Relation between lipolysis and glycolysis during ischemia in the isolated rat heart

Summary The relation between lipolysis and glycolysis during ischemia was investigated in isolated perfused rat hearts. In hearts perfused with 11 mM glucose, ischemia caused a marked increase of glycerol release from 10 to 33 nmol/g wt weight/min. Substrate-free perfusion induced an initial stimulation of glycerol release, but lipolysis was subsequently reduced to values comparable to normoxic conditions. Neither did perfusion in the presence of acetate (10 mM) and -hydroxybutyrate (10 mM) stimulate lipolysis. Inhibition of glycolysis by pyruvate prevented the increase of glycerol release during ischemia. These data suggest a tight link between glycolysis and lipolysis during ischemia which is probably mediated by the availability of glycolytically produced glycerol-3-phosphate for reesterification. In the absence of glycerol-3-phosphate, the lipolysis is regulated by product inhibition. As a consequence, the tissue triglyceride levels after perfusion remained fairly constant in all groups of hearts.The calculated energy loss by the reesterification cycle during ischemia was found to be approximately 2.5% of the total energy production. These data are inconsistent with the assumption that this energy loss contributes significantly to the negative energetic balance of the heart during ischemia. Removal of fatty acids by reesterification may constitute a protective mechanism in order to prevent excessive intracellular accumulation of fatty acids and derivative esters during ischemia.     

Effect of biventricular pacing on heart rate variability in patients with chronic heart failure

BACKGROUND: Biventricular pacing is emerging as a long-term therapy for symptomatic heart failure. Analysis of heart rate variability (HRV) has become an important predictive tool in this syndrome. AIM OF THE STUDY: To assess whether chronic resynchronization therapy can affect HRV in patients with heart failure. METHODS AND RESULTS: Thirteen patients with heart failure were studied (mean age+/-1 S.E. 65+/-2.2 years, QRS 195+/-5.3 ms, NYHA class 3.2+/-0.1, LVEF 21+/-1.7%). The protocol included a preliminary no pacing period for 1 month following device implantation. Twenty-four hour Holter ECG recordings were performed at the end of this period (baseline) and after 3 months of biventricular stimulation (VDD mode). Prior to and following pacing patients underwent NYHA class evaluation, 6-min walk test, Quality of Life Assessment and a cardiopulmonary exercise test. Biventricular pacing improved functional class (P<0.0001) and Quality of life (P<0.0001), increased 6-min walk distance, (P=0.008) and exercise duration (P<0.0001) but had no significant effect on peak exercise VO(2). Resynchronization therapy increased mean 24-h RR (922+/-58 vs. 809+/-41 ms at baseline, P=0.006), SDNN (111+/-11 vs. 83+/-8 ms, P=0.003), SDNN-I (56+/-10 vs. 40+/-5 ms, P=0.02), rMSSD (66+/-14 vs. 41+/-8 ms, P=0.003), Total Power (5724+/-1875 vs. 2074+/-553 ms(2), P=0.03), Ultra Low Frequency Power (1969+/-789 vs. 653+/-405 ms(2), P=0.03) and Very Low Frequency Power (2407+/-561 vs. 902+/-155 ms(2), P=0.004). CONCLUSION: Biventricular pacing in heart failure improves autonomic function by increasing HRV. This may have important prognostic implications.     

