MS23对大鼠血流动力学指标和血压的影响

目的 观察MS23对麻醉正常血压大鼠血流动力学和对清醒无拘束自发性高血压大鼠(SHR)血压的影响.方法 采用PowerLab系统记录MS23对麻醉正常血压大鼠的血压、心电和血流动力学指标的影响;采用DSI心电和血压遥测系统观察MS23对清醒无拘束自发性高血压大鼠血压的影响.结果 MS23 0.1mg/kg～1.0mg/kg 静脉给药降低麻醉正常血压大鼠的平均动脉压、左心室收缩压和左心室压最大上升速率,减慢心率,对左心室舒张末压、左心室压最大下降速率和心电图其他指标无统计学意义;而Ami降低收缩压的同时,增快心率、增大左心室收缩压和左心室压最大上升速率.MS23 1.0 mg/kg 灌胃给药对清醒无拘束自发性高血压大鼠的收缩压和舒张压均有显著的降低作用,且以对舒张压的作用更明显;对心率无显著性影响.结论 MS23对正常血压大鼠和自发性高血压大鼠的血压均有显著的降低作用,而对心脏无兴奋作用.     

黄芪皂苷注射液对急性心衰犬心功能和血流动力学的影响

目的 观察黄芪皂苷注射液对实验性心衰犬心功能和血流动力学的影响.方法 采用β受体阻滞剂心得安诱发麻醉犬在体急性心衰模型,静脉注射黄芪皂苷注射液,同时测定心输出量(CO)、心脏指数(CI)、左心室收缩压(LVSP )、左室舒张末压(LVEDP)、收缩压最大上升速率(+dp/dtmax)及舒张压最大下降速率(-dp/dtmax)等心功能指标.结果 黄芪皂苷注射液对心衰犬CO 、CI 及LVSP、+dp/dtmax、-dp/dtmax均有明显的增加作用.结论 黄芪皂苷注射液具有增加col、增强心肌收缩力和改善心脏舒缩功能的作用.将其研制成强心和改善心功能药物具有良好的应用前景.     

缩醛基毛冬青提取化合物R4对麻醉犬心功能与血流动力学的影响

目的 研究缩醛基毛冬青提取化合物R4对麻醉犬心功能与血流动力学的影响.方法 采用麻醉犬开胸,测定心脏血流动力学参数,并分离冠状动脉左旋支,放置探头测量冠脉血流量,同步测量心输出量.结果 缩醛基毛冬青提取化合物R4 (0.5 mg/kg、1.0 mg/kg、2.0 mg/kg)可降低麻醉犬的血压,减少心肌耗氧量以及减慢心率,降低左室舒张末期压,左心室内压最大上升和下降速率,同时增加冠脉血流量.结论 缩醛基毛冬青提取化合物R4通过减少心肌耗氧量,降低左室舒张末期压及左心室内压最大上升和下降速率,使冠脉流量增加等环节发挥改善麻醉犬心功能与血流动力学的作用.     

氢对家兔缺血再灌注损伤心脏血流动力学的影响

目的应用家兔缺血再灌注损伤模型探讨氢对心脏血流动力学的影响。方法新西兰白兔40只随机分组,正常组(n=10)为假手术组分离但不结扎前降支;模型组结扎60min再灌注后分别给予静脉盐水(n=5)10mLkg和腹腔空气(n=5)10mL/kg;静脉氢盐水组(n=10)结扎60min再灌注后,静脉泵入氢盐水10mL/kg;腹腔氢气组(n=10)结扎60min再灌注后给予腹腔氢气10mL/kg。结果氢对缺血再灌注家兔心血流动力学的左心收缩压(LVSP)、左心舒张压(LVDP)、左心室舒张压未压(LVEDP)及等容收缩期左心室内压上升最大速率(+dp/dtmax)等观察指标产生良好的有益影响,而且除个别指标外,腹腔氢气这种作用优于静脉氢水。结论氢气对家兔缺血再灌注损伤心脏血流动力学具有一定有益作用。     

