重组人脑钠肽及米力农对麻醉犬血流动力学及肾功能的影响

目的观察重组人脑钠肽(rhBNP)对麻醉犬血流动力学和肾功能的作用。方法给麻醉开胸犬恒速输注rhBNP(采用累积给药方式),或iv米力农后,进行血流动力学测定,并测定尿量、尿钠和血钠含量。结果rhBNP可使MAP,LVSP,LVdP/d_t,PAP,LVEDP,TPR及RVR呈剂量依赖性下降,CO有增加趋势,尿量和尿钠排出量呈剂量依赖性增加。米力农则明显降低MAP,PAP,LVEDP,TPR,RBF及RVR,升高LVSP,LVdP/d_t和CO,加快心率,对尿量、尿钠排出量和血钠无明显影响。结论rhBNP能明显降低心脏前后负荷,改善心脏功能;可舒张肾动脉,有扩张血管和利尿排钠作用。米力农则有正性肌力和频率作用,无利尿利钠作用。     

注射用红景天苷对麻醉犬血流动力学的影响

目的:观察注射用红景天苷对麻醉犬血流动力学的影响。方法:杂种犬36只,人工呼吸下开胸,给药后观察其心率(HR)、血压(MAP)、心输出量(CO)、冠脉血流量(CBF)、左室压(LVP)、左心室舒张末期压(LVEDP)、左室等容收缩期压力最大变化率(±LVdP/dtmax)等指标,计算冠脉阻力(CVR)和体循环总外周阻力(TPR)等血流动力学指标。结果:红景天苷(2,4,8 mg.kg-1)对MAP,HR和LVP无明显影响,能显著增加CBF和CO,±LVdP/dtm ax也出现不同程度的增加,同时LVEDP,CVR和TPR降低。结论:注射用红景天苷能明显改善麻醉开胸犬的血流动力学指标。     

阿司匹林与卡托普利合用对麻醉犬血液动力学的影响

目的观察阿司匹林(Asp),卡托普利(Cap)单用和合用对麻醉开胸犬血液动力学的作用。方法张力指数(TTI)、左室做功指数(LVWI)、平均动脉压(MAP)、总外周血管阻力(TPVR)、股动脉血流量(FBF)、左室内压(LVSP)、 dp/dtmax、左室舒张末期压(LVEDP)、心率(HR)均同步记录于多导生理记录仪及电磁流量计上。结果Asp5、10mg·kg-1iv对血液动力学各项指标均无明显影响,Cap0.5mg·kg-1iv对LVSP、 dp/dtmax、LVEDP、HR无明显影响 ,CI稍增加 ,但可使TTI、LVWI、TPVR显著下降 ,Asp与Cap 合用与Cap 单用结果相似。结论Asp不影响Cap对心血管功能的改善     

麝香保心分散片对冠脉结扎犬血流动力学的影响

目的研究麝香保心分散片对冠脉结扎犬血流动力学的影响。方法采用麻醉犬开胸结扎左冠状动脉前降支 (LAD)产生急性心肌梗死 (AMI)模型 ,测定AMI 3h犬的心脏血流动力学参数。结果十二指肠给予麝香保心分散片 ,能明显增加心输出量 (CO)和搏出量 ,增加心肌血流量 ,降低冠脉阻力 ,增加左室收缩内压 (LVSP)及室内压最大上升和下降速率 (±dp/dtmax) ,轻度减慢心率 ,明显降低左室舒张末期压 (LVEDP) ,增加冠脉结扎犬心脏指数 (CI)及搏功 ,降低总外周阻力 ,对平均动脉压有下降趋势。结论麝香保心分散片主要以改善心肌收缩和舒张功能 ,增加缺血心肌供血等环节 ,发挥抗心肌缺血作用     

麻醉开胸犬静脉注射EMD56431血液动力学研究

目的:研究ATP敏感钾通道开放剂EMD56431对麻醉开胸犬血流动力学的作用.方法:采用静注(i.v.)给药方式,动态监测麻醉开胸犬左心室收缩压(LVSP)、左室压上升和下降速率(±dp/dtmax),左室舒张末期压(LVEDP)、收缩压(SAP)、舒张压(DAP)、平均动脉压(MAP)、ECG等指标,并计算出心率(HR)、心脏指数(CI)和外周阻力(TPR).结果:静注EMD56431在一定范围内可使麻醉开胸犬呈时间和剂量依赖性的血压降低,尤以DAP下降为甚,在降压的同时,可见HR减慢.除大剂量EMD56431外,其余各剂量对心脏泵功能、血流量、ECG均无明显影响.结论:EMMD56431可显著降低血压,改善心脏供血.     