Effect of iron overload in the isolated ischemic and reperfused rat heart

Summary It has been suggested that iron might play a pivotal role in the development of reperfusion-induced cellular injury through the activation of oxygen free radical producing reactions. The present study examined the effects of myocardial iron overload on cardiac vulnerability to ischemia and reperfusion. Moreover, the effect of the iron chelator deferoxamine in reversing ischemia-reperfusion injury was studied. Animals were treated with iron dextran solution (i.m. injection, 25 mg every third day during a 5 week period). The control group received the same treatment without iron. Isolated rat hearts were perfused at constant flow (11 ml/min) and subjected to a 15 minute period of global normothermic ischemia followed by reperfusion for 15 minutes. The effects of iron overload were investigated using functional and biochemical parameters, as well as ultrastructural characteristics of the ischemic-reperfused myocardium compared with placebo values. The results suggest that (a) a significant iron overload was obtained in plasma and hepatic and cardiac tissues (×2.5, ×16, and ×8, respectively) after chronic intramuscular administration of iron dextran (25 mg); (b) during normoxia, iron overload was associated with a slight reduction in cardiac function and an increase in lactate dehydrogenase (LDH) release (×1.5); (c) upon reperfusion, functional recovery was similar whether the heart had been subjected to iron overload or not. However, in the control group left ventricular end-diastolic pressure remained higher than in preischemic conditions, an effect that was not observed in the iron-overloaded group. Moreover, LDH release was markedly increased in the iron-loaded group (×4.2); (d) iron overload was associated with a significant worsening of the structural alterations observed during reperfusion, particularly at the mitochondrial and sarcomere level; (e) after 15 minutes of reperfusion, the activity of the anti-free-radical enzyme, glutathione peroxidase (GPX), was significantly reduced in ironoverloaded hearts, whereas catalase activity was increased; (e) the overall modifications observed in the presence of iron overload were prevented by deferoxamine. In conclusion, this study underlines the possible role of cardiac iron in the development of injury associated with ischemia and reperfusion, and the possible importance of the use of an iron-chelating agent in antiischemic therapy.     

Coronary hemodynamic data in ischemic heart disease according to ischemic behavior during pacing

In order to study the circulatory changes induced by maximal atrial pacing in coronary patients, coronary sinus blood flow (CBF) measured by continuous thermodilution, lactate extraction coefficient (K), arteriovenous difference in oxygen (AVO₂ diff), and aortic blood pressure (BP) were measured at basal state and at maximal heart rate (HR_max) in 11 patients without coronary disease (group I) and in 28 patients with severe coronary lesions, divided into two groups according to the absence (group IIa) or the presence (group IIb) of chest pain and ST-segment depression at HR_max. K was inverted in group IIb (24±17% vs −23±39%, p < 0.001), but remained unchanged in group I and group IIa. Despite similar HR_max, percent increase in CBF was significantly lower in group IIb (54±34%), than in group I (113±54%, p < 0.01). This contrasts with the higher values of the product of heart rate times systolic blood pressure (HR × SBP) as well as of diastolic blood pressure (DBP) in group IIb. The decrease in coronary resistances was lower in group IIb than in group I (p < 0.001), and also lower than in group IIa (p < 0.05). The ratio MO₂ × CBF/systolic BP × HR_max was significantly lowered only in group IIb (p < 0.001) confirming the imbalance between myocardial oxygen supply and oxygen demand. In coronary patients, myocardial ischemia induced by atrial pacing is related to an insufficient increase in CBF, well evidenced by continuous thermodilution.     

Involvement of lysosome-like particles in the metabolism of endogenous myocardial triglycerides during ischemia/reperfusion. Uptake and degradation of triglycerides by lysosomes isolated from rat heart

Summary The hormonal regulation and enzymatic basis of endogenous lipolysis in heart are not yet completely elucidated. The lysosomal fraction from rat heart appeared to be markedly enriched in triglycerides and a significant reduction in triglycerides in this fraction was found after prolonged perfusion or stimulation of lipolysis with glucagon. The enhanced rate of lipolysis, measured as glycerol release from the isolated perfused rat heart, was abolished 10–15 min after continuous glucagon administration. Omission of glucagon for another 60 min restored the ability of glucagon to stimulate lipolysis, indicating the limited availability of endogenous triglycerides and the presence of a transfer-system for triglycerides from a non-metabolically active pool to a metabolically active pool. The enhanced lipolysis induced by low-flow ischemia was found to be inhibited by the lysosomotropic agent methylamine (5 mM). Methylamine-perfusion during low-flow ischemia was accompanied by an increased recovery of myocardial triglycerides in the lysosomal fraction. The possible role of lysosome-like particles in myocardial triglyceride homeostasis was further investigated by studying the kinetics of uptake and degradation of labeled triglycerides by membrane-particles recovered in the subcellular fraction enriched with lysosomal marker enzymes. It appeared that isolated lysosomal membranes take up added triglycerides at an average rate of 30 nmoles/min/g protein. The bulk of these triglycerides taken up is stored whereas 20% is degraded to diglycerides and free fatty acids. More than 90% of the free fatty acids formed were released from the lysosomes into the supernatant. The uptake and degradation of triglyceride-filled liposomes by isolated myocardial lysosomes was inhibited during incubation with methylamine (5 mM). On the other hand, a lowering of pH during in vitro incubation increased the rate of uptake and degradation of added triglycerides by isolated lysosomes. These results indicate that lysosomes or lysosome-like particles are involved in the enhanced lipolysis during myocardial ischemia.     