芦丁对大鼠离体心脏冠脉流量和血流动力学参数的影响

目的研究芦丁对大鼠离体心脏冠脉流量(CF)及血流动力学参数的影响。方法利用Langendorff实验系统,将36只大鼠随机分为6组,每组6只,观察溶剂及不同浓度芦丁(0.3μmol/L,1μmol/L,3μmol/L,10μmol/L,30μmol/L)对大鼠离体心脏冠脉流量及血流动力学参数的影响。先用正常台式液灌流大鼠心脏,待各指标稳定后,记录冠脉流量(CF)、左心室收缩压(LVDP)、左心室舒张压(LVEDP)、左心室内压最大上升速率(+dp/dtmax)和左心室内压最大下降速率(-dp/dtmax)。30min后,用含溶剂或芦丁的台式液灌流大鼠心脏,再记录各参数。观察芦丁对大鼠离体心脏冠脉流量及血流动力学参数的影响。结果 0.3μmol/L,1μmol/L,3μmol/L,10μmol/L,30μmol/L芦丁浓度依赖性增大CF值,使CF值从7.3mL/min±1.2mL/min增大到12.6mL/min±1.1 mL/min;芦丁浓度依赖性增大LVDP值和+dp/dtmax值,使LVDP值从60mmHg±2mmHg增大到73mmHg±4mmHg,使+dp/dtmax值从1 135mmHg/s±102mmHg/s增大到1 427mmHg/s±115mmHg/s;不同浓度芦丁对LVEDP和-dp/dtmax值无显著影响。结论芦丁增加离体大鼠心脏冠脉流量,对离体大鼠心脏有正性肌力作用。     

抑郁对急性心肌梗死大鼠心室重构的影响

目的 观察抑郁对急性心肌梗死(AMI)大鼠心室重构及血流动力学的影响.方法实验大鼠46只,随机分为四组:假手术组(n=10),梗死模型组(n=12)、抑郁模型组(n=12)、路优泰组(每天90 mg/kg)(n=12).4 w后用Open-field法观察各组大鼠行为学变化以及血流动力学测定和病理及光镜下心肌组织切片观察.结果①行为学观察:与假手术组相比,抑郁模型组,水平穿越格数、竖立次数、理毛时间,均减少,中央格停留时间、粪便粒数均增加(P＜0.01);与抑郁模型组相比,梗死模型组、路优泰组水平穿越格数、竖立次数、理毛时间明显增加,中央格停留时间、粪便粒数明显减少(P＜0.05,P＜0.01).②心室重构指标测定:与假手术组相比,梗死模型组、抑郁模型组、路优泰组,心率、左心室舒张末压、左、右室相对重量、室间隔厚度明显增加,主动脉收缩压、主动脉舒张压、左心室收缩压、左心室内压最大上升及下降速率明显减少(P＜0.05,P＜0.01).与抑郁模型组相比,梗死模型组、路优泰组,主动脉收缩压、左心室收缩压、左心室内压最大上升及下降速率明显增加,心率、左心室舒张末压、左、右室相对重量、室间隔厚度减少(P＜0.05,P＜0.01),且抑郁组大鼠光镜下心肌损伤最为严重.结论 AMI后抑郁可加重心肌梗死后心室重构过程,对血流动力学、心功能均有极为不利影响.     

三七总皂苷对腹主动脉缩窄致大鼠心肌肥厚能量代谢紊乱的抑制作用

目的 探讨三七总皂苷(PNS)对腹主动脉缩窄致大鼠心肌肥厚的抑制作用及机制.方法 取75只大鼠,采用腹主动脉缩窄法致心肌肥厚;随机取15只大鼠进行假手术作为对照(假手术组).1周后,手术大鼠随机分为4组:模型组、低剂量PNS组(50 mg/kg)、中剂量PNS组(100 mg/kg)和高剂量PNS组(150 mg/kg).给药11周,测定大鼠血流动力学改变;计算心脏指数和左心室质量指数;病理切片作HE染色观察大鼠左心室心肌形态学改变;取出左心室部分心肌组织进行乳酸、游离脂肪酸测定;采用逆转录聚合酶链反应测定心肌组织心房钠尿肽mRNA的表达;采用高效液相色谱法测定心肌中的三磷酸腺苷(ATP)、二磷酸腺苷(ADP)和一磷酸腺苷(AMP)含量.结果 与模型组相比,PNS可以降低肥厚指数,改善其血流动力学,降低心房钠尿肽mRNA的表达,降低心肌肥厚大鼠心肌乳酸和游离脂肪酸含量,增高心肌ATP、ADP和AMP含量.结论 PNS能够有效抑制腹主动脉缩窄大鼠心肌肥厚并改善其能量代谢紊乱.     

