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。     

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     

高原肺水肿患者血流动力学变化及对吸氧反应的测定

目的:探讨高原肺水肿的发病机理。方法:采用右心漂浮导管检测法, 对9例高原肺水肿患者及9例同海拔高原健康人的血流动力学指标进行了检测, 同时也观察了吸入纯氧对高原肺水肿患者血流动力学的影响。结果:高原肺水肿患者发病时, 肺动脉平均压、肺血管阻力、心脏指数均明显高于同海拔高度健康人, 而患者肺动脉楔压, 右心房压力同对照组相比, 未见显著差异;吸氧后, 高原肺水肿患者心率、肺动脉平均压力, 肺血管阻力及心脏指数均较吸氧前明显下降, 特别是肺动脉平均压及肺血管阻力下降尤为明显, 肺动脉平均压力在吸氧1min后即明显下降, 吸氧5min后, 下降至最低值, 但吸氧20min后仍未达对照组水平。结论:高原肺水肿是非心源性肺水肿, 肺动脉高压在其发病中起重要作用。     

前列腺素E_2对家兔血液动力学的影响及对急性心肌梗塞后的心肌保护作用

本实验结果表明,家兔静注PGE_2(Iμg/min/kg)后,动脉收缩压、静脉舒张压、平动脉压均显著下降,左室 dp/dt max,-dp/dt max、心肌耗氧量亦显著下降;心率、左室射血时间、左室收缩成分缩短速率,左室等容舒张期压力下降的时间常数均无明显改变。结果提示:家兔静注PGE_2,可降低动脉血压,减少心脏负荷,降低心肌耗氧量,但对心脏舒缩功能无明显影响。急性心肌梗塞的家兔,静注同剂量的PGE_2,可使 dP/dt max、-dp/dt max显著高于对照组;ST段抬高值亦显著低于对照组,LVSP高于对照组但无统计学意义。本结果亦进一步表明PGE_2可改善心肌血供,降低室壁张力,减少心肌耗氧量,以维持心脏功能。提示PGE_2对心肌梗塞具有保护作用。     

氨联苯啶酮对高原动物肺动脉压和肺气体交换的影响

9只出生、生长在高原的猪,静脉注入氨联吡啶酮,剂量为2.5mg/Kg,在注药后不同时间分别重复测定指标。给药后左室和右室dp/dtmax和心指数稍增加但无显著差异;对照期肺动咏平均压为39.7±7.4mmHg,肺血管阻力为9.43±3.34mmHg/L/min,给药后     

硝苯吡啶对幼猪缺氧性肺动脉压增高和右心室肥大的影响

在本实验中,观察了缺氧(模拟4000米高原)和在缺氧条件下注入硝苯吡啶溶液对幼猪(n=18)血流动力学指标和血液气体参数的影响。结果表明:1.缺氧时,肺动脉平均压(Psa)和肺血管阻力(PVR)显著增高,颈总动脉压(Psa)和总外周阻力(TPR)亦增高,心输出量(CO)则无明显改变,2.在4000米模拟高原注入硝苯吡啶(40μg/kg,IV)溶液后,Psa和PVR显著下降,Psa和TPR亦下降,CO明显增加;3.每天肌注两次硝苯吡啶(40mg/kg/次)溶液的幼猪,经过慢性间断性缺氧(模拟4000米高原,8小时/天,共30天)后,右心室并无明显肥大。实验结果说明硝苯吡啶能防治猪的缺氧性肺动脉高压及慢性间断性缺氧引起的右心室肥大。     

大鼠心肌梗塞致脑缺血的研究

本文观察了大鼠心肌梗塞后心、脑组织生理和生化指标的动态改变,结果显示:BP、BBF、±dp/dt max在结扎后6h显著降低。BBF于72h恢复,BP、±dp/dt max于7天恢复。心、脑组织MDA在72h升至峰值,7天恢复。NAGase则于7天达高峰,14天恢复。MDA与NAGase的改变与大鼠心梗后心泵功能的变化呈一致性,说明心源性脑缺血反应的存在。     

慢性缺氧对肺动脉压与肺血管反应性的影响

一般认为,慢性缺氧动物肺血管反应性增高与收缩增强是产生肺动脉高压的重要基础。本文的目的是探讨在肺动脉压随缺氧时间延长而递增的过程中,肺血管反应性是否也平行地增高。实验用雄性Wistar大鼠,体重200～270克,随机分为平原对照组、模拟5000米高度低压舱内连续缺氧4天、10天、20天、30天等五个组,每组8只动物。在12％乌拉坦溶液(10ml/kgBW)腹腔麻醉下行右心导管术测肺动脉压(PAP)与右室内压最大上升速率(dp/dt max)后,处死动物,取主肺动脉制备血管条(10×1mm),垂直悬挂于管状恒     