实验性阻塞性呼吸暂停对犬左心室心肌力学的急性影响

目的 :观察阻塞性呼吸暂停 (OA)对犬左心室收缩和舒张功能的急性影响。方法 :选用健康犬10只 ,通过循环在呼气末闭塞 (呼吸暂停期 ,AP)和开放 (间歇期 ,IP)上气道模拟OA ,应用心导管技术测定实验前和第10个循环过程中犬心肌力学和部分血流动力学参数的变化及实验前后动脉血气、血浆去甲肾上腺素 (NE)和肾上腺素 (Ep)的变化。结果 :(1)与实验前比较 ,除IP晚期外 ,心率显著减慢 ,平均动脉压 (MAP)显著增加 ;在AP晚期 ,左室收缩压 (LVSP)、左室压力最大上升和下降速率 (±dp/dt)及心肌收缩因子缩短最大速度 (Vmax)均显著下降 ,左室舒张末压 (LVEDP)显著升高 ,左室压力下降时间常数 (T)显著延长。(2)在一个循环过程中 ,与IP晚期比较 ,心率、LVSP、±dp/dt和Vmax 在AP晚期显著下降 ,LVEDP显著升高 ,T值显著延长 ;MAP在IP早期显著升高。(3)OA导致PaO2 和 pH值显著下降 ,PaCO2、NE和Ep显著升高。结论 :OA可引起犬左心室舒张功能和心肌收缩性一过性下降及交感神经兴奋性增强     

心喘灵(XC-1)及其衍生物XC-2对麻醉犬血流动力学的作用

本工作比较研究了心喘灵(XC-1)及其衍生物XC-2(8204) 对麻醉开胸犬心脏血流动力学的作用。用递加剂量法静注心喘灵0.5,1.0,2.0和4.0 mg/kg,每二个剂量之间的间隔为5 min,给药后MAP和LVP下降,HR减慢,CI和SI增加,TPR降低,冠状、颈内和股动脉血流增加,血管阻力下降,±LVdp/dt max增加,而LV dp/dt/p改变不明显,LVW,CVP和MVO₂无明显变化。用同法静注同样剂量XC-2的作用和心喘灵相似,但较弱;一次静注5 mg/kg也出现柑似但较弱的作用。它们的作用是通过阻断α和β受体及直接扩张血管所引起。     

肉毒碱对实验性衰竭心脏功能的影响

肉毒碱carnitine是一广泛存在于组织中的氨基酸,本文报告人工合成d,l-carnitine盐酸盐(VBt)对麻醉猫衰竭心脏及离体豚鼠衰竭心脏功能的影响。用缓慢恒速静注戊巴比妥钠引起猫急性心衰。给心衰猫静注VBt 50 mg/kg/min,共5分钟。给药后,MAP、LVP及LVdp/dt max均明显升高,CVP及LVEDP轻度下降,HR无明显改变。当VBt与毒毛旋花子甙K合用时,能增加后者引起心律失常的剂量和治疗宽度。VBt对正常离体豚鼠心脏除引起HR减慢外,对心收缩力和冠脉血流量均无明显影响。当用乏氧灌流引起急性心衰时,VBt则加强心收缩力和增加冠脉血流,并推迟心衰的发展。此外VBt还能使大鼠心肌组织耗氧量明显降低。     

西洋参茎叶皂甙对犬血流动力学的影响

iv西洋参茎叶皂甙25mg.kg(-1)、50mg.kg~(-1)能明显降低麻醉正常犬动脉血压、左室压及左室压最大上升速率,而对左室舒张期末压无明显影响,从而使心脏做功和耗氧减少,有利于抗心肌缺血作用。能明显减轻实验性心肌梗塞犬左室舒张期末压的增加及心脏指数的减少,也使左室压最大下降速率的降低明显减轻,表明西洋参茎叶皂甙能够改善心肌梗塞犬的循环功能.且对心肌舒张功能具有保护作用。     

