多巴酚丁胺、米力农干预美托洛尔致心脏负性肌力效应的实验研究

目的观察在美托洛尔使大鼠心脏左室收缩功能减弱后,临床常用正性肌力药物(多巴酚丁胺、米力农)对大鼠心功能的改善作用。方法将Wistar雄性健康大鼠32只,随机分为正常对照组、美托洛尔5 mg/kg组、美托洛尔10 mg/kg组、美托洛尔20 mg/kg组,各8只,观察不同浓度多巴酚丁胺、米力农给药前后各组大鼠心率(HR)、左心室发展压(LVDP)、左室内压上升最大速率(+dp/dt_(max))、左室内压下降最大速率(-dp/dt_(max))等心功能指标变化。结果美托洛尔20 mg/kg组健康大鼠的心率、LVDP、+dp/dt_(max)、-dp/dt_(max)的绝对值明显小于正常对照组(P0.05)。多巴酚丁胺具有明显加快心率的作用,且增大+dp/dt_(max)、-dp/dt_(max)的绝对值,但对健康大鼠LVDP的影响并没有明显增加,多巴酚丁胺的正性变时、正性变力效应明显被美托洛尔减弱,米力农不影响心率,LVDP及+dp/dt_(max)、-dp/dt_(max)的绝对值在正常对照组和美托洛尔各浓度组都有很大的提高。结论米力农可以改善美托洛尔引起的心功能减弱,用多巴酚丁胺则未得到改善。     

压力-容积环评价压力负荷型慢性心力衰竭大鼠左心室功能的意义

目的采用压力-容积(P-V)环研究压力超负荷对大鼠左心室血流动力学的影响。方法 13只SD大鼠随机分为2组:假手术(Sham)组(n=7)和心力衰竭(HF)组(n=6)。HF组采用腹主动脉缩窄法制备模型,Sham组只穿线不缩窄。对两组大鼠进行血流动力学检测,大鼠麻醉后经右颈总动脉向左心室内插入Millar导管(SPR-838),记录两组大鼠的P-V变化。结果与Sham组相比,HF组大鼠的心脏(P0.01)和肺脏(P0.05)重量均显著增加。在稳定状态的P-V环中可以看到,和Sham组相比,在压力超负荷的影响下,HF组左心室P-V环明显增高、右移,P-V曲线斜率也明显高于Sham组,左心室收缩/舒张末期压力(P_(es)/P_(ed))、收缩/舒张末容积(V_(es)/V_(ed))、压力衰退的时间常数(Tau)均增高(P0.05),而室内压最大上升速率(dP/dt_(max))、左室压力最大下降速率(-dP/dt_(min))、射血分数(EF)和每搏输出量(SV)均出现降低(P0.05)。结论压力负荷型慢性HF大鼠左心室发生了舒张和收缩功能障碍,并且伴有一定程度的左心室肥大。P-V环能够准确地定性、定量评价大鼠的心功能。     

中药脑肺康对实验性犬心力衰竭的影响

目的 研究中药脑肺康对实验性心衰的影响.方法 用戊巴比妥钠诱发犬的急性心衰,采用RM-6000生理仪、电磁流量计、AP-6dG放大器和AC-601放大器测定心输出量(CO)、左室压(LVP)、左室末期舒张压(LVEDP)、±dp/dt_(max)和心电图(ECG).结果 十二指肠给脑肺康(2.5、5、10g/kg)后心输出量、左室压、+dp/dt_(max)和血压明显上升(P<0.05),与阴性对照组有明显差异(P<0.05),但左室末期舒张压下降(P<0.05).结论 脑肺康对犬急性心衰有较好的保护作用.     

非诺贝特治疗大鼠左心室肥厚

目的研究非诺贝特逆转腹主动脉缩窄(AAC)大鼠左心室肥厚的作用,并初步探讨其对 Akt/GSK3β信号通路的影响。方法采用 AAC 法建立心肌肥厚模型。术前1周和术后4周灌胃给予非诺贝特[80 mg/(kg·d)],观察了其对血流动力学参数、超声参数、左室质量(LVM)/体质量(BM)、心肌超微结构的影响。同时检测了心肌组织中 Akt 和 GSK3β蛋白磷酸化的表达变化。结果 1)与假手术组相比,大鼠腹主动脉缩窄4周后,主动脉收缩压(AoSP)、主动脉舒张压(AoDP)、左室内压(LVESP、LVEDP)明显升高(P<0.05);室内压最大上升速率(+dp/dt_(max))和室内压最大下降速率(-dp/dt_(min))明显减少(P<0.05),而非诺贝特治疗后,+dp/dt_(max)、-dp/dt_(min)明显上升(P<0.05);AoSP、AoDP、LVESP 无明显变化(P>0.05)而 LVEDP 稍降(P<0.05)。2)手术后4周 AAC 大鼠呈现出明显的向心性肥厚,室间隔(IVSd 和 IVSs)及左室后壁厚度(PWTd 和 PWTs)(P<0.05)、LVM/BM[LVM:(2.94±0...     