慢性缺氧对大鼠肺动脉和主动脉舒缩反应的影响

大鼠经模拟高原5000m缺氧15d后,右肺动脉对Ach所致的舒张反应显著减弱,对5-HT所致的收缩反应显著增强,胸主动脉则无这种变化。结果提示,慢性缺氧对肺血管和体血管血管反应性的不同影响可能是高原缺氧环境下肺动脉压升高、体动脉压下降或不变的重要原因之一。     

慢性肺动脉高压肺血管力学特性的评价

本文以风心病二尖瓣病变合并被动性肺动脉高压为研究对象,借助右心导管技术和利用压力波形面积确定动脉顺应性的改进方法,通过测定肺血管阻力和顺应性,以评价慢性肺动脉高压肺血管力学特性的变化规律。发现慢性肺动脉高压患者肺动脉血管阻力明显升高（P＜0.01）;而反映血管壁固有结构的零压顺应性Co明显下降(P＜0.01),与术前肺动脉平均压呈显著负相关(r＝－0.745P＜0.05);扩血管药物试验提示不同程度肺动脉高压组的肺血管阻力均有显著下降(P＜0.01),轻度肺高压组零压顺应性和平均压顺应性均明显升高(P＜0.01);而重度肺高压组零压顺应性Co无明显变化(P＞0.05)。由此我们认为慢性肺高压肺血管都存在不同程度的重建,肺血管外周血管阻力和顺应性是影响其肺动脉压力水平的主要因素。     

Comparative study of the effect of pacing mode on the interaction of the right and left ventricles

This study was designed to evaluate ventricular dyssynchrony from the viewpoint of the interaction of right and left ventricular contractions. Forty-three patients, 24 with sick sinus syndrome, 9 with complete atrioventricular block, and 10 with normal sinus rhythm were involved in this study. Microtip transducer catheters were advanced into both the left and right ventricles and ventricular pressure and the associated dp/dt were recorded simultaneously. Hemodynamic differences in various pacing modes were analyzed using pressure and dp/dt recordings obtained from the left and right ventricles. When an asynchrony between the right and left ventricular contractions existed, the right ventricular positive peak dp/dt developed a dual-peak waveform, the second peak corresponding in time to the peak of the left ventricular positive peak dp/dt. This dual-peak dp/dt waveform was seen with ventricular (VVI) and atrioventricular sequential (DVI) pacing, whereas a single-peak waveform was seen with atrial (AAI) pacing or sinus rhythm. In cases where DVI or VVI pacing modes are selected, an asynchronous effect between contractions of the right and left ventricles may occur, with dual-peak dp/dt of the right ventricle. Because the dual-peak dp/dt waveform indicates ventricular dyssynchrony, reducing the distance from peak I to peak II could maintain the synchronization of the right and left ventricles. It is considered particularly vital to give sufficient consideration to this point in chronic heart failure patients with left bundle branch block requiring biventricular pacing.     

心肌梗死模型大鼠心功能与血管活性物质释放关键蛋白NSF-siRNA

背景：如何通过有效的干预手段,降低心血管疾病发病率与死亡率,已经成为一个日益迫切的重大公共卫生问题。 目的：探索腺病毒介导的血管活性物质释放关键蛋白NSF-siRNA对心肌梗死模型大鼠心脏功能的影响。 方法：36只成年SD大鼠,经结扎左冠状动脉前降支建立急性心肌梗死模型。心电图确定模型成功后,分别给予大鼠心脏左室壁梗死区周围局部注射NSF-siRNA腺病毒(实验组)、阴性腺病毒(对照组)及生理盐水(生理盐水组)。2周后通过无创超声心动图测定心脏左室射血分数(LVEF)值;并通过右颈外动脉置管,连接BL-420生物机能实验系统测定左心室舒张末期压(LVEDP)及心室内压力变化率峰值(dp/dtmax)评价心功能;随后取材、连续切片,观察心肌梗死范围。 结果与结论：2周时实验组左室射血分数值与对照组及生理盐水组相比明显增加(P < 0.05);实验组左室舒张末压与对照组及生理盐水组相比显著降低(P < 0.05);实验组左室最大压力上升速率与对照组及生理盐水组比较明显增加(P < 0.05);心肌梗死面积各组比较差异均无显著性意义(P > 0.05)。结果可见梗死局部周围注射腺病毒介导的NSF-siRNA表达载体,能显著改善模型大鼠心肌梗死后2周左室射血分数、左心室舒张末期压、心室内压力变化率峰值3项心功能指标,但对心肌梗死面积无明显影响。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

