The effect of uridine and uridine nucleotides on isolated rat heart performance in regional myocardial ischemia

We studied the effects of uridine, uridine-5'-monophosphate (UMP), uridine-5'-diphosphate (UDP) and uridine-5'-triphosphate on contractility, coronary flow and heart rate in isolated perfused rat hearts under 60-minute regional ischemia of the left ventricle. All the compounds (50 mumol/l) induced a positive inotropic effect but had no effect on the heart rate. Uridine and UMP prevented the development of the contracture. UDP and especially UTP increased coronary flow. Probably, a protective effect of uridine and UMP is due to activation of myocardial glycogen synthesis while favourable effects of UDP and UTP on contractility and coronary flow are explained by their influence on P2U-receptors of cardiomyocytes. In addition, coronary dilatation induced by UDP and UTP promoted the reduction of the damaged zone.     

蛋白激酶C活化对大鼠缺血/再灌注心肌细胞凋亡和Bcl-2表达的影响

目的:探讨PKC活化对大鼠I/R心肌细胞死亡和凋亡抑制基因bcl-2表达的影响。方法:采用TUNEL法以及免疫组化和原位杂交方法。结果:①PMA+IR_3h组TUNEL法阳性心肌细胞核数量及阳性心肌细胞核占总心肌细胞核数的百分比均明显少于IR_3h组(P＜0.05,＜0.01);②PMA+IR_3h组表达Bcl-2蛋白阳性的心肌细胞数及阳性心肌细胞占心肌细胞总数的百分比均明显多于IR_3h组(P＜0.01);PMA+IR_1h组表达bcl-2mRNA阳性的心肌细胞数及阳性心肌细胞占心肌细胞总数的百分比均明显多于IR_1h组(P＜0.01)。结论:①PKC活化能够显著减少大鼠I/R心肌细胞死亡;②PKC活化通过上调凋亡抑制基因bcl-2的基因表达可能是其减少大鼠I/R心肌细胞死亡的机制之一。     

大鼠肠系膜动脉血流短暂阻断对缺血/再灌注心肌细胞凋亡及Bcl-2表达的影响

目的: 探讨短暂阻断肠系膜动脉血流(MAO)对大鼠缺血再灌注(I/R)心肌细胞凋亡及bcl-2表达的影响。方法: 采用TUNEL法观察心肌细胞凋亡数以及免疫组化和原位杂交方法检测Bcl-2蛋白及其mRNA表达。结果: ①MAO+IR_3h组TUNEL法阳性心肌细胞核数量及阳性心肌细胞核占总心肌细胞核数的百分比均明显少于IR_3h组(P＜0.01);②MAO+IR_3h组表达Bcl-2蛋白阳性的心肌细胞数及阳性心肌细胞占心肌细胞总数的百分比均明显高于IR_3h组(P＜0.01);MAO+IR_1h组表达bcl-2mRNA阳性的心肌细胞数及阳性心肌细胞占心肌细胞总数的百分比均明显高于IR_1h组(P＜0.01)。结论: ①大鼠MAO能够显著减少I/R心肌细胞凋亡;②MAO通过上调凋亡抑制基因bcl-2基因表达、提高心肌中Bcl-2蛋白量可能是其减少I/R心肌细胞凋亡的机制之一。     

Quantitative assessment of cardiac pump performance.

1. A means of quantitating left ventricular performance in the conscious dog is presented. Changes in heart rate, stroke volume and cardiac output during elevation of left atrial pressure by acute volume expansion were measured in the conscious dog. 2. The changes in heart rate and stroke volume could be described by y = ym - (ym-yi)e-kp, where yi and ym are initial and maximum values of the variable and p is the change in mean left atrial pressure. 3. Because cardiac output is a derived variable (stroke volume X heart rate) its response is described by a multiple exponential relationship. 4. For a given initial heart rate and inotropic state, the stroke volume response is determined by the Frank-Starling mechanism and the pressure-volume characteristics of the myocardium.     