丹参水提物对心肌缺血-再灌注损伤大鼠血流动力学的影响

目的观察丹参水提物(SME)对心肌缺血-再灌注损伤(I/R)大鼠血流动力学的影响,探讨其对I/R大鼠心肌梗死的保护作用。方法采用SD♂大鼠左冠状动脉前降支结扎法制备I/R大鼠模型,同时给予不同剂量的SME(29.76、59.52 mg·kg-1)和复方丹参片(FDT,1.21 g·kg-1),3 d后测定心电图,记录再灌注2 h后的心率(HR)、动脉血压(MABP)、左室舒张末期内压(LVEDP)、左室收缩内压(LVSP)、左室内压最大上升/下降速率(LVdp/dtmax);计算心脏组织的梗死范围。结果29.76、59.52 mg·kg-1SME和1.21 g·kg-1FDT可使LVEDP降低,MABP、LVdp/dtmax和LVSP升高,心肌组织的梗死面积缩小;59.52 mg·kg-1SME较1.21 mg·kg-1FDT可明显改善各项指标。结论 SME对大鼠I/R具有保护作用。     

The haemodynamic and metabolic effects of tolmesoxide with special reference to impaired myocardial function.

The haemodynamic, metabolic and regional blood flow effects of the vasodilator, tolmesoxide (1 mg kg-1 min-1 for 20 min by intravenous infusion) were examined in two groups of greyhound dogs anaesthetized with alpha-chloralose and mechanically ventilated. One group of dogs was thoracotomized and subjected to acute coronary artery occlusion. In these dogs tolmesoxide was infused 2.5 h after occlusion when there was evidence of impaired myocardial function. Tolmesoxide administration resulted in marked systemic hypotension which was associated with myocardial stimulation (increase in heart rate and LVdP/dtmax). These effects were less marked in thoracotomized dogs subjected to coronary artery occlusion. Cardiac stimulation was attenuated by pretreatment with the beta-adrenoceptor antagonist, atenolol. Peripheral resistance and left ventricular end-diastolic pressure (LVEDP) were reduced by tolmesoxide. In spite of the systemic hypotension, the marked reduction in LVEDP resulted in an enhanced subendocardial driving pressure and an increased blood flow to ischaemic regions of the left ventricular wall as measured with Xe133 clearance. Blood flow to normal regions of the left ventricular wall was also increased by tolmesoxide. A metabolic and respiratory acidosis may have contributed to the haemodynamic effects of tolmesoxide. Plasma renin levels were significantly elevated by the drug. Tolmesoxide administration thus resulted in cardiac stimulation, reduced both pre-load and after-load, yet maintained coronary and pulmonary perfusion. This haemodynamic profile of tolmesoxide would explain the beneficial effects obtained with this drug in the treatment of cardiac failure.     

重组人脑钠肽对慢性心力衰竭兔的实验研究

目的研究重组人脑钠肽（rhBNP）对慢性心力衰竭（CHF）兔血流动力学及心功能的影响。方法用导管捅破兔主动脉瓣,导致超容量负荷型兔的心衰模型。造模成功后动物饲养约5周。心力衰竭兔随机分为三组,分别给予rhBNP、硝普钠和安慰剂（5%葡萄糖）静脉滴注。采用心脏超声图观察用药前后心功能指标。1周后静脉给予同样三种药物,观察用药前后HF兔血流动力学参数的变化。结果HF兔静脉滴注rhBNP后心脏超声检查示LVEF较治疗前明显升高（P〈0.05）,LVEF从（0.63±0.06）L上升至（0.70±0.07）L（P〈0.05）;CO无明显变化;LVESV、LAD较治疗前下降明显（P〈0.05）,LVESV从（2.1±0.7）m l降至（1.2±0.9）m、lLAD由（11.0±1.9）mm下降至（10.1±1.8）mm。而硝普钠治疗组和安慰剂组上述参数无明显变化（P〉0.05）。血流动力学监测：给药3 h后三组比较发现：rhBNP组LVEDP、MAP和DBP下降差异具有统计学意义,LVEDP从（19.1±2.8）mm Hg下降至（6.4±5.9）mm Hg（P〈0.05）;DBP从（72.6±6.3）mm Hg降至（64.6±6.1）mm Hg（P〈0.05）;硝普钠组SBP、DBP、MAP、LVSP、LVEDP均明显下降（P〈0.05）,而且以LVSP和SBP下降最为显著;安慰剂组上述参数无明显变化。结论慢性HF兔应用rhBNP后可以增加LVEF,缩小LVESV和LAD。rhBNP能明显降低慢性HF兔的心脏前后负荷,使DBP、MAP明显下降,尤其是LVEDP下降显著。     

