免疫损伤对离体培养心肌细胞力学特性的影响

目的：探讨病毒性心肌炎时免疫损伤对心肌细胞损害的发病机理。方法：成功建立自身免疫离体心肌细胞模型，在此基础上进行心肌细胞的细胞力学特性的分析。结果：免疫损伤对心肌细胞有明显的损害，心肌细胞收缩力下降，其中免疫损伤的心肌细胞在２４小时的心肌收缩力下降比１２小时更为明显。结论：免疫损伤使心肌细胞收缩力下降。     

藏羚羊和藏系绵羊左心室收缩功能的比较研究

目的:探讨藏羚羊适应高原低氧环境的左心功能特点。方法:捕捉海拔4 300 m藏羚羊9只、藏系绵羊10只运至格尔木(海拔2 800 m)实验基地。测定二者的心脏/体重比(HW/BW)、右心室/(左心室+室间隔)重量比[RV/(LV+IVS)];应用心导管技术测定心率(HR)、收缩压(SBP)、舒张压(DBP)、左室等容收缩期心室内压力上升最大速率和左室等容舒张期心室内压力下降最大速率(±dp/dt)。以格尔木市的氧浓度(21.1%)为基线,分别给予更低浓度氧14.6%、12.5%(分别相当于海拔5 300 m、6 300 m)的低氧吸入15 min后重复测定以上指标。应用透射电镜观察心肌超微结构。结果:藏羚羊HW/BW显著高于藏系绵羊(P0.01),基础状态下藏羚羊SBP低于藏系绵羊(P0.05),+dp/dt与藏系绵羊比无显著差异,吸入14.6%和12.5%的低氧气体后藏羚羊+dp/dt分别升高至145.1%和148.1%,而藏系绵羊分别降低至68.4%和70.5%(P0.05);电镜下观察藏羚羊心肌超微结构与藏系绵羊比较,其心肌细胞线粒体较为丰富。结论:藏羚羊心脏对高海拔低氧环境的适应,是通过增加心脏器官的重量及心肌细胞线粒体的含量来实现,其心肌收缩功能的适应性特征为:在静息状态下以较低的左心室心肌收缩力来降低氧耗量以此适应高原低氧环境,而以海拔更高的较低氧浓度为应激条件下,左心室心肌收缩力明显升高。提示:藏羚羊作为高原适应性动物,经过漫长的自然选择其心脏对高原低氧环境的适应不同于藏系绵羊。     

电针对实验性家兔急性心肌缺血时心肌收缩性能的影响

实验采用LVP、V_(CE)类等指标观察针刺对家兔急性心肌缺血时心肌收缩性能的影响。 灰兔28只,电针“内关”组15只,不给电针对照组13只。结扎冠状动脉左室支,造成急性心肌缺血。 描记结扎冠脉前的LVP,dp/dt曲线及肢体Ⅱ导心电图,拍摄P-dP/dt环及P-(dp/dt)/P环。再分别描记结扎冠脉5分、10分、15分的上述参数及拍摄两环。于结扎冠脉15分时松结。电针组于松结前5分钟开始电针,留针10分钟。共观察75分     

八肽胆囊收缩素逆转内毒素休克大鼠心功能降低的实验研究

目的: 观察八肽胆囊收缩素(CCK-8)改善内毒素休克(ES)大鼠心功能的变化,探讨CCK-8抗ES的作用及机制。方法: 实验分对照组、脂多糖(LPS)组、CCK组及CCK+LPS组;监测左室内收缩压(LVP)、左室收缩与舒张期内压变化的最大速率、心率(HR)和平均动脉压(MAP)的动态变化;分别测定2h血清、心肌组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)和一氧化氮(NO)含量的变化。结果: 静脉注射CCK-8(40μg·kg^-1),引起短时间心率减慢,轻度MAP、LVP和±LVdp/dt_max上升;静脉注时LPS(8mg·kg^-1),引起HR生快后慢双向改变MAP、LVP和±LVdp/dt_max快速持续下降;整体预先注射CCK-8,可明显缓解ES大鼠HR的快速变化,逆转MAP、LVP和±LVdp/dt_max下降,但未恢复至正常水平。CCK-8可提高ES大鼠血清、心肌组织中SOD活性,降低MDA和NO含量。结论: CCK-8可引起短时间心率减慢、轻度MAP上升和心肌收缩力增强;预先应用CCK-8可以减轻ES大鼠心肌氧化损伤,减少NO合成,恢复心肌收缩力,逆转心功能降低及顽固性低血压,是其发挥抗ES的重要机制之一。     