丙泊酚对心肌肥厚大鼠离体心脏功能的保护作用

目的观察丙泊酚(propofol)对心肌肥厚大鼠离体心脏功能的影响,并探讨其作用机制。方法采用Langendorff心脏灌流实验方法,观察Propofol对心肌肥厚大鼠离体心脏功能的影响。观察不同阻断剂对Propofol作用的影响。结果 Propofol可增强心肌肥厚大鼠离体心脏心功能,心率减慢,主动脉收缩压(LVSP-LVDP)升高,左室压最大上升速率(+dp/dt_(max))升高,左室压最大下降速率(-dp/dt_(max))降低,吲哚美辛预处理后,Propofol对心脏功能的影响减弱。结论 Propofol可以明显改善心肌肥厚大鼠离体心脏功能,其作用可能与前列环素(PGI_2)的合成有关。     

异莲心碱防止高血压大鼠左室肥厚的可能机制

背景 既往报告异莲心碱是从莲子心中分离的一种双苄基喹啉生物碱单体,具有抗心律失常、Ca2 拮抗及阻断α受体作用,对高血压左室肥厚有不同程度的改善.高血压左室肥厚心肌肌浆网钙泵(SERCA)活力较正常心肌降低.目的 探讨异莲心碱对高血压大鼠左室肥厚及SERCA活力的影响.方法 将二肾一夹肾血管性高血压大鼠(RHR)模型,随机分为3组:正常对照组、肾血管性高血压大鼠对照组(未治疗RHR组)和异莲心碱治疗组.在异莲心碱治疗组持续给药10周后,分别测定各组大鼠的血压、左室质量/体质量,以及左室心肌SERCA活力.结果 治疗后,异莲心碱治疗组血压(136.4±14.6)mm Hg较未治疗RHR组(189.8±4.4)mm Hg显著降低(P＜0.01);异莲心碱治疗组左室质量/体质量(2.23±0.43)也较未治疗RHR组(2.93±0.52)显著降低(P＜0.05);异莲心碱治疗组左室心肌SERCA活力[(0.91±0.18)μmol/(g protein·min)]较未治疗RHR组[(0.61±0.23)μmol/(g protein·min)]显著升高(P＜0.05),但仍较正常对照组[(1.32±0.18)μmol/(g protein·min)]低(P＜0.01).结论 异莲心碱能降低RHR的血压,减低RHR的左室质量/体质量,对高血压左室肥厚具有一定的防治作用;其机制可能与异莲心碱能升高RHR肥厚心肌肌浆网SERCA活力,改善心肌细胞内钙超载有关.     

不同时间左心室注射地尔硫对大鼠顿抑心肌功能的影响

目的观测不同时间左心室注射地尔硫对大鼠顿抑心肌功能的影响。方法 Wistar雄性大鼠25只,随机分为5组,假手术组(A组)、顿抑心肌组(B组)、缺血期注射地尔硫组(C组)、再灌注早期注射地尔硫组(D组),再灌注晚期注射地尔硫组(E组),每组5只,观察心率(HR)、左心室收缩末期压(LVESP)、左心室舒张末期压(LVEDP)、左心室内压最大上升速率及最大下降速率(±dp/dt_(max))的变化。结果与A组大鼠比较,除C组再灌注30、60、90、120 min,D组再灌注60、90、120 min时,其他各组在缺血及再灌注后均出现HR增快,LVESP、LVEDP、±dp/dt_(max)降低(P<0.05);C组再灌注30 min、D组再灌注90 min时HR、LVESP、LVEDP、±dp/dt_(max)已恢复至术前水平。与B组大鼠比较,C组再灌注15、30、60、90、120 min,D组再灌注90、120 min HR下降,LVESP、LVEDP、±dp/dt_(max)明显改善(P<0.05)。结论在缺血和再灌注早期左心室注射地尔硫可促进顿抑心肌功能的恢复,而再灌注晚期应用则无明显作用。     