人参皂苷Rg_2对犬戊巴比妥钠心力衰竭的影响

目的 观察人参皂苷Rg_2(Rg_2)对犬戊巴比妥钠心力衰竭的影响。方法 复制戊巴比妥钠致心力衰竭模型,静脉注射Rg_2 0.5、1.0、2.0 mg·kg~(-1),观察对血流动力学的影响。结果 Rg_2 0.5、1.0、2.0mg·kg~(-1)静脉注射,可加快HR、升高SBP、DBP、MAP、LVSP及±dp/dt_(max);降低LV-EDP。结论 Rg_2能改善心功能不全犬的血流动力学状况,具有强心作用。     

强心扩血管药羟苯氨酮对大鼠,猫和狗心脏血流动力学的影响

为了解强心扩血管新药羟苯氨酮( oxyphenamone,9003 )对在体心血管系统的效应,用多导生理仪与电磁流量计测定大鼠,猫与狗的心脏血流动力学参数。结果表明,静注羟苯氨酮引起血压与血管阻力中度下降,心输出量,心肌收缩力与收缩力变化速度,冠状动脉和股动脉血流量明显增加。羟苯氨酮对心率与左室压的影响呈现种系差别,它增加狗的左室收缩压与压力变化速度,降低左室舒张末期压力,小剂量羟苯氨酮(1或3mg·kg^-1)引起狗的心率轻度降低,剂量增到6mg·kg^-1,心率中度加快。羟苯氨酮不影响猫的心率与左室压。大鼠静注羟苯氨酮后引起心率,左室收缩压与压力变化速度降低,左室舒张末期压力无变化。羟苯氨酮对心脏血流动力学的影响有待用病理模型作进一步观察。     

蝙蝠葛酚性碱对犬血流动力学及冠脉循环的影响蝙蝠葛酚性碱对犬血流动力学及冠脉循环的影响

目的研究蝙蝠葛酚性碱（PAMD）对正常麻醉犬血流动力学、冠脉循环及心肌氧代谢的影响。方法设立生理盐水阴性对照组及PAMD 3.5和7.0 mg·kg^-1两剂量组，在不同时间点观察各组犬血流动力学、冠脉循环及心肌氧代谢的相关指标的改变。结果与药前相比，PAMD两剂量组均可降低左心室收缩压（LVSP）和±dP/dt_max，减慢心率，增加心肌氧含量、降低心肌氧利用率，且具有增加冠状动脉血流量，降低冠状动脉阻力和外周阻力的作用。对血压、心输出量和左室舒张末压（LVEDP）无显著影响。结论PAMD能改善血流动力学、冠脉循环及心肌氧代谢。     

5／6肾切除致慢性肾衰诱发左室心衰大鼠模型的病理生理

目的研究5／6肾切除引起慢性肾衰诱发左室心衰大鼠模型的病理生理机制。方法雄性SD大鼠经“两次手术切除法”行5／6肾切除,6周后造成慢性肾衰,8周后诱发左室心衰。试剂盒法测定血清钙、磷、肌酐、尿素氮。Bradford法测定24h尿蛋白量。左心室插管术测定心脏血流动力学指标心率（HR）、左室收缩压（LVSP）、左室舒张压（LVDP）、左室舒张末期压（LVEDP）及左室最大压力上升速度（dp／dtmax）和下降速度（-dp／dtmax）。称重法测定心脏重量参数。病理切片HE染色观测心肌病理情况。结果与假手术组相比,除血清钙水平外,病理组大鼠各项指标均比假手术组明显升高,表明慢性肾衰造模成功。与假手术组大鼠比较,病理组大鼠LVSP下降,LVDP和LVEDP均上升。病理组心脏重量参数均比假手术组升高。提示左室舒张和收缩（主要是舒张）功能损伤,发生左室心衰和左室心肌肥厚重构。结论5／6肾切除慢性肾衰诱发的大鼠左室心衰,病理生理学特点是左室舒张和收缩（主要是舒张）功能衰竭,和左室心肌肥厚重构。     

Cardiovascular effects of the calcium sensitizer, levosimendan, in heart failure induced by rapid pacing in the presence of aortic constriction.