用ESR检测兔心肌顿抑时一氧化氮的动态变化

目的：用顺磁共振技术（ESR）测定兔在心肌缺血再灌注过程中心肌顿抑时，血液中一氧化氮（NO）动态变化。方法：结扎前降支制成心肌缺血-再灌注模型，经颈动脉左心室插管，多导生理仪记录左心室最大上升速率（dp/dt_max）、心室舒张末压力、动脉血压、心率等血液动力学指标。分别于缺血前、缺血5 min、10 min，再灌注5 min、10 min、30 min、60 min、90 min、120 min各时点取静脉血1 mL，在电子自旋共振仪记录NO波谱，测定NO水平。结果：在再灌注5 min、120 min时，NO浓度明显高于缺血前[(23.4±4.8) mm vs (12.0±0.5) mm，(21.4±1.8) mm vs (12.0±0.5) mm，P<0.01]。心肌收缩功能在缺血5 min时已经开始受损[(4965±295.6) mmHg/s vs (3967±315.3) mmHg/s，与缺血前比较P<0.01]，但是在再灌注5 min时明显低于缺血5 min时[(3327±120.4) mmHg/s vs(3967±315.3) mmHg/s，P<0.05]。结论：再灌注早期NO升高而心肌收缩力下降，提示NO对早期缺血再灌时心肌顿抑有加重作用。     

缺氧性肺动脉高压的发展与左右心功能变化关系的进一步探讨

我们曾在“缺氧性肺动脉高压的发展与心输出量动态变化的关系”中报道:大鼠在模拟5,000m高度的低压舱内连续减压缺氧4、10、20天,其右心室收缩压RVP(相当于肺动脉收缩压)、右室±(dp/dt)max(反映心肌舒缩功能)、心输出量CO,每搏量SV和心指数CI均随缺氧时间的延长而逐步升高,左室压LVP与左室±(dp/dt)max则无明显改变。本文延     

病毒性心肌炎辅助治疗疗效观察

病毒性心肌炎是一种由病毒感染而引起的心肌疾病 ,近年来病毒性心肌炎的相对发病率有上升趋势。引起病毒性心肌炎的病毒有近 2 0余种 ,一般情况下病毒通过血液循环直接侵犯心肌细胞 ,引起细胞的溶解、坏死、水肿、断裂 ;另外病原也可不侵犯心肌 ,而在心肌表面形成新抗原和特异性抗体 ,在补体的参与下 ,抗原—抗体相互作用使心肌细胞破坏 ,而产生心肌炎症病变。不管以哪一种病变为主 ,最后均引起心肌松弛无力 ,心脏扩大 ,心肌收缩功能障碍 ,进而导致心脏功能衰竭 ,病毒性心肌炎是心血管系统的常见病 ,国内外学者对其诊断和治疗做了大量的研究…     

缺血预适应对青年与老年大鼠缺血/再灌注心肌氧化应激及线粒体功能的影响

目的:探讨缺血预适应(ischemic preconditioning,IPC)对青年与老年大鼠缺血/再灌注(ischemia/reperfusion,IR)心肌损伤的影响。方法:雄性3月龄(青年)与20月龄(老年)Wistar大鼠,应用离体心脏灌流方法复制心肌IR与IPC模型。实验分为青年缺血/再灌注(YIR)组、青年缺血预适应(YPC)组、老年缺血再灌注(OIR)组与老年缺血预适应(OPC)组。透射电镜观察心肌及心肌线粒体超微结构变化;TTC染色测定心肌梗死面积;比色法测定冠脉流出液中乳酸脱氢酶(LDH)活性、心肌组织中超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量;酶联免疫吸附法测定心肌组织硝基化与羰基化蛋白质含量,TUNEL方法检测心肌细胞凋亡;氧电极法测定线粒体呼吸功能及钙诱导的线粒体渗透性转运孔开放情况。结果:与YIR组比较,YPC组心肌梗死面积明显减少,冠脉流出液中LDH活性降低,心肌组织的SOD活性增加,MDA含量降低,心肌硝基化与羰基化蛋白含量降低。电镜下可见YPC组心肌及分离的心肌线粒体膜结构完整、基质致密。YIR组心肌线粒体呼吸控制率与Ⅲ态耗氧量及P/O比值均明显增加,质子漏出减少,钙诱导的线粒体肿胀明显减轻,心肌细胞凋亡率下降。而与OIR组比较,OPC组上述指标均无显著统计学差异。与YPC组比较,OPC组心肌超微结构损伤明显增加,心肌氧化应激水平增加,线粒体呼吸功能下降,心肌细胞凋亡与坏死增多。结论:缺血预适应能够保护青年大鼠心肌缺血/再灌注损伤;而老年大鼠心脏对预适应刺激减敏,导致缺血预适应心肌保护作用钝化,这可能与老龄IPC心脏氧化应激水平增加导致线粒体损伤、细胞凋亡有关。     