伊贝沙坦对快速心房起搏家兔心房电重构的影响

目的观察伊贝沙坦对心房快速起搏8h家兔心房电重构及心房肌细胞超微结构改变的影响。方法将12只家兔随机分为伊贝沙坦组和对照组。经颈内静脉将电极置入右心房,以600次/min行快速心房起搏,分别测定起搏前及起搏后0.5h、1h、4h、8h及停止起搏后10min、20min、30min,S1S1为200ms、150ms时的心房有效不应期(AERP200、AERP150);取未起搏家兔及每组起搏8h后家兔右心耳组织观察超微结构。结果①心房快速起搏8h,对照组家兔AERP缩短,起搏0.5h内AERP缩短幅度最明显;AERP频率自适应性出现了下降—逆转;停止起搏后30minAERP及AERP频率自适应性基本恢复至起搏前水平(最初10min恢复迅速)。②伊贝沙坦组家兔8h心房快速起搏过程中各时间点AERP较起搏前无明显变化。③8h心房快速起搏后对照组家兔心房肌细胞超微结构可见线粒体肿胀、脊溶解、糖原聚集,伊贝沙坦组家兔心房肌细胞超微结构基本正常。结论伊贝沙坦可阻止8h心房快速起搏所致的心房电重构和心房肌细胞超微结构改变。     

心脏缺血和再灌注对冠状动脉内起搏效能的影响

目的 探讨心脏缺血再灌注(ischemia-reperfusion,I/R)过程中,冠状动脉内起搏阈值的动态变化及规律.方法 10只小型约克猪,按照常规经皮冠状动脉成形术(PTCA)方法,使用0.014英寸的BWM导丝进入左前降支(LAD)远端.使用over-the-wire(OTW)球囊沿导丝进入血管,到达距导丝远端1 cm处.采用球囊堵闭造成心脏I/B模型,血管堵闭和再灌注通过冠状动脉造影证实.导丝外端和临时起搏测试仪相连,分别检测LAD堵闭前以及堵闭后5、10、20、30、40 min及再灌注5、10、20、30、60、90、120 min的起搏阈值和阻抗.结果 基础起搏阈值为(0.71±0.24)V.与缺血前相比,缺血早期冠状动脉内起搏阈值无明显变化;缺血30 min时,冠状动脉内起搏阈值明显增加,直到40 min时,冠状动脉内起搏阈值增至(1.99±1.36)V,几乎达缺血前3倍.再灌注后5 min后冠状动脉内起搏阈值明显回落至(1.06±0.46)V,直至再灌注末均保持相同趋势.缺血前、缺血中和再灌注末阻抗在912 Q与1133 Q之间波动,但各时间点之间差异无统计学意义.结论 心肌较长时间急性缺血可导致冠状动脉内起搏阈值明显增高,但即使发生心肌坏死后,增高的阈值仍在可起搏范围内.再灌注可使增高的起搏阈值明显回落;但和缺血前相比,仍有增高趋势.在缺血期和再灌注期,冠状动脉内起搏阻抗变化差异无统计学意义.     