急性大量饮酒对犬血流动力学和心肌力学的影响

目的　探讨急性大量饮酒对犬血流动力学和心肌力学的影响。方法　选用健康犬 10只 ,应用心导管技术观察急性大量饮酒 ( 2 g/kg酒精 )后犬血流动力学和心肌力学各项参数的变化以及血浆肾上腺素 ( AD)、去甲肾上腺素( NE)、肾素活性 ( RNA)、血管紧张素 ( AT- )和动脉血气的变化 ,进行自身对照研究。结果　急性大量饮酒后 ,心率加快 ,心排血量下降 ,平均肺动脉压升高 ,外周动脉收缩压下降、舒张压升高 ,左心室收缩压下降、舒张末压增高 ( P<0 .0 1或 P<0 .0 5 ) ;左心室压力最大上升速率和下降速率、心肌收缩因子缩短最大速度均下降 ,等容舒张期左心室压力下降时间常数延长 ( P<0 .0 1) ;血浆 AD、NE、RNA和 AT- 水平升高 ( P<0 .0 1或 P<0 .0 5 ) ;动脉血p H值、Pa O2 下降 ,Pa CO2 上升 ( P<0 .0 1)。结论　犬急性大量饮酒引起心脏整体泵血功能下降 ,左心室收缩和舒张功能下降 ,交感 -肾上腺髓质系统和肾素 -血管紧张素系统活动增强 ;交感神经兴奋效应不足以代偿酒精及其代谢产物对心肌毒性作用所引起的心室收缩和舒张功能的下降     

氨酰心安限制心肌梗塞范围的实验研究

目的 了解氨酰心安对限制实验性心肌梗死范围的效应.方法 杂种犬22条,均开胸结扎冠状动脉左前降支结扎,造成急性心肌梗塞模型,然后分三组,A组注射酰心安0.375 mg/kg山组注射氨酰心安0.75 mg/kg(每次0.25 mg/kg,每8小时一次,三次总量为0.75mg/kg);C组仅注射生理盐水.并观察血流动力学指标,24 小时处死剖检心脏,计算心肌梗死范围.结果A、B二组用药后比对照组心肌梗塞范围有明显减少;用药后二小时血流动力学亦有明显变化.结论 静脉注射氨酰心安有限制急性心肌梗塞效应.     

知母百合与厄贝沙坦联合运用对高血压大鼠血压和血流动力学的影响

目的观察中药方剂知母百合与厄贝沙坦联合运用对高血压大鼠的血压和血流动力学的影响。方法采用自发性高血压大鼠(SHR)和肾血管狭窄性高血压大鼠(RVHR)模型,将高血压大鼠随机分成4组:对照组(CMC溶剂,n=10)、厄贝组(厄贝沙坦40mg/kg,n=10)、联合组(厄贝沙坦40mg/kg加知母百合浓缩药粉1250mg/kg,n=10)及中药组(知母百合浓缩药粉1250mg/kg,n=10)。动态观察灌胃给药后以下指标的变化:清醒状态下的SHR和RVHR的收缩压(SBP)、舒张压(DBP)、脉压(PP)及收缩压变异率(SBPV)变化;SHR的左心室收缩末期内压(LVESP)、左心室舒张末期内压(LVEDP)、心室内压最大上升速率( dp/dtmax)、心室内压最大下降速率(-dp/dtmax)的变化。结果在SHR和RVHR急性清醒测压中,厄贝组及联合组的SBP及DBP较给药前均明显降低,下降幅度可达20mmHg～28mmHg(1mmHg=0.133kPa,P<0.05);与对照组相比,两组SBP及DBP降低幅度为19mmHg～28mmHg(P<0.05);联合组与厄贝组相比,SBP和DBP降低幅度为6mmHg～9mmHg(P<0.05)。不论给药前后或者与对照组相比,中药组的血压参数无统计学意义(P>0.05)。在SHR的血流动力学实验中,厄贝组及联合组的SBP及DBP较对照组明显下降(15mmHg～24mmHg,P<0.05);各组之间的LVESP、LVEDP、 dp/dtmax、-dp/dtmax无统计学意义(P>0.05)。结论常规剂量的知母百合本身没有降压作用,对大鼠心脏的血流动力学也没有明显影响,但可协同厄贝沙坦的降压作用(幅度6mmHg～9mmHg)。     