二肾一夹和肾下主动脉缩窄模型对高血压大鼠右室纤维化的影响

目的探讨二肾一夹（2K1C）及肾下主动脉缩窄（INAC）高血压模型大鼠右室功能与结构的改变及其Ang（1-7）的影响。方法建立2K1C及INAC模型，并采用微渗泵植入技术，用Ang（1-7）进行体内干预，采用无创及有创方法检测动物血压及右心功能；定性及定量分析这两种高血压模型右室心肌细胞及纤维化程度的变化。结果在血压增高的过程中，2K1C模型右室的功能和结构均发生明显的变化，术后14d时其右室收缩及舒张功能均已受损；其心肌细胞无明显变化，但其胶原已明显增多，CVF及PVCA均明显增加；应用Ang（1-7）干预可明显改善2K1C大鼠右室功能并减轻心肌纤维化的发生。在INAC动物模型，14d时其右心功能并无明显变化，无心肌细胞的改变及心肌纤维化的发生，Ang（1-7）对其亦无明显影响。结论在这两种动物模型，其右心功能的改变与其是否发生心肌纤维化有关，而心肌纤维化的发生是RAAS激活的结果。Ang（1-7）可抑制2K1C模型右室心肌纤维化进而改善右心功能，其机制可能与直接抑制RAAS有关。     

The effect of changes in cardiac frequency on left and right ventricular dP/dt max at different contractile states of the myocardium

Summary In 17 canine heart-lung preparations the dependence of frequency potentiation of the right and left ventricular myocardium on the basic inotropic state of the heart was investigated. The effect of unipolar stimulation of the right atrium on dP/dt max in both ventricles was measured. The aortic pressure was maintained constant.Shortly after isolation of the heart, a stepwise increase of rate from 140 to 200 beats/min only had a very weak influence on left ventricular dP/dt max. With deterioration of the myocardium the frequency potentiation of dP/dt max increased considerably. End-diastolic pressure regularly decreased with rising cardiac frequency. Since the real positive inotropic effect is masked by the concomitant fall in diastolic loading, the end-diastolic pressure was maintained constant in a second group of 8 hearts during rate variation. The most pronounced inotropic effect was now found shortly after isolation of the heart. A rate increase of 30 beats/min resulted in a 20% rise of dP/dt max. The frequency potentiation decreased with deterioration of the heart resulting in a 12% dP/dt max increase at an estimated inotropic state of 50% of control. When the contractile state of the heart was improved above the control state by calcium application the frequency potentiation of the myocardium decreased.In the right ventricle similar results were obtained except for the fact that no significant correlation between the steepness of the frequency characteristics and the contractile state of the heart could be found when the end-diastolic pressure was kept constant.Portions of this study have been presented at the 45th Congress of the German Physiological Society     

Norepinephrine and isoprenaline induced changes of peripheral blood flow acceleration caused by changes of cardiac inotropy

Summary In anesthetized dogs the norepinephrine (NE) and isoprenaline (ISO) (1–1024 ng/kg i.v.)-induced increase of maximum peripheral flow acceleration (celiac artery, cranial mesenteric artery, renal artery, and femoral artery) and the changes of the maximum first derivative of arterial pressure were compared with the increases of maximum ascending aortic flow acceleration and maximum first derivative of left ventricle pressure (LV dP/dt max).The maximum effect of each dose on maximum acceleration of flows (dF/dt max) and maximum first derivative of pressures (dP/dt max) occurred simultaneously for all variables. The effect was dose-dependent. Sensitivity was similar for NE (D₅₀:2256–512 ng/kg) and for ISO (D₅₀: 128–256 ng/kg).We demonstrated that other variables than inotropic action (heart rate, left ventricular end diastolic pressure and diastolic aortic pressure) played only a minor role in the increases of LV dP/dt max in our studies.In contrast with the uniform response of dF/dt max and dP/dt max, the reaction of peripheral vascular resistance varied. In particular in the gastrointestinal tract the resistance could either be increased (NE, D₅₀: 115 ng/kg) or decreased (ISO, D₅₀: 15 ng/kg). Gastrointestinal resistance was a more sensitive variable for catecholamine stimulation than dF/dt max and dP/dt max.The data show that under the present experimental conditions enhancement of peripheral flow acceleration induced by NE and ISO is due to increase of cardiac inotropy.Supported by the Foundation for Medical Research FUNGO     

Left ventricular inotropic and peripheral vasomotor responses from independent changes in pressure in the carotid sinuses and cerebral arteries in anaesthetized dogs