Evaluation of free radical and lipid peroxide formation during global ischemia and reperfusion in isolated perfused rat heart

Summary Free radical species have been implicated as important agents involved in myocardial ischemic and reperfusion injuries. In our study, formation of free radicals was measured directly with electron paramagnetic resonance spectroscopy before ischemia, during 10 minutes of global ischemia, and 20 seconds after reperfusion in the rat heart. We also investigated the formation of thiobarbituric acid-reactive material as index of lipoperoxidation induced by free radicals and measured arrhythmias. Production of free radicals takes place during ischemia since the signal intensity with a g value of 2.004 attributed to free radical species was increased by 50% after 10 minutes of global ischemia. In hearts reperfused with oxygenated perfusate for 20 seconds, the signal doubled. These experiments supply evidence that free radicals are generated in isolated rat heart during a short period of global ischemia and reperfusion. However, this increase was not associated with a concomitant increase of lipid peroxides in the myocardium nor with the development of reperfusion arrhythmias.     

双心室同步起搏治疗充血性心力衰竭的临床应用

目的　观察三腔双心室起搏治疗充血性心力衰竭效果。方法　患者男性 2例 ,女性 1例 ,平均年龄 5 7岁 ,为充血性心功能衰竭伴左束支阻滞 ,植入三 (四 )腔双心室起搏器。左心室起搏通过冠状静脉窦植入 2 187或 2 188电极导线 ,置于心后静脉起搏左心室 ,左右心室电极导线通过 Y形转接器与双腔起搏器连接。结果　双心室起搏并辅以合适的 AV延迟后 ,患者心力衰竭症状明显改善 ,N YHA分级从 ～ 级改善至 级 ,二尖瓣返流明显减少。结论　初步临床应用提示 ,双心室同步起搏治疗充血性心力衰竭是可行而有效的     

Ventricular dyssynchrony in dilated cardiomyopathy: the role of biventricular pacing in the treatment of congestive heart failure

Despite advances in pharmacologic therapy, the prognosis of patients with advanced congestive heart failure (CHF) remains poor. Many of these patients have cardiac conduction abnormalities, such as left bundle-branch block or interventricular conduction delays, that can lead to ventricular dyssynchrony (abnormal ventricular activation that results in decreased ventricular filling and abnormal ventricular wall motion). Biventricular pacing is an alternative, nonpharmacologic therapy under active investigation for the treatment of CHF. Resynchronization devices with transvenous leads in the right atrium, right ventricle, and left ventricle (via the coronary sinus) have been implanted in patients to provide atrial triggered biventricular pacing. The use of such devices has been associated with improvement in ejection fraction, dP/dt, stroke work, and functional class. The proposed mechanisms involved in improving ventricular function with biventricular pacing include improved septal contribution to ventricular ejection, increased diastolic filling times, and reduced mitral regurgitation. This article reviews the pathophysiology of ventricular dyssynchrony and examine insights from clinical trials that are evaluating cardiac resynchronization therapy for CHF.     

右室心尖部起搏对老年患者心功能的影响

目的:评价右室心尖部起搏对老年患者心脏功能的影响。方法:入选因缓慢性心律失常安装心脏永久起搏器的老年患者(年龄≥60岁)115例。所有患者均为心房电极位于右心耳,心室电极置于右室心尖部;VVI型起搏器60例,DDD型起搏器55例。按最终心室累积起搏百分比(Cum%VP)分为3组:A组Cum%VP<50%(34例),B组Cum%VP≥50%~<100%(38例),C组为完全心室起搏,即Cum%VP=100%(43例)。通过询问患者自觉症状,行运动耐量、左室射血分数(LVEF)及脑利钠肽(BNP)水平的检查,了解各组及不同起搏模式患者术前、后心功能的变化。结果:①术后18个月,与术前比较,3组均有心功能恶化趋势,即LVEF、BNP均有降低、升高的改变,但A组的改变幅度最小,C组的改变幅度最大,B组介于两者之间;②VVI与DDD起搏相比,对心功能的影响无差异,VVI起搏患者心房颤动和脑栓塞发生率略高。结论:①老年患者在右室心尖部起搏情况下,随着Cum%VP的增加,心功能恶化程度增大;②VVI或DDD起搏模式不是影响老年患者心功能的决定因素。     