钩藤总碱与天麻素联用对自发性高血压大鼠血压和血压变异性的影响

背景钩藤和天麻是治疗高血压的传统中药,常联合应用。目的研究钩藤、天麻的活性成分钩藤总碱及天麻素抗高血压和改善血压变异性的协同作用。方法 60只自发性高血压大鼠随机分为11组,分别是:对照组、钩藤总碱4组(25、50、100、200mg/kg)、天麻素3组(8、80、800mg/kg)、钩藤总碱+天麻素3组[(50+8)、(50+80)、(50+800)mg/kg],腹腔给药。采用清醒自由活动大鼠血压测定系统监测给药前后大鼠的血压和血压变异性。用两因素多水平析因设计、概率和法和q检验方法评价钩藤总碱和天麻素降压以及改善血压变异性的协同作用。结果在25～200mg/kg剂量范围内,钩藤总碱给药量与血压降低幅度有量效关系。其中,200mg/kg剂量组给药前后收缩压分别为(182±16)和(142±12)mmHg,舒张压分别为(133±21)和(100±19)mmHg,给药前后血压平均值的差异有统计学意义(P<0.01)。天麻素单独注射剂量达到800mg/kg也没有降低自发性高血压大鼠的血压。而钩藤总碱+天麻素组[(50+8)、(50+80)、(50+800)mg/kg]有降压作用,钩藤总碱和天麻素联用具有协同降压作用,对血压变异性没有不良影响。结论钩藤总碱具有确切的降压作用,但对血压变异性没有影响。天麻素本身不降低血压,但与钩藤总碱联用具有协同降压作用。     

心肌梗死大鼠左心室收缩与舒张功能的改变及其影响因素

目的 探讨心肌梗死大鼠左心室收缩和舒张功能的改变、以及心室重构对心室舒缩功能的影响.材料和方法结扎Wistar大鼠左冠状动脉、制成心肌梗死模型,6周后测定左室心肌力学指标,心肌胶原含量、血浆及心肌的血管紧张素Ⅱ(Aug Ⅱ)浓度.结果 心肌梗死组与对照组比较,LVPSP、+dp/dt_(max)、dp/dt_(max)绝对值及V_(max)明显降低(P<0.01),LVEDP增加(P<0.01),T值延长(P<0.01),MAP无差异.心肌梗死组与对照组比较、心肌羟脯氨酸和心肌胶原含量明显增高(P均0.01),心肌AngⅡ含量明显升高(P<0.01)、血浆AngⅡ浓度无显著差异.结论 心肌梗死后左室收缩与舒张　功能明显降低,同时出现心肌细胞的肥大和纤维细胞的增生以及间质纤维化、后者可进一步导致和加重心脏泵血功能的异常.     

依普利酮对慢性心力衰竭大鼠血流动力学和运动能力的影响

目的探讨依普利酮对慢性心力衰竭大鼠血流动力学和运动能力的影响。方法将18只成年健康清洁级SD雄性大鼠随机分为空白组、心力衰竭组与依普利酮组,每组6只大鼠。心力衰竭组与依普利酮组均采用结扎左冠状动脉前降支建立心力衰竭模型,依普利酮组在心力衰竭模型建立后2周给予依普利酮20 mg/(kg·d)灌胃,连续应用4周。记录大鼠不同时间点的血流动力学和运动能力。结果所有大鼠都成活,心力衰竭组与依普利酮组实验2周、6周的收缩压与舒张压均明显高于空白组(P0.05),依普利酮组实验6周的收缩压与舒张压均明显低于心力衰竭组(P0.05)。实验6周,心力衰竭组与依普利酮组左室收缩末期内径(LVESD)明显高于空白组(P0.05),依普利酮组LVESD低于心力衰竭组(P0.05)。实验6周心力衰竭组与依普利酮组左室内压最大上升速率(+dp/dt_(max))和左室内压最大下降速率(-dp/dt_(max))值均低于空白组(P0.05),依普利酮组+dp/dt_(max)、-dp/dt_(max)均高于心力衰竭组(P0.05)。结论采用结扎左冠状动脉前降支建立心力衰竭模型能反映大鼠的心力衰竭状况,依普利酮可改善慢性心力衰竭大鼠血流动力学状况,提高心功能与运动能力。     