莲心碱对正常大鼠血压和左室收缩功能的影响

目的 了解莲心碱对正常大鼠的降压作用与左室收缩功能的关系。方法 分别经大鼠静脉注射2mg/kg和6mg/kg的莲心碱,左心室插管,同步记录左心室压力和微分,测算心肌收缩因子最大缩短速度(V_(Max))等参数。结果 2mg/kg和6mg/kg莲心碱可不同程度的降低大鼠收缩压(SAP)、舒张压(DAP)、左室压力(LVP)上升最大速率(dp/dt_(Max))和V_(Max),对心率和左室开始收缩到开始射血的时间(t-dp/dt_(Max))则无明显影响。莲心碱降低V_(Max)的有效作用时间与SAP基本一致,莲心碱降低DAP的有效作用时间长于LVP、dp/dt_(Max)和V_(Max) 结论 经心碱具有明显的降低血压作用,莲心碱降低DAP的作用大于SAP,莲心碱降低血压的主要作用部位在外周血管。莲心碱可降低正常大鼠左室收缩功能,这一效应可能参与莲心碱的早期降压作用。     

Effects of aminophylline in the conscious dog after coronary occlusion

The effects of aminophylline were examined in 19 conscious dogs subjected to coronary arterial occlusion. Measurements were made of left ventricular pressure and its first derivative (dP/dt), segment length and the velocity of segment length shortening in normal and severely ischemic zones. Regional blood flow was measured in these zones using the radioactive microsphere technique. Coronary occlusion increased heart rate, mean arterial pressure and left ventricular end-diastolic pressure but did not change left ventricular systolic pressure or dP/dt significantly. It also resulted in increased end-diastolic segment length and reduced segment length shortening (114 ± 6 percent, that is, paradoxical bulging) associated with marked reduction of blood flow to ischemic myocardium. Aminophylline, 1 mg/kg per min for 9 to 15 minutes administered after occlusion, increased heart rate 6 ± 2 beats/min, mean arterial pressure 5 ± 1 mm Hg, left ventricular systolic pressure 9 ± 2 mm Hg and left ventricular dP/dt 670 ± 50 mm Hg/s while reducing left ventricular end-diastolic pressure by 3.4 ± 0.3 mm Hg. In severely ischemic zones aminophylline increased transmural blood flow by 21 ± 8.0 percent (p < 0.02), reduced end-diastolic segment length by 0.23 ± 0.05 mm (p < 0.01) and reduced paradoxical bulging by 0.15 ± 0.06 mm (p < 0.02). Thus, in the presence of coronary arterial occlusion, aminophylline increased mean arterial pressure, left ventricular dP/dt and heart rate while reducing left ventricular end-diastolic pressure. In severely ischemic myocardium aminophylline appeared to exert a salutary effect and improved both regional perfusion and function.     

Bradykinin improves left ventricular diastolic function under long-term angiotensin-converting enzyme inhibition in heart failure

Both systolic and diastolic cardiac dysfunction coexist in various degrees in the majority of patients with heart failure. Although ACE inhibitors are useful in the treatment of heart failure, the roles of bradykinin in the systolic and diastolic properties of left ventricular function under long-term treatment of ACE inhibitor have not been fully elucidated. We therefore evaluated the changes in left ventricular function, histomorphometry, and the expression of several failing heart related genes, by use of an orally active specific bradykinin type 2 receptor antagonist, FR173657 (0.3 mg/kg per day), with an ACE inhibitor, enalapril (1 mg/kg per day), in dogs with tachycardia-induced heart failure (270 ppm, 22 days) and compared the effects to enalapril alone. Although there were no differences observed in blood pressure, left ventricular dimension, and percentage of fractional shortening, FR173657 significantly increased left ventricular filling pressure (P<0.01), prolonged the time constant of relaxation (P<0.05), and suppressed the expression of endothelial NO synthase and sarcoplasmic reticulum Ca(2+)-ATPase mRNA (P<0.05). FR173657 also upregulated collagen type I and III mRNA (P<0.05) and increased the total amount of cardiac collagen deposits (P<0.05) in left ventricle compared with that in the enalapril-treated group. In conclusion, endogenous bradykinin contributes to the cardioprotective effect of ACE inhibitor, improving left ventricular diastolic dysfunction rather than systolic dysfunction, via modification of NO release and Ca(2+) handling and suppression of collagen accumulation.     