Temporal changes in the subcellular distribution of protein kinase C in rabbit heart during global ischemia

Our recent studies utilizing an in vivo regional ischemia model revealed no changes in the subcellular distribution of protein kinase C (PKC) in dog and rabbit hearts after repeated 5 min episodes of preconditioning ischemia/reperfusion. However, 10 min of sustained ischemia resulted in an increase in PKC activity in the membrane fraction. These findings indicate that prolonged ischemia may cause changes in the subcellular distribution of PKC. However, the detailed time course of these changes during sustained severe ischemia is poorly resolved. Thus, our objective was to study temporal changes in PKC distribution in the cytosolic, nuclear, and membrane fractions isolated from globally ischemic rabbit heart. Hearts were removed under deep anesthesia, placed into normal saline at 37°C, and repeatedly sampled from apex to base at baseline, 2, 5, and 10 min into global ischemia, with matched samples obtained in every heart. PKC activity was increased at 2 min into global ischemia in both the nuclear fraction (1069±75 vs 893±49 pmol/min/g at baseline; p=0.05) and the membrane fraction (1374±95 vs 1187±59 pmol/min/g at baseline; p<0.05) with persistent translocation observed at 5 and 10 min into the protocol. Thus, direct biochemical determination of PKC activity in the isolated rabbit heart revealed increased activity in the nuclear and the membrane fractions as early as 2 min into global ischemia. Received: 27 August 1997, Returned for revision: 17 September 1997, Revision received: 13 October 1997, Accepted: 6 November 1997     

Effects of felodipine on the ischemic heart: Insight into the mechanism of cytoprotection

Summary To assess whether the administration of felodipine protects the myocardium in a dose-dependent manner against ischemia and reperfusion, isolated rabbit hearts were infused with three different concentrations of felodipine: 10^-10, 10^-9, and 10^-8 M. Diastolic and developed pressures were monitored; coronary effluent was collected and assayed for CPK activity and for noradrenaline concentration; mitochondria were harvested and assayed for respiratory activity; and ATP production and calcium content and tissue concentration of ATP, creatine phosphate (CP), and calcium were determined. The occurrence of oxidative stress during ischemia and reperfusion was also monitored in terms of tissue content and release of reduced (GSH) and oxidized (GSSG) glutathione. Treatment with felodipine at 10^-10 and 10^-9 M had no effect on the hearts when perfused under aerobic conditions, whilst the higher dose reduced developed pressure from 57.7 ± 2.6 to 30.0 ± 2.6 mmHg (p < 0.01). On reperfusion treated hearts recovered better than the untreated hearts with respect to left ventricular performance, replenishment of ATP and CP stores, and mitochondrial function. Recovery of developed pressure was 100% at 10^-8 M, 55% at 10^-9 M, and 46% at 10^-10 M. The reperfusion-induced tissue and mitochondrial calcium overload, release of CPK and noradrenaline, and oxidative stress were also significantly reduced. The effects of felodipine were dose dependent. Felodipine inhibited the initial rate of ATP-driven calcium uptake but failed to affect the initial rate of mitochondrial calcium transport. It is concluded that felodipine infusion provides dose-dependent protection of the heart against ischemia and reperfusion. Because this protection also occurred at 10^-9 M and 10^-10 M in the absence of a negative inotropic effect during normoxia and of a coronary dilatory effect during ischaemia, it cannot be attributed to an energy-sparing effect or to improvement in oxygen delivery. From our data we can envisage two other major mechanisms—(1) membrane protection and (2) reduction in oxygen toxicity. The ATP-sparing effect occurring at 10^-8 M is likely to be responsible for the further protection.Cattedra di Cardiologia, Universita' degli Studi di Brescia     