射频消融犬心脏脂肪垫消弱Bezold-Jarisch反射

目的观察经心外膜射频消融犬右肺静脉脂肪垫、下腔静脉脂肪垫及心脏第3脂肪垫对藜芦定诱发的Bezold—Jarisch反射（BJR）及相关的血流动力学指标的影响,并探讨其临床意义。方法30只杂种犬麻醉后经右侧开胸,随机分为对照组（不消融）、消融组（经心外膜消融上述3个脂肪垫）。经左心室导管弹丸式推注藜芦定15μg/kg,比较两组推药前后心率、动脉收缩压、动脉舒张压、平均动脉压、左心室收缩压、左心室舒张末压、左心室压最大上升及下降速率的变化。结果推注藜芦定前两组各项指标差异无统计学意义（P〉0．05）,推注藜芦定后消融组心率的下降显著低于对照组（（22．9±8．5）次／minvs（93．3±18．4）次／min,P〈0．01）],但动脉压、左心室压、左心室压最大上升及下降速率的变化与对照组相比差异无统计学意义（P〉0．05）。结论经心外膜射频消融犬上述3个脂肪垫能明显消弱藜芦定诱发的BJR的心率抑制成分,但不能消弱BJR的血管抑制成分。此方法对防治心脏抑制型以及混合型血管迷走性晕厥可能有效．但对血管抑制型血管迷走性晕厥可能无效．     

Cardioprotective Effects of Angiotensin II Type 1 Receptor Blockade with Olmesartan on Reperfusion Injury in a Rat Myocardial Ischemia‐Reperfusion Model

We determined the effects of olmesartan on infarct size and cardiac function in a rat ischemia/reperfusion model. Rats underwent 30 min of left coronary artery (CA) occlusion followed by 2 h of reperfusion. In protocol 1, the rats received (by i.v.) 1 mL of vehicle at 10 min after CA occlusion (Group 1, n = 15); olmesartan (0.3 mg/kg) at 10 min after CA occlusion (Group 2, n = 15); 1 mL of vehicle at 5 min before CA reperfusion (Group 3, n = 15); or olmesartan (0.3 mg/kg) 5 min before CA reperfusion (Group 4, n = 15). In protocol 2, the rats received (by i.v.) 1 mL of vehicle at 5 min before CA reperfusion (Group 5, n = 21); or olmesartan (3 mg/kg) at 5 min before CA reperfusion (Group 6, n = 21). Systemic hemodynamics, left ventricular (LV) function, LV ischemic risk zone, no‐reflow zone, and infarct size were determined. In protocol 1, olmesartan (0.3 mg/kg) did not affect blood pressure (BP), heart rate, LV ± dp/dt or LV fractional shortening during the experimental procedure, and did not alter no‐reflow or infarct size. In protocol 2, olmesartan (3 mg/kg) significantly reduced infarct size to 21.7 ± 4.1% from 34.3 ± 4.1% of risk zone in the vehicle group (P= 0.035), but did not alter the no‐reflow size. Prior to CA reperfusion, olmesartan (3 mg/kg) significantly reduced mean BP by 22% and LV ±dp/dt, but did not affect heart rate. At 2 h after reperfusion, olmesartan significantly decreased heart rate by 21%, mean BP by 14%, and significantly increased LV fractional shortening from 54.1 ± 1.4% to 61.3 ± 1.6% (P= 0.0018). Olmesartan significantly reduced myocardial infarct size and improved LV contractility at a dose (3 mg/kg) with systemic vasodilating effects but not at a lower dose (0.3 mg/kg) without hemodynamic effects.     

Experimental studies of the hemodynamics of disopyramide in comparison with quinidine