Phasic right coronary artery blood flow in conscious dogs with normal and elevated right ventricular pressures.

We studied phasic right coronary blood flow in well trained normal dogs and dogs with pulmonic stenosis. We installed electromagnetic flow transducers and pressure tubes under anesthesia to monitor right coronary blood flow, cardiac output, central aortic blood pressure, and right ventribular pressure. In normotensive dogs, systolic flow amplitude equaled early diastolic flow levels. The ratio of systolic to diastolic flow at rest was substantially greater in the right coronary bed (36+/-1.3%) than in the left circumflex bed (13+/-3.6%). Right diastolid flow runoff, including the cove late in diastole, resembled left circumflex runoff. Blood flow to the normotensive right (37+/-1.1 ml/min 100(-1) g) and the left (35+/-1.0 ml/min(-1) g) ventricular myocardium indicated equal perfusion of both cardiac walls. Throttling of systolic flow was related directly to the right ventricular systolic pressure level in the dogs with pulmonic stenosis. Retrograde systolic flow occurred in severe right ventricular hypertension. The late diastolic runoff pattern in dogs with pulmonic stenosis appeared the same as for the normotensive dogs. We obtained systolic to diastolic flow ratios of 1/3 the value of normotensive hearts in high and severe pulmonic hypertension. Electrocardiograms and studies of pathology suggested restricted blood flow to the inner layers of the right myocardium in the dogs with severe and high right ventricular hypertension. Normotensive and hypertensive peak hyperemic flow responses were similar, except for an increased magnitude of diastolic flow, with proportionately less systolic flow in hypertensive states.     

Segmental systolic responses to brief ischemia and reperfusion in the hypertrophied canine left ventricle.

OBJECTIVES AND BACKGROUND. Left ventricular hypertrophy is associated with increased mortality, increased myocardial infarct size and an increased incidence of sudden death. Although reperfusion after ischemia has been shown to result in decreased infarct size and recovery of systolic thickening, it is unknown how left ventricular hypertrophy might influence recovery of regional systolic thickening after ischemia and reperfusion. We hypothesized that left ventricular hypertrophy might attenuate or abolish the functional response to reperfusion. METHODS. Three groups of chronically instrumented, conscious dogs (dogs with left ventricular hypertrophy and hypertension; dogs with left ventricular hypertrophy and reduced blood pressure and a control group without hypertrophy and with normal blood pressure) underwent 15 min of ischemia and 24 h of reperfusion. Segmental systolic thickening was measured by sonomicrometers and myocardial segments were grouped by percent of control segmental systolic thickening retained at 15 min of ischemia (class 1 greater than or equal to 67%, class 2 from 0% to 66%, class 3 less than 0% control systolic thickening). The recovery of each class of segment was measured serially during reperfusion. Hemodynamic variables and regional myocardial blood flow were also measured. RESULTS. There were no differences among groups in recovery of segmental systolic thickening for class 1 segments. Systolic thickening in class 2 (hypokinetic) segments was significantly depressed (p less than 0.05 compared with control value) in the group with left ventricular hypertrophy and reduced blood pressure (but not in the group with hypertrophy and hypertension) during early reperfusion; systolic thickening in class 3 (dyskinetic) segments showed a similar trend in the group with hypertrophy and reduced pressure. CONCLUSIONS. Although left ventricular hypertrophy with hypertension did not attenuate the contractile response to reperfusion, hypertrophy with reduced blood pressure was associated with significantly greater depression of segmental systolic thickening early during reperfusion.     

福辛普利对急性心肌梗死大鼠心室重构的影响

目的 观察福辛普利对急性心肌梗死大鼠心室重构的防治作用。方法 大鼠结扎左冠状动脉前降支造成急性心肌梗死,同时应用福辛普利进行治疗,给药4周后测定心室重构大鼠血液动力学、生化学及形态学参数。结果 福辛普利对急性心肌梗死心室重构大鼠,能明显升高左心室内压最大上升和下降速率(±dp/dtmax)及其校正值(±dp/dtmax/LVSP),降低左心室收缩压(LVSP)及左心室舒张末压(LVEDP),亦能明显降低左心室容积(LVV)、左心室长轴(LVLA)长度、左心室短轴(LVSA)长度、左心室绝对重量(LVAW)、左心室相对重量(LVRW)、左心室绝对重量(RVAW)和右心室相对重量(RVRW),但对心率(HR)、收缩压(SBP)、舒张压(DBP)、平均动脉压(MAP)及体重(BW)均无明显影响。此外,可明显降低血清脂质过氧化物(LPO)及心肌血管紧张素Ⅱ(Ang Ⅱ)和肾上腺素(E)含量,提高超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性。结论 福辛普利能有效防治急性心肌梗死大鼠的心室重构。     