大鼠实验性左室心肌梗塞对右室收缩性能的影响

对左室心肌梗塞(MI)是否会直接影响右室功能,至今尚有争议。本实验观察大鼠左室MI时右室dp/dt max的改变及其与左室dp/dt max和梗塞范围(IS)间的关系。结果发现冠脉结扎后1天,在左室dp/dt max显著降低的同时,右室dp/dt max也显著降低,且与左室dp/dt max呈显著的直线正相关,而与IS呈显著的直线负相关。在冠脉结扎后3天时,左室dp/dt max有显著恢复,但仍低于对照水平,而右室dp/dt max已恢复正常,且与左室的dp/dt max和IS间不再具有显著的直线相关关系。由此证明;在大鼠左室MI早期,右室收缩性能可受到直接影响,影响的程度与IS及左室收缩性能降低的程度相关;但当左室收缩性能恢复到一定程度时,这种影响消失。     

扩张性心肌病的预防及护理

1病理病因
　　扩张型心肌病是多种因素长期作用引起心肌损害的最终结果。感染或非感染性心肌炎、酒精中毒、代谢等多种因素均可能与扩张型心肌病发病有关。短暂的原发性心肌损伤(如接触毒性物质)对某些心肌细胞来说可能是致死性的,但残存的心肌细胞会因此而增加负荷,发生代偿性肥厚。这种代偿性变化在早期尚能维持心脏的整体功能,但最终将表现为心肌的收缩和舒张功能障碍。心肌炎既有不可逆的心肌细胞死亡,又有由细胞因子所介导的可逆性心肌抑制[1]。     

Repeated normoxic hyperbaric exposures induce haemodynamic and myocardial changes in rats

Summary The effect of repeated exposure to ambient pressures of 5 bar (500 kPa), in atmospheres comprising normal partial pressures of oxygen [0.2 bar (20 kPa)] and nitrogen [0.8 bar (80 kPa)] and 4 bar (400 kPa) helium, on cardiac function and morphology was assessed in conscious rats. Ten test rats underwent chamber dives daily for 40 consecutive days, and ten control rats were exposed in the same chamber for an equal period of time, but in air at 1 bar (100 kPa). Cardiac output (Q_c) and myocardial blood flow (Q_myocardial) were determined by the microsphere method. After 40 days, the body mass was 7% greater in the control than in the test rats (P<0.05), although they were given exactly the same amount of standard food. The test rats had a significantly higher (7% absolute, 12% ventricular mass to body mass, P<0.05) heart mass (left ventricular myocardium, including the ventricular septum) than the control rats. The percentage tissue dry mass of the right and left ventricles was equal in the two groups. Microscopic examination revealed a number of small focal necroses in the left ventricle of the test rats but none in the control rats. The left ventricular pressure (LVP) and the maximum velocity of LVP increase (contractility) and decrease were significantly increased (25%–96%, P<0.001) in the pre-exposed compared to the control rats at 1 bar (100 kPa). The systolic arterial pressure, heart rate and respiratory frequency were similar in the two groups at 1 bar (100 kPa). The LVP and + dP/dt increased linearly and in parallel in both groups during compression, although at 5 bar (500 kPa) the test rats had reached a significantly higher LVP and + dP/dt level. However, the heart rate was unchanged in both groups. The pre-exposed rats had a higher left Q_myocardial [1 bar (100 kPa)=33%, P<0.05; and 5 bar (500 kPa)=maximum 40%, P<0.05] than the control rats. The systolic arterial blood pressure also increased during compression to its maximum after 20 min at 5 bar (500 kPa) in both groups. The mean arterial pressure, respiratory frequency, end-diastolic pressure and Q_c were unchanged throughout the experiments. A pressure drop of 42 mmHg (5.6 kPa) between the left ventricle and the arteries would suggest stenosis in the aortic valve region in the test rats. In conclusion, the cardiac function as well as myocardial mass and morphology were changed after 40 consecutive exposures to 5 bar (500 kPa) in conscious rats.     