实验性心肌缺血内皮素的动态变化

目的:观察心肌缺血对血浆及心肌组织内皮素(ET)浓度影响的量效及时效改变,并初步探讨其机制。方法:用不同剂量的垂体后叶素(Pit)诱发大鼠在体心肌缺血并观察了相同剂量Pit作用下的不同时点的大鼠心肌组织及血浆的ET浓度的变化,然后做心肌ET-1的免疫组化及基因表达。结果:随着Pit剂量的加大,血浆及心肌组织ET浓度逐渐升高,当Pit剂量升至15U/kg体重时,其ET浓度高于对照组(P＜0.05);Pit注射后1hET浓度升至高峰,当缺血时间大于1h后,ET浓度有所回降,但仍明显高于对照组。免疫组化显示ET-1主要定位在心肌细胞和血管内皮细胞,缺血组心肌ET-1染色灰度值明显低于对照组(P＜0.01);RT-PCR结果显示缺血组PCR产物条带灰度值显著高于对照组(P＜0.01)。结论:垂体后叶素性心肌缺血可引起血浆及心肌ET浓度的升高并呈现一定的量效及时效关系,这可能与缺血刺激心肌ET-1基因的表达及蛋白合成有关。     

Effect of different temperature conditions of reperfusion on recovery of myocardial contractility after hypothermal cardiac ischemia

Central Research Laboratory, S. M. Kirov Medical Institute, Gor'kii, (Presented by Academician of the Academy of Medical Sciences of the USSR B. A. Korolev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 111, No. 2, pp. 128–129, February, 1990.     

Effect of single-leg resistance exercise on regional arterial stiffness

To examine the effects of lower-limb unilateral resistance exercise on central and peripheral arterial stiffness, thirteen participants (7 male and 6 female, mean age = 21.5 ± 0.7 years) performed leg press exercise using their dominant leg. Pulse wave velocity (PWV) was used to measure central (carotid to femoral) and peripheral (femoral to dorsalis pedis of both legs) arterial stiffness before, 5 min post, and 25 min post exercise. No change was found in central PWV. A leg-by-time interaction was found as peripheral PWV in the non-exercised leg did not change (7.9 ± 0.3 m/s to 7.9 ± 0.3 m/s to 8.0 ± 0.3 m/s, P = 0.907) while peripheral PWV in the exercised leg significantly decreased from pre (8.7 ± 0.4 m/s) to 5 min post exercise (7.5 ± 0.3 m/s, P = 0.008) and 25 min post exercise (7.8 ± 0.3 m/s, P = 0.031). Systolic blood pressure (BP) increased significantly from pre (126.9 ± 3.4 mmHg) to 5 min post exercise (133.7 ± 4.3 mmHg, P = 0.023) and was not different than resting values 25 min post exercise (123.2 ± 3.1 mmHg). There was no change in diastolic BP. Compared to heart rate (HR) pre-exercise (55.4 ± 1.4 bpm), HR was significantly increased 5 min post exercise (70.7 ± 3.0 bpm, P = 0.001) and 25 min post exercise (69.1 ± 2.0, P = 0.001). Acute resistance exercise appears to decrease arterial stiffness in the exercised leg while having no effect on central arterial stiffness or arterial stiffness of the non-exercised leg. These findings suggest that regional changes rather than systemic alterations may influence arterial stiffness following acute resistance exercise.     

清醒兔反复短阵心肌缺血对心肌梗塞影响的研究

本文旨在以清醒兔反复短阵心肌缺血(RBMI)模型,观察RBMI对局部心肌的影响。每24h缺血3分钟,连续10次,结果并不致心肌超微结构的明显改变及心电图的累积性损伤变化,但可致局部心肌毛细血管密度增加(P<0.001,X±SD)及线粒体横截面积增大(0.5302±0.1060 VS 0.5923±0.1305(μm~2),P<0.05);经历RBMI的动物在再次4h心肌缺血中的死亡率(1/9VS 9/17,P<0.001,卡方检验)、Q波出现的频率、梗塞范围(IS)(33.23±2.82 VS 56.61±8.01,坏死区/缺血区%,P<0.001)及ST段的抬高量均明显低于单纯4h缺血组,而两组血浆NAGase活性则明显增加,但组间比较并无差别。上述表明,RBMI不仅对兔心肌无累积性损伤,却能减少心肌严重缺血时的损伤,其机制可能与侧支循环的开放或重建有关;线粒体横截面积增大在其中的意义也值得重视。     

Afferent impulses from cardiac vagal fibers in myocardial ischemia

Summary When the descending branch of the left coronary artery is compressed the rate of flow of impulses in different cardiac fibers may be affected variously: there may be an increase, a decrease or a fluctuating change at different times after compression of the coronary vessels.In certain fibers there was no change in impulse rate although these fibers ran from cardiac mechanoceptors located in or near the ischemic zone.Presented by Active Member AMN SSSR V. V. Parin Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 59, No. 5, pp. 31–35, May, 1965     