西洋参茎叶三醇组皂苷对大鼠压力超负荷性心室重构的保护作用

目的 观察西洋参叶20s-原人参三醇组皂苷(PQTS)对压力超负荷性大鼠心室重构的保护作用.方法 Wistar大鼠随机分为假手术组、模型组、阳性药卡托普利组及PQTS低、中、高剂量组.结扎大鼠腹主动脉建立压力超负荷性心室重构模型,PQTS按12.5、25.0、50.0mg·kg-1·d-1连续腹腔注射6周,检测心室脏器系数、心肌组织病理学及血流动力学参数,测定血清丙二醛( MDA)含量及超氧物歧化酶(SOD)活性,血浆前列环素(PGI2)、血栓素A2 (TXA2)、内皮素(ET)及血管紧张素Ⅱ(AngⅡ)含量.结果 与重构模型组比较,PQTS能明显抑制心室重构大鼠心肌组织的病理性改变,降低心室质量及心脏系数,明显升高收缩压、舒张压、平均动脉压、左室收缩压及左心室内压最大上升和下降速率(±dp/dtmax),降低心率及左室舒张末压,可明显降低血清MDA含量,升高SOD活性,亦能明显降低血浆ET、AngⅡ及TXA2含量,提高PGI2含量及PGI2/TXA2比值(P＜0.05或P＜0.01).结论 PQTS对大鼠心室重构具有明显保护作用,可能与其改善心室重构大鼠的左心收缩和舒张功能,增强抗氧化酶活性,减少自由基及缩血管活性物质对心肌的损伤,纠正PGI2/TXA2失衡等机制有关.     

Influence of minoxidil on myocardial hemodynamics,regional blood flow,and morphology in beagle dogs

Summary Studies were made of the effects of two doses of minoxidil (3 mg/kg), given 24 hours apart, on cardiovascular hemodynamics, regional myocardial blood flow, and cardiac morphology in beagle dogs. Minoxidil caused increases in mean right atrial and left ventricular end-diastolic pressure. Systemic and pulmonary vascular resistance were reduced; cardiac output was increased. Left ventricular stroke work and the systolic pressure time index were unchanged by monoxidil administration. The diastolic pressure time index and ratio of diastolic/systolic pressure time index were decreased by minoxidil. Regional myocardial blood flow, measured with radioactive microspheres, increased in all regions of the heart except to the left ventricular papillary muscles. Minoxidil increased blood flow to left ventricular subendocardial tissue; however, this increase was significantly less than that observed in corresponding areas of subepicardial tissue, thus reducing the subendocardial/subepicardial tissue blood flow ratio. These results suggest that minoxidil is an effective peripheral vasodilator but may result in inadequate subendocardial perfusion. Morphologic studies disclosed two types of minoxidil-induced cardiac lesions: left ventricular papillary muscle necroses, and hemorrhagic lesions which were most prominent in right atrium and were associated with inflammation, intramural hemorrhage, and fibrinoid necrosis of small arteries. The papillary muscle necroses were attributed to hypoxia. The atrial lesions were not of ischemic or hypoxic origin, because minoxidil did not decrease blood flow to atrial tissue. It is suggested that the atrial lesions are related to excessive vasodilatation.     

川芎大复方对麻醉开胸犬血流动力学的影响

目的 :探讨川芎大复方 （CR）静脉给药后对血流动力学的影响。方法 :以 0 .3,0 .6 ,0 .9,1.2 g/kg剂量注入健康麻醉开胸犬的心房内 ,观察血流动力学的变化。结果 :低剂量的 CR无药效变化 ,CR有剂量依赖性地引起 HR的明显减慢 ,L VSP,L Vdp /dtmax显著降低 ,冠脉血流量 （CBF）快速增加和平均主动脉血压 （m Ao P）下降。结论 :川芎伍用其它中药组成的大复方引起明显的负性变时和变力作用 ,CBF增加以及 m Ao P下降