保心胶囊对实验性犬心肌缺血血流动力学的影响

目的:观察保心胶囊对结扎犬心肌缺血时心脏血流动力学的影响。 方法:实验分假手术对照组,缺血组,缺血+地奥组,缺血+保心低剂量组,缺血+保心中剂量组,各组犬连续灌胃(生理盐水或药物)三天后,结扎犬心脏冠脉左前降支复制急性心肌缺血模型,测定犬不同时点的血压、血流量及左室等容期压力最大变化速率的变化。结果:保心中剂量组对血压、血流量及左室等容期压力最大变化速率的作用与缺血组比较有显著差异(P＜0.05)。结论:保心胶囊具有改善心肌缺血、增强心肌舒缩能力的作用。     

Organ blood flow and cardiac contractility in anaesthetized cats at 5 bar (500 kPa) ambient pressure

Summary Previous in vivo and in vitro experiments have demonstrated increased cardiac contractility and increased total myocardial blood flow ( ) when rats were exposed to normoxic 5-bar (500 kPa) ambient pressure. In the present study, regional blood flow was measured using the microsphere method on nine anaesthetized cats at surface and normoxic 5-bar (500 kPa) ambient pressure. Left ventricular pressure (LVP) and cadiac contractility, measured as peak left ventricular +dP/dt and –dP/dt were measured in six of the cats. Arterial pressure, heart rate and cardiac output remained unchanged after compression, but total increased by 29% (P<0.01) and cerebral blood flow increased by 66% (P<0.05). At the same time +dP/dt and –dP/dt was increased by 83% and 102%, respectively (P<0.01), while LVP was enhanced by 14% (P<0.05). Except for a moderate decrease in partial pressure of oxygen, acid base status in arterial blood remained unchanged. The results indicate that the effects of increased ambient pressure on the heart are general physiological phenomena, which are not only limited to the laboratory rat.     

Cardiac changes to signalled shock avoidance in dogs

Alterations in heart rate (HR), left ventricular pressure (LVP), and maximum left ventricular dp/dt (LVdp/dt max) during a signalled avoidance task were studied in eight chronically prepared dogs. Four of these animals comprised a non-shock control group. In experimental animals, HR increased during the first two days of the avoidance task but did not change significantly during the last two days, while LVP remained at the supranormal post-training levels and LVdp/dt max increased over the course of the experiment. Control animals showed no change in HR or LVP, but LVdp/dt max decreased over the four experimental days. Changes in LVdp/dt max in experimentals reflect a consistent increase in cardiac sympathetic activation. However, HR changes indicate an initial increase and a subsequent decrease in sympathetic activity. It was therefore postulated that either differential activation of sympathetic cardiac fibers occurred such that during non-stress periods and subsequent exposure to stress, sympathetic influences predominate which are reflected only in LVdp/dt max changes, or sympathetic and parasympathetic fibers differentially control cardiac function during stress and non-stress conditions.     

Temporal relationship of contractility and myocardial potassium balance following beta-adrenergic stimulation of the in situ pig heart

Lower intracellular Na+ during beta-adrenergic stimulation provides an increased driving force for Na-Ca exchange, which might attenuate the inotropic response. Since (1) Na+ reduction is coupled to K+ uptake, and (2) K+ uptake lags behind the positive inotropic response to isoproterenol, we could examine the effect of Na-Ca exchange by comparing cardiac contractility and K+ balance following intracoronary isoproterenol infusion (0.6-0.8 microgram min-1). In 8 open-chest pigs, potassium concentrations were continuously measured by PVC-valinomycin mini-electrodes in arterial blood (a), and in myocardial venous blood in a shunt from the coronary sinus (cs) to the right atrium. Shunt flow, aortic flow, a left ventricular segment length and left ventricular pressure (LVP) were also continuously recorded. 64 (41-85)% (median and 95% confidence interval) of the LV dP/dt increase occurred within 1 min; thereafter contractility rose slowly. During the first minute of isoproterenol infusion, there was a small net myocardial K+ release, which then reversed to K+ accumulation. A maximum a-cs K+ concentration difference of 0.20 (0.09-0.39) mM occurred at 3.0 (2.0-4.25) min, falling to 0.05 (0.01-0.10) mM after 6.5 (3.75-8.75) min, at which point accumulated myocardial K+ uptake was 135 (27-219) mumol 100 g-1. Heart rate remained unchanged and intramural ECG indicated no sign of ischemia during the first 1.5 min of isoproterenol infusion. At 6.25 (5.0-8.0) min after stop of isoproterenol, LV dP/dt was 12 (9-24)% lower than before infusion (P less than 0.02) whereas myocardial K+ content remained higher than control. Thus, the monovalent cation shift succeeding the positive inotropic response was not associated with reduced contractility, but could explain the undershoot of LV dP/dt after stopping isoproterenol.     