Mitochondrial damage during ischemia determines post-ischemic contractile dysfunction in perfused rat heart

Possible mechanisms underlying sodium overload-induced ischemia/reperfusion injury in perfused rat hearts were examined. Massive accumulation of myocardial Na(+) occurred during ischemia, suggesting cytosolic sodium overload in cardiac cells. Treatment of the pre-ischemic heart with 0.3 micromol/l tetrodotoxin or 3 micromol/l ethyl-isopropyl amiloride enhanced post-ischemic contractile recovery (72 or 82% of initial vs 24% for untreated group), which was associated with suppression of tissue Na(+) accumulation (138 or 141% of initial vs 270% for untreated group), restoration of tissue high-energy phosphates, and preservation of the ability of mitochondria to produce ATP in the ischemic/reperfused heart. The release of cytochrome c from the ischemic heart was observed, which was blocked by treatment of the pre-ischemic heart with these agents. The improvement of post-ischemic contractile recovery by these agents was closely correlated with the ability of mitochondria to produce ATP during ischemia. To examine the effects of sodium overload on mitochondrial function, isolated mitochondria were incubated in the presence of various concentrations of Na(+). Na(+) induced mitochondrial membrane perturbations such as depolarization of the membrane potential, mitochondrial swelling, cytochrome c release from isolated mitochondria, and a reduction in oxidative phosphorylation. These events in the isolated mitochondria were not blocked by the presence of the above agents. The results suggest that cytosolic sodium overload in cardiac cells may induce deterioration of the mitochondrial function during ischemia and that this mitochondrial damage may determine post-ischemic contractile dysfunction in perfused rat hearts.     

Regional myocardial perfusion during chronic biventricular pacing and after acute change of the pacing mode in patients with congestive heart failure and bundle branch block treated with an atrioventricular sequential biventricular pacemaker

BACKGROUND: Biventricular (BiV) pacing has been found to improve systolic function and exercise tolerance in patients with severe congestive heart failure and bundle branch block. The mechanisms behind this beneficial effect is still not sufficiently clarified. AIM: To evaluate the regional myocardial perfusion (MP) during BiV pacing and after acute change of the pacing mode to conventional dual chamber (DDD) pacing, and single chamber atrial (AAI) pacing in patients with severe congestive heart failure and prolonged QRS width treated with chronic BiV pacing. METHODS AND RESULTS: Fourteen patients (age 63+/-7 years, 13 male) were evaluated 13+/-7 months after implantation of a triple-chamber biventricular pacemaker. MP was quantified with 13N-labeled ammonia positron emission tomography during BiV pacing, DDD pacing, and AAI pacing. MP was assessed in the anterior, lateral, inferior, and septal regions, and the global mean MP was calculated. Clinical assessment was performed before pacemaker implantation and after at least 3 months of BiV pacing including a 6-min walk test (WT), New York Heart Association (NYHA) class functional score and echocardiography. Global mean MP (BiV: 0.65+/-0.20 vs. DDD: 0.65+/-0.21 vs. AAI: 0.65+/-0.18 mlg(-1)min(-1)) and MP in each of the four regions did not differ between the three pacing modes. The patients improved clinically during BiV pacing; 6 min WT increased (338+/-59 vs. 415+/-73 m, P<0.001), NYHA class score improved (class I/II/III/IV: 0/0/11/3 vs. 1/9/2/0, P<0.001), and left ventricular ejection fraction increased (21+/-5 vs. 29+/-8%, P=0.004). CONCLUSION: No differences in regional MP are detectable after chronic BiV pacing when the pacing mode is changed acutely in patients with severe congestive heart failure and bundle branch block. This finding indicates, that the clinical improvement caused by BiV pacing is not associated with any increase in the MP and thereby oxygen demand.     