1. The haemodynamic effects of a novel cardiotonic drug, levosimendan, which has both calcium-sensitizing and phosphodiesterase III (PDE III) inhibitory properties, were studied in conscious dogs in which heart failure had been induced by prolonged cardiac pacing in the presence of aortic constriction. These effects were compared with those in sham-operated dogs with essentially normal cardiac function. 2. Eighteen mongrel dogs were instrumented for the measurement of left ventricular pressure (LVSP, LVEDP) and contractile function (dP/dt; dP/dt/P). In twelve dogs a balloon catheter, positioned in the thoracic aorta, was inflated producing an approximate 60% reduction in effective aortic diameter. Twenty min later rapid ventricular pacing (240 beats mean-1) was commenced and maintained for 48 h by means of a bipolar pacing electrode introduced into the right ventricle. This electrode served also for recording changes in the endocardial electrogram in the absence of pacing. Six of these dogs were used to evaluate the haemodynamic changes of pacing-induced heart failure; a further six of these dogs the haemodynamic changes elicited by levosimendan under these conditions. Six sham-operated dogs (group 2) served as controls. 3. In six dogs (group 1) the haemodynamic alterations were assessed after the development of heart failure. In the presence of aortic constriction, 48 h continuous rapid cardiac pacing resulted in a marked deterioration in left ventricular function which remained stable for at least 48 h after cessation of pacing. Thus, there was a marked reduction in LVSP (15%), +dP/dtmax (35%), -dP/dtmax (36%) and also in dP/dt/P (29%), whereas LVEDP was increased considerably (from 6.4 +/- 1.4 to 20.0 +/- 2.2 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular and adenylate cyclase stimulant properties of NKH477, a novel water-soluble forskolin derivative.

The cardiovascular effects of NKH477 (6-(3-dimethylaminopropionyl)forskolin hydrochloride), a novel water-soluble forskolin derivative, were investigated in dogs. Intravenous (i.v.) injections of NKH477 (1-30 micrograms/kg) caused dose-related increases in left ventricular dP/dtmax (LVdP/dtmax), coronary and femoral artery blood flow (CBF, FBF), heart rate (HR), and myocardial oxygen consumption (MVO2) and a dose-related decrease in blood pressure (BP) in anesthetized dogs. The regression analysis between CBF and MVO2 showed that NKH477 did not influence substantially the balance of oxygen supply and demand. Infusions of NKH477 (0.15-0.6 microgram/kg/min i.v.) also increased LVdP/dtmax, cardiac output (CO), and HR and decreased BP, pulmonary arterial diastolic pressure, and total peripheral resistance (TPR) in a dose-dependent manner. In contrast to forskolin, NKH477 administered intraduodenally (0.05-0.2 mg/kg) and orally (0.15 and 0.3 mg/kg) clearly exhibited cardiovascular actions, as it did in i.v. administration, indicating that NKH477 is orally active. No arrhythmias were induced by NKH477 in any study. NKH477, like forskolin, showed adenylate cyclase stimulant activity in guinea pig ventricular membrane but did not inhibit Na+, K(+)-ATPase or phosphodiesterase (PDE) activity. Thus, NKH477 can be characterized as a potent, orally active, water-soluble forskolin derivative, which suggests that NKH477 is a useful inodilator for treatment of heart failure, especially in the severe stage with beta-adrenoceptor downregulation.     

Cardioprotective effect of fluvastatin on isoproterenol-induced myocardial infarction in rat

The present study was designed to investigate whether fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, would attenuate the acute myocardial infarction in isoproterenol-treated rat model via maintaining activities of endogenous antioxidant enzymes. Hemodynamic and electrocardiograph parameters were monitored and recorded continuously, cardiac marker enzymes and antioxidative parameters of plasma and heart tissues were measured, and histopathological examination of heart tissues was performed. Isoproterenol-treated rats showed lower of left-ventricular systolic pressure (LVSP), maximum (LVdP/dtmax) and minimum rate of developed left ventricular pressure (LVdP/dtmin), and higher of left ventricular end-diastolic pressure (LVEDP), in addition, a significant rise in ST-segment and increase in content of lactate dehydrogenase, glutamic oxalacetic transaminase, creatine kinase and malondialdehyde, as well as fall in activities of glutathione peroxidase, superoxide dismutase and catalase were observed. Oral administration of fluvastatin (5, 10 and 20 mg/kg, respectively) significantly prevented almost all the parameters of isoproterenol-induced heart failure and myocardial injury that mentioned above. The protective role of fluvastatin on isoproterenol-induced myocardial damage was further confirmed by histopathological examination. There was no significant change in heart rate in all experimental groups. Compared with control group, any indexes in sham rats treated with fluvastatin (20 mg/kg) alone were unaltered (all P>0.05). Our results suggest that fluvastatin has a significant effect on the protection of heart against isoproterenol-induced myocardial infarction through maintaining endogenous antioxidant enzyme activities.