黑木耳多糖对抗大鼠慢性缺血性心肌损伤

目的： 在整体大鼠心脏冠脉结扎模型上研究黑木耳多糖(AAP)的心肌保护作用,并探讨其作用机制。方法：在体大鼠实验模型,结扎冠状动脉左前降支,测定心肌梗死面积、血清乳酸脱氢酶（LDH）含量、超氧化物歧化酶（SOD）的活性、丙二醛（MDA）的含量以及心肌纤维化程度,观察不同剂量的黑木耳多糖（50、100和200 mg·kg-1·d-1,共20 d）的心肌保护作用,复方丹参作为阳性对照。结果：黑木耳多糖灌胃可明显减小在体大鼠缺血心肌的梗死面积,降低血清中LDH的含量。黑木耳多糖可明显减少MDA的生成,增强SOD活性,使心肌胶原纤维蛋白的含量降低。结论：黑木耳多糖能对抗大鼠缺血性心肌损伤,其机制可能与其抗氧化作用有关。     

Pathogenic and adaptive changes of the heart in regional myocardial ischemia and postischemic myocardial reperfusion

The evidence is presented and on development of both adaptive and pathogenic changes in the heart in its regional ischemia followed by renewal of circulation in major branches of coronary arteries. Cellular and molecular mechanisms of cardiac changes are characterized: energy supply to cardiomyocytes; their membrane physico-chemical status and structure, enzymes activity, ion-liquid balance, electrophysiological parameters; genetic program of myocardial cells; mechanisms of neurohumoral regulation. Mechanisms and role of the phenomenon of hormone-neuromediator dissociation of catecholamines (adrenaline and noradrenaline) correlations in long-term ischemia and reperfusion of the myocardium are described.     

Substrate oxidation and cardiac performance during exercise in disorders of long chain fatty acid oxidation

BackgroundThe use of long-chain fatty acids (LCFAs) for energy is inhibited in inherited disorders of long-chain fatty acid oxidation (FAO). Increased energy demands during exercise can lead to cardiomyopathy and rhabdomyolysis. Medium-chain triglycerides (MCTs) bypass the block in long-chain FAO and may provide an alternative energy substrate to exercising muscle.ObjectivesTo determine the influence of isocaloric MCT versus carbohydrate (CHO) supplementation prior to exercise on substrate oxidation and cardiac workload in participants with carnitine palmitoyltransferase 2 (CPT2), very long-chain acyl-CoA dehydrogenase (VLCAD) and long-chain 3-hydroxyacyl CoA dehydrogenase (LCHAD) deficiencies.DesignEleven subjects completed two 45-minute, moderate intensity, treadmill exercise studies in a randomized crossover design. An isocaloric oral dose of CHO or MCT-oil was administered prior to exercise; hemodynamic and metabolic indices were assessed during exertion.ResultsWhen exercise was pretreated with MCT, respiratory exchange ratio (RER), steady state heart rate and generation of glycolytic intermediates significantly decreased while circulating ketone bodies significantly increased.ConclusionsMCT supplementation prior to exercise increases the oxidation of medium chain fats, decreases the oxidation of glucose and acutely lowers cardiac workload during exercise for the same amount of work performed when compared with CHO pre-supplementation. We propose that MCT may expand the usable energy supply, particularly in the form of ketone bodies, and improve the oxidative capacity of the heart in this population.     

Effect of stress adaptation on cyclic nucleotide content in myocardial tissue during acute ischemia/reperfusion

We studied the effect of adaptation to chronic immobilization stress on the contents of cyclic adenosine monophosphate and cyclic guanosine monophosphate in myocardial tissue during coronary occlusion and reperfusion. The contents of cyclic adenosine monophosphate and cyclic guanosine monophosphate in the ischemic area and nonischemic myocardium of unadapted rats increased during coronary artery ligation for 10 min. Reperfusion for 10 min was followed by an increase in the content of cyclic adenosine monophosphate. During coronary occlusion, the content of cyclic adenosine monophosphate in the myocardium of stress-adapted rats increased less significantly than in control animals. No significant differences were found in the content of cyclic guanosine monophosphate in control and adapted rats. Our results suggest that poor response of the myocardial cyclic nucleotide system to ischemia/reperfusion in adapted animals is associated with the antiarrhythmic and cardioprotective effect of adaptation. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 145, No. 5, pp. 525–528, May, 2008