双心室起搏治疗心力衰竭的有关临床试验

起博治疗充血性心力衰竭有了新的进展 ,试验证明多点起搏或单独左心室起搏比单独的右心 DDD起搏更有益于改善患者血流动力学功能及生活质量     

缺血再灌注不同时间点大鼠海马细胞内Ca~(2+)含量比较

目的研究脑缺血再灌注损伤中大鼠海马神经细胞内Ca~(2+)含量的变化,检测环磷腺苷葡胺(MAC)预处理对其的影响。方法将SD大鼠60只按实验分为正常组(5只)、假手术组(5只)、缺血再灌注组(再灌注组)和MAC预处理组(预处理组)。再灌注组和预处理组又分为再灌注后2、24、48、72 h和7天5个时间点,每个时间点5只大鼠,线栓法建立大鼠局灶性脑缺血再灌注损伤模型,流式细胞仪检测缺血侧海马神经细胞内Ca~(2+)的含量,观察MAC预处理对细胞内Ca~(2+)含量变化的影响。结果与假手术组比较,再灌注组2 h细胞内Ca~(2+)含量开始增高,24、48 h Ca~(2+)含量达到高峰(P0.01),72 h Ca~(2+)含量开始下降,7天Ca~(2+)含量进一步降低,但仍高于假手术组水平;与再灌注组比较,预处理组缺血再灌注2 h Ca~(2+)含量差异无统计学意义,24、48、72 h Ca~(2+)含量显著降低(P0.01)。结论细胞内Ca~(2+)含量增高为缺血再灌注损伤的病理机制之一,MAC预处理能有效抑制细胞内Ca~(2+)含量增高,在大鼠局灶性脑缺血再灌注损伤中起到保护作用。     

双心室起搏治疗心力衰竭的初步经验

目的 介绍双心室起搏治疗心力衰竭衰竭的初步经验。方法 ６例充血性心力衰竭患者,男性４例,女性２例,平均年龄５８岁;心功能ＮＹＨＡ分级：Ⅲ～Ⅳ级：均伴有心室内阻滞。患者均植入了三腔双心室起搏器,左心室导线通过冠状静脉窦插入心脏静脉侧分支或侧后分支。结果 所有患者植入起搏器后临床症状改善,超声心动图检查显示左心室收缩功能和同步性改善,舒张期充盈改善,二尖瓣返流减少,此外,双心定起搏后,所有病例ＱＲＳ时     

Optimized perioperative biventricular pacing in setting of right heart failure.

AIMS: A 78-year-old female with prior atrioventricular junctional ablation for paroxysmal atrial fibrillation and implantation of DDDR pacemaker underwent repair of severe tricuspid insufficiency. Effects of biventricular pacing were tested with temporary wires at the conclusion of cardiopulmonary bypass. METHODS: An ultrasonic flow probe was placed on the ascending aorta for real time cardiac output measurements. Atrioventricular delay optimization was performed and biventricular pacing was initiated while right-left ventricular delays were varied. RESULTS: There was no advantage of biventricular pacing (optimum right-left ventricular delay of +80 ms) compared with existing DDD. CONCLUSIONS: This study confirms the physiological effects of right-left ventricular delay on cardiac output after cardiopulmonary bypass.     

大鼠脑缺血再灌注后脑源性神经营养因子的表达及意义

目的　研究脑局灶缺血再灌注后脑源性神经营养因子 (BDNF)的表达规律及其意义。方法　健康雄性Wistar大鼠 30只 ,随机分为正常对照组、假手术组和缺血再灌注组 ,按照改良的栓线法建立大脑中动脉缺血再灌注大鼠模型。用免疫组织化学方法检测BDNF在脑组织中的表达情况。结果　BDNF免疫阳性表达在缺血再灌注组的梗死中心区梗死灶边缘带有显著增强的阳性表达。再灌注 15min开始增多 ,再灌注 1h明显增多 ,2h达到高峰 ,4h开始下降 ,2 4h恢复至正常对照组水平。结论　缺血再灌注损伤可诱导BDNF极早表达 ,并迅速升高 ,有利于缺血再灌注损伤后神经细胞的存活及后期神经功能恢复