尾加压素预处理对大鼠心脏缺血再灌注损伤的影响

目的:探讨尾加压素(UII)预处理对于离体灌流大鼠心脏缺血再灌注(I/R)损伤的影响。方法:在离体灌流的SD大鼠心脏I/R模型上,以UII预灌注心脏,采用MFLLab200心功能软件监测心功能,以试剂盒测定心肌细胞ATP、总钙、丙二醛含量和乳酸脱氢酶(LDH)漏出,并观察其对于冠脉流出量(CPF)的影响。结果:UII预处理组与单纯I/R组比较,冠脉流出液中LDH低28%[(78.3±18.1)U/Lvs(10.93±23.9)U/L,P<0.05],心肌组织MDA和钙含量分别低24%和27%(P<0.05);ATP含量高73%(P<0.05)。与I/R组比较,UII预处理组CPF高42%[(5.4±0.7)mL/minvs(3.8±0.8)mL/min,P<0.05],LVEDP低20%(P<0.05),±dp/dtmax分别高25%和45%(P<0.05);冠脉流出液中NO₂^-/NO₃^-含量高63%(P<0.05)。结论:UII预处理可以减轻离体灌注大鼠心脏I/R所造成的损伤,其机制与NO介导的冠脉扩张效应有关。     

硫化氢对大鼠离体灌流心脏心功能的影响

目的：观察H2S对大鼠离体心脏心功能的影响，以探讨内源性H2S对心肌活动的调节意义。方法： 检测大鼠心肌组织中H2S的含量及生成率，并采用RT-PCR方法检测心肌组织CSE(内源性硫化氢合成的关键酶)mRNA的表达；应用Langendorff灌流大鼠离体心脏，用不同浓度NaHS(10-6-10-3mmol/L)灌流心脏，及用生理浓度NaHS(4×10-4mol/L)持续灌流20 min，测量心率(HR)、左室内压差(△LVP＝左室收缩压-左室舒张压)、左室内压变化速率(±dp/dtmax)、冠脉灌流量(CPF)等指标；应用KATP通道阻断剂格列苯脲预灌流，后给予生理剂量NaHS灌流，观察其是否可以阻断NaHS的效应。结果： NaHS可以呈浓度依赖性抑制左心室±dp/dtmax及△LVP(P＜0.05)，但对HR、CPF没有影响，生理剂量NaHS持续灌流20 min内，可以持续抑制±dp/dtmax及△LVP(P＜0.05)，而对HR、CPF几乎没有影响。KATP通道阻断剂格列苯脲可以大部分(85.7%)阻断生理剂量NaHS对心功能的抑制效应。结论： 内源性H2S可能通过开放心肌KATP通道，抑制大鼠离体心脏左心室的收缩功能。     

Decreases in left ventricular contractility during endotoxin shock in rabbits

The participation of the heart in shock syndrome formation during endotoxin shock is a problem still awaiting solution. The task undertaken is to assess the work of the left ventricle and arterial pressure in rabbits before and after endotoxin injection at a dose of 2 mg.kg-1. Heart rate is the first to reach significantly lower values--at 30 min (p less than 0.05). At 45 min, there are significant reductions in dP/dtmax (p less than 0.01), (dp/dt)/P40 (p less than 0.001), LVP (p less than 0.05), and increase in dP/dtneg (p less than 0.02). Both the systolic and diastolic blood pressures were significantly decreased at 60 min. The data obtained warrant the assumption that impaired myocardial contractility plays a part in the formation of shock syndrome in rabbits exposed to endotoxin.