1. The pressure perfusing the isolated carotid sinuses and the pressure perfusing the cerebral circulation were changed independently, and the resulting inotropic responses in the left ventricle and peripheral vasomotor responses were determined.2. Inotropic responses were assessed by measuring changes in the maximum rate of change of left ventricular pressure (dP/dt max) with heart rate and mean aortic pressure held constant. Vascular resistance changes were usually assessed by perfusing the descending thoracic aorta at constant flow and measuring changes in perfusion pressure.3. Decreases in carotid sinus pressure over the baroreceptor sensitivity range resulted in a 45% increase in dP/dt max and a 59% increase in vascular resistance.4. Unless arterial oxygen tension was abnormally low, lowering cerebral perfusion pressure to 50 mm Hg resulted in little or no inotropic and vasomotor responses. In the presence of hypoxaemia (P(a,O2) < 60 mm Hg), lowering cerebral perfusion pressure to below about 80 mm Hg resulted in marked responses.5. These experiments suggest that, unless arterial oxygen tension is abnormally low, the carotid sinus reflex and not cerebral hypotension is important in the control of the inotropic state of the heart and of vasomotor activity. With hypoxaemia, responses from cerebral hypotension may also be important.     

不同β-肾上腺素能受体对低氧应激大鼠心脏舒缩功能的影响

目的:探讨不同β-肾上腺素能受体(β-adrenergic receptor,β-AR)在急性低氧应激中对大鼠左、右心室舒缩功能的影响。方法:健康雄性SD大鼠随机分为4组(n=7):对照组(control group)、非选择性β-肾上腺素能受体阻断剂普萘洛尔组(propranolol group)、选择性β_1-肾上腺素能受体阻断剂阿替洛尔组(atenolol group)和选择性β2-肾上腺素能受体阻断剂ICI 118,551组(ICI 118,551 group),各组大鼠分别在常氧(西宁,海拔2 260 m,20.9% O_2,79.1% N_2)和急性低氧(15.0% O_2,85.0% N_2)通气的状态下进行实验,监测各组大鼠心率(heart rate,HR)、左心室收缩压(left ventricular systolic pressure,LVSP)、右心室收缩压(right ventricular systolic pressure,RVSP)及左、右心室内压最大上升和下降速率(±dp/dt_(max))等心功能指标变化;同时,比较低氧通气前后动脉血气的变化。结果:常氧下,propranolol组、atenolol组与ICI 118,551组LVSP和左心室±dp/dt_(max)较给药前降低,同时propranolol组与atenolol组RVSP和右心室±dp/dt_(max)较给药前明显降低(P0.05)。低氧通气5 min后,各组大鼠与常氧组相比动脉血氧分压(PaO_2)、LVSP和左心室±dp/dt_(max)均降低(P0.05);但右心室±dp/dt_(max)明显升高(P0.05);且低氧条件下control组心功能指标的变化程度均比propranolol组和atenolol组明显。结论:低氧应激时心脏β_1-AR的激活可能是心脏发挥代偿调节的重要方式,但右心室通过紧张源性扩张代偿表现出的右心舒缩功能增强对低氧下机体循环血流量的维持更为重要。     

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.     

肺高血流模型大鼠肺动脉重构与奈必洛尔的影响

背景：血管舒张型肾上腺素β1受体阻断药奈必洛尔能否有效降低肺动脉压,对肺血管重构有何影响,目前尚不清楚。 目的：观察奈比洛尔对肺高血流模型大鼠肺动脉重构的影响。 方法：将40只SD大鼠随机均分为4组,模型组、奈比洛尔组、卡托普利组均制备肺动脉高压并肺血管重构大鼠模型,假手术组仅分离腹主动脉及下腔动脉;造模后5 d,奈比洛尔组、卡托普利组分别于灌胃给予奈比洛尔溶液1 mg/(kg•d)与卡托普利溶液5 mg/(kg•d),模型组与假手术组灌胃给予等体积生理盐水。给药8周后,对比4组平均肺动脉压、右心室肥厚指数、肺动脉形态学变化、肺动脉超微结构及肺动脉环舒张率。 结果与结论：与假手术组比较,模型组大鼠肺间小动脉肌化  程度明显,平均肺动脉压和右心室湿质量/(左心室湿质量+室间隔湿质量)显著增高(P < 0.01或P < 0.05),肺动脉环舒张率降低(P < 0.05或P < 0.01)。与模型组比较,奈必洛尔组、卡托普利组平均肺动脉压、右心室湿质量/(左心室湿质量+室间隔湿质量)显著降低   (P < 0.05或P < 0.01),肺间小动脉肌化程度降低,肺动脉环舒张率增加(P < 0.05或P < 0.01)。说明奈比洛尔能够减轻肺高血流模型大鼠的肺动脉重构,其机制与奈必洛尔保护血管内皮和降低肺动脉压有关。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程