular compartment appears to be due to a greater sensitivity of the parenchyma to the inhibitory effects of hypothyroidism on growth. This finding is compatible with a decrease in cellular size of the hearts of hypothyroid rats; a compartmental shift in water from the cellular to the extracellular compartment need not be postulated. Most or all of the enlargement of ECS is due to an expansion of the interstitial compartment. No changes in tissue water content were detected. Plasma concentrations of potassium, calcium and magnesium declined, whereas the concentrations of sodium and chloride remained constant. Depending on whether the electrolytes are predominantly intracellular or extracellular, tissue electrolyte contents showed alterations appropriate to the relative changes in compartmental volumes. Assuming homogeneous distributions of the electrolytes throughout the ECS, the calculated cellular concentrations slightly increased for sodium and potassium, decreased for magnesium, and remained unchanged for calcium and chloride.