The haemodynamic effects of quinidine and disopyramide i.v. were investigated in 79 rats. Measurements were performed in the intact circulation (LVP, AoP, dp/dtmax). Myocardial function was examined independently of circulatory changes by isovolumetric registrations (peak LVP). Animals with NaCl infusion served as controls. After infusion of 5 mg/kg (10 mg/kg) quinidine, we obtained a reduction (p less than 0.05) in the left ventricular pressure to 81.6 +/- 3.1% (82.6 +/- 3.7%), in the mean aortic pressure to 70.7 +/- 3.4% (79.3 +/- 6.7%), in dp/dtmax to 73.9 +/- 5.6% (72.8 +/- 6.2%), and in the heart rate to 69.7 +/- 7.4% (69.9 +/- 5.4%). Isovolumic pressure maxima after quinidine were not different from the controls (90.7 +/- 2.4% and 93.6 +/- 1.5% respectively vs. 96.1 +/- 1.0%). 1 mg/kg disopyramide caused no significant haemodynamic changes. 2 mg/kg disopyramide led to a slight increase in dp/dtmax (107.2 +/- 5.6%, N.S.), while 4 mg/kg disopyramide had a tendency to reduce the left ventricular pressure (88.5 +/- 6.2%), mean aortic pressure (80.5 +/- 14.8%) and dp/dtmax (75.1 +/- 8.0%). After 4 mg/kg disopyramide, the isovolumic maxima were reduced. Our results indicate that the haemodynamic side effects of class-I antiarrhythmic drugs are different. Quinidine i.v. caused a reduction in pressures and heart rate, but had no influence on the isovolumic pressure maxima. Disopyramide i.v., on the other hand, had no significant haemodynamic effects in clinical doses. After high (not clinically used) doses of disopyramide (4 mg/kg), which also led to high plasma levels, myocardial performance was depressed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Negative inotropic effect of flecainide on the post-ischemic heart with limited contractile function

The hemodynamic effects of 7 min i.v. flecainide were examined in rats with postischemic left ventricular dysfunction. For quantification of contractile function the isovolumic left ventricular pressure generating capacity and dp/dtmax were determined. Fifteen min after infusion the isovolumic maximum pressure was reduced for 33 mm Hg after flecainide (2 mg/kg; n = 12), whereas in the controls only a minimal reduction (12 mm Hg; n = 13) was found; dp/dtmax was also significantly reduced after flecainide. The results indicate - in contrast to prior investigations on normal hearts - a considerable negative action of 2 mg/kg flecainide i.v. on postischemic myocardium with reduced contractile function.     

Acute effects of alcohol, beta blockade, and their combination on left ventricular function and hemodynamics in normal man

Twenty-three healthy males, aged 23 to 62 years, were examinedby M-mode echocardiography and systolic time intervals for 3h after (1) ethanol 1 g/kg by mouth taken over 60 minutes; (2)atenolol 100 mg by mouth; (3) ethanol (1 g/kg) + atenolol (100mg). The peak mean blood ethanol (± s.e.) was 112 ±4mg/100 ml in test 1 and 104 ± 7 mg/100 ml in test 3.During increasing blood ethanol, heart rate (HR), systolic bloodpressure (BP), cardiac output (CO) and echocardiographic indicesof left ventricular (LV) function were significantly augmented,while total peripheral resistance (TPR) decreased. During decliningblood ethanol, systolic BP, L V end-diastolic and end-systolicdiameters, stroke volume (SV) and circumferential wall stresswere significantly reduced; echocardiographic indices of LVfunction were unaltered, but the pre-ejection period/LV ejectiontime ratio was increased, Atenolol decreased llR, systolic BP,SV, CO, and all estimates of LV function, but increased TPR.Ethanol + atenolol tended to cause smaller depressions in theindices of LV function than did atenolol alone, in spite ofsimilar plasma atenolol concentrations (n = 6). It is concludedthat ingestion of modest doses of ethanol evokes vasodilationand enhances LV function during increasing blood ethanol, andreduces LV preload and afterload during decreasing blood ethanolwithout impairing contractility. Social drinking and beta blockadeseem not to have any harmful acute combined effects on the heartand circulation, at least in normal subjects.     

Catheter ablation of cardiac fat pads attenuates Bezold-Jarisch reflex in dogs

Ablation of Cardiac Fat Pads and BJR . Background: Bezold–Jarisch reflex (BJR) plays an important role in the pathophysiology of several cardiovascular disorders. Radiofrequency catheter ablation (RFCA) of the vagal ganglia in cardiac fat pads (FPs) may attenuate BJR. The purpose of this study was to examine the effects of RFCA of the cardiac FPs on veratridine‐induced BJR in dogs. Methods and Results: This study was performed in 30 pentobarbital‐anesthetized and open‐chest dogs: control group received no ablation (n = 15); and ablation group (n = 15) received epicardial ablation of the 3 FPs located near the right pulmonary vein, the inferior vena cava, and the aortic root. The BJR was induced by injection of veratridine (15 μg/kg) into the left ventricle. Before injection of veratridine, there were no significant differences in heart rate (HR), systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), left ventricle end‐diastolic pressure (LVEDP), left ventricular peak systolic and diastolic velocity (±dp/dt_max) between these 2 groups (P > 0.05). However, the veratridine‐induced decrease of HR in ablation group was significantly lower than that in control group (22.9 ± 8.5 bpm vs 93.3 ± 18.4 bpm, P < 0.01). There were no differences in the reduction of SAP, DAP, MAP, LVSP, LVEDP and dp/dt_max between both groups (P > 0.05). Conclusions: RFCA of the cardiac FPs significantly attenuated veratridine‐induced cardio‐vagal component but not the vasodepressor component of the BJR. This might have therapeutic implications in BJR‐related disorders such as cardio‐inhibitory vasovagal syncope. (J Cardiovasc Electrophysiol, Vol. 22, pp. 573‐578 May 2011)     

Ghrelin注射对大鼠血压和心肌收缩功能的影响

目的: 探讨促生长激素释放多肽(ghrelin,GRL)对大鼠心血管功能的影响及其意义。方法: 将40只成年雄性SD大鼠分为对照组和4个剂量的GRL组，静脉注射GRL后测量血流动力学指标。随后采用单细胞动态边缘检测系统测定细胞收缩功能的变化。结果: ①GRL各组平均动脉血压（MABP）较对照组明显下降（P<0.05）。②GRL各组单个心肌细胞收缩功能指标最大收缩幅度（PTA）、最大缩短和复长速率（±dL/dtmax）较对照组明显降低（P<0.05）。结论: GRL可剂量依赖性地降低大鼠的MABP，降低心肌细胞的收缩功能。     

射频消融犬心脏第三脂肪垫消弱Bezold-Jarisch反射

目的观察射频消融犬心脏第3脂肪垫(上腔静脉与主动脉根部之间的脂肪垫,SVC-AO FP)对Bezold-Jarisch反射(BJR)及相关的血流动力学指标的影响。方法30只杂种犬麻醉后经右侧开胸,随机分为对照组(不消融)、消融组(消融SVC-AO FP),每组15只。经左室导管弹丸式推注藜芦定15μg/kg诱发BJR,比较两组推药前后心率(HR)、动脉压、左室压、左室压最大上升速率(+dp/dtmax)及最大下降速率(-dp/dtmax)的变化。结果推注藜芦定前两组的各项指标无显著差异(P>0.05),推注藜芦定后两组的各项指标均呈一过性下降,消融组HR的最大下降值ΔHR显著低于对照组(27.7±8.2次/分vs 93.3±18.4次/分,P<0.01),但动脉压、左室压及±dp/dtmax的最大下降值两组相比无显著差异(P>0.05)。结论射频消融犬SVC-AO FP能明显消弱藜芦定诱发的BJR的HR抑制,但不能消弱BJR的血管抑制。     

Diastolic vibration improves systolic function in cases of incomplete relaxation.

BACKGROUND. Incomplete relaxation of the left ventricle (LV) affects LV filling, but the subsequent effect on LV systolic function remains unclear. We attempted to improve relaxation by applying oscillatory mechanical perturbation during diastole (diastolic vibration) and examined the extent to which systolic function improved. METHODS AND RESULTS. Using 10 open-chest canine preparations, pacing tachycardia and administration of propranolol were imposed to induce various levels of incomplete relaxation. Myocardial length perturbation was induced with an oscillator attached to the LV surface (50 Hz, 1-mm amplitude) and was restricted to the period from the beginning of isovolumic relaxation to end diastole. At resting heart rates, diastolic vibration caused an immediate decrease in the time constant (T) of LV pressure fall without any influence on heart rate, LV peak systolic pressure (peak LVP), stroke volume (SV), LV peak positive dP/dt, and total systemic vascular resistance. With pacing tachycardia, diastolic vibration increased both peak LVP and SV at 160 beats per minute (before) and 120 beats per minute (after propranolol), simultaneously decreasing both T and LV diastolic pressures and increasing end-diastolic segment length. The increase in peak LVP and SV caused by diastolic vibration correlated with the T/diastolic interval (r = 0.82), the assumed index of severity of incomplete relaxation. CONCLUSIONS. These results suggest that diastolic vibration accelerates the LV relaxation rate and that this increased relaxation improves systolic function through the Frank-Starling mechanism.