前胡丙素与硝苯啶对大鼠工作心脏缺血再灌注损伤的保护作用

大鼠ip前胡丙素(Pra-C 15 mg/kg,bid×3d)和硝苯啶(Nif 60μg/kg,bid×3d),使离体缺血再灌注工作心脏的收缩(AP,LVSP,+dP/dt_max)舒张(-dP/dt_max LVEDP和T值)性能在35min时得到改善,尤以舒张性能改善明显,并能促进CO,CF,SV及HR恢复,改善心脏工作效率,减少CK释放和心肌线粒体钙含量,表明Pra-C和Nif对心肌缺血都有保护作用,Pra-C的效应与Nif相近。     

7-甲氧基-4′-羟基-3′-二乙胺甲基异黄酮(MHDF)对大鼠血流动力学和主动脉的作用

本实验观察了MHDF对整体大鼠血流动力学和离体大鼠胸主动脉的作用。结果表明iv MHDF(3～12.8 mg/kg)能降低大鼠左心室±dp/dt_max,V_max,V_pm和LVSP,延长T-dp/dt_max,减慢心率。MHDF还能舒张大鼠胸主动脉,ED₅₀为6.5×10^-6mol/L;非竞争拮抗NA和CaCl₂致主脉收缩,pD₂′为3.11±0.21和3.73±0.07;抑制高K⁺致主动脉收缩,IC₅₀为1.76×10^-5mol/L。提示MHDF对血管的作用与α受体阻断剂不同,而可能与钙拮抗有关。     

多柔比星诱导的心衰大鼠迷走神经的功能性改变

目的 探讨心衰大鼠迷走神经对心脏调节功能的变化以及电刺激迷走神经对心脏舒缩功能的影响。方法 将大鼠分为对照组、心衰模型组及迷走神经刺激组,对照组10只,每只给予生理盐水1 mL,心衰模型组及迷走神经刺激组共30只给予多柔比星腹腔注射2.5 mg·kg-1,每周1次,共6次。给药结束后行血流动力学检测、压力反射敏感性检测及迷走神经刺激(刺激频率:2.0 Hz,波宽:1.0 ms,刺激幅度:3 V,持续时间:240 min)。结果 与对照组相比,心衰组大鼠压力反射敏感性明显下降(n=10,3.29±0.47 vs 1.90±0.24,P＜0.05)。迷走神经刺激后,与心衰模型组大鼠比较,其左室舒张末压(LVEDP)明显降低(P＜0.01),而左室舒张期压力最大下降速率(-dP/dt_max)、左室等容收缩期压力最大上升速率(+dP/dt_max)、左室内压峰值(LVSP)均明显升高(均P＜0.01)。结论 多柔比星诱导的心衰大鼠迷走神经张力下降,电刺激迷走神经可明显改善心衰大鼠心脏的舒缩功能。迷走神经刺激有望成为治疗心力衰竭的有效方法之一。     

辽吉冰凉花总甙对心功能影响的实验研究

辽吉冰凉花总甙(APAW)1.0mg/kg iv,能使麻醉家兔正常心脏的P-dP/dt环体面积(LO),LV-dP/dt_max,Vpm及LVSP比药前增大,HR减慢。APAW和冰凉花(AAR)及毒毛旋花子甙K(SK)一样,能明显改善衰竭兔心的心功能。静脉恒速输入0.5 mg/ml APAW,25min后,心衰家兔的LVSP,LV—dP/dt max,LO均明显回升,LVEDP降低,t-dP/dt max缩短。三种强心甙的最大强心效力无显著性差异。但APAW的治疗宽度和治疗指数均较AAR和SK为大,而AAR和SK间则无显著性差异。     

粉防己碱对DOCA盐性高血压心肌肥厚大鼠心脏血流动力学的影响

粉防己碱可显著降低DOCA盐性高血压心肌肥厚大鼠的血压,左室湿重;在工作心脏研究中发现其改善肥厚心室的收缩(AP,LVSP,+dp/dt_max)舒张(一dp/dt_max,LVEDP,T值)性能,尤以舒张性能改善明显,并恢复泵功能(CO)和冠脉流量(CF);在左室压力容积关系法研究显示有改善肥厚心室左室顺应性和左室僵硬度的作用。提示:Tet有逆转心肌肥厚和改善肥厚心肌舒张收缩功能,左室顺应性和心肌劲度的作用。     

细辛对狗左室功能的作用及其与去甲乌药硷、异丙肾上腺素的比较

实验表明细辛可使狗左室泵功能和心肌收缩性能明显改善。在心肺制备狗,主要表现为LVSP↑,LVEDP↓,MAP↑,CO↑,HR↑,SV↓,dp/dt_max↑,-dp/dt_max↑,t—dp/dt_max↓,V_px↑,V_ce-cpip↑,V_max↑;在麻醉开胸狗,除MAP降低和SV增加外,对其它指标的作用方向与心肺制备实验结果基本一致;两个实验中测取的Lissajous图形的正向前降支均向右上方移位。从而排除了前、后负荷的影响,说明泵功能的改善似由于细辛增强心肌收缩性能所致。通过细辛与去甲乌药硷、异丙肾上腺素的比较研究,提示三者的作用基本相似,唯SV显示不同的结果。细辛使SV增加,去甲乌药硷、异丙肾上腺素却使SV减少,这可能与细辛增加HR的比率较二者为低密切相关。肾上腺素能β受体阻滞后,细辛增加CO的作用仍然存在,值得进一步研究。     

蝙蝠葛酚性碱对离体大鼠心肌顿抑的保护作用

目的　探讨蝙蝠葛酚性碱(PAMD)对离体大鼠心肌顿抑的作用。方法　采用缺血10min后再灌注30min造成心肌顿抑模型(S) ,灌流液中加0.5mg·mL^-1 PAMD(P)组同样缺血再灌注。结果　灌注末S组LVSP ,+dp/dt_max和-dp/dt_max分别降至预灌末的49% ,53%和58% ,LVEDP则增至422% ;心肌钙含量为(514±142 ) μg·g^-1 (干重) ;出现可逆性心肌超微结构损伤。而P组再灌注末LVSP ,LVEDP ,+dp/dt_max和-dp/dt_max恢复为预灌末值的70% ,205% ,78%和79% ;心肌钙为(316±84) μg·g^-1 (干重) ;以上变化均有显著差异。结论　PAMD对离体大鼠顿抑心肌有保护作用     

氟碳乳剂稀释血液对心肌缺血时左心室舒张功能的影响

本实验在40只麻醉开胸兔心脏上观察了阻断冠脉血流后左心室舒张功能的变化和氟碳乳剂稀释血液对心肌缺血时左心室-dp/dt_max,-V_CE和T值变化的影响。实验结果表明,阻断冠脉血流后,-dp/dt_max和-V_CE均明显降低,T值显著延长。阻断冠脉血流前或阻断冠脉后15min时用氟碳乳剂行等容血液稀释,可使心肌缺血时左心室舒张功能损害明显减轻。     

萘甲异喹对离体豚鼠心肌的作用

萘甲异喹(NI)呈浓度依赖性地降低离体豚鼠心房收缩力和频率。其拮抗豚鼠左房肌Iso正性肌力作用的PD2₂′值为5.4,Ver为5.8。NI10μmol/L明显降低豚鼠乳头肌收缩力;缩短快反应APD,以对APD₂₀影响最大,但不影响APA和V_max。对高K⁺去极化慢反应动作电位,NI产生浓度依赖性负性肌力作用,同时明显降低APA,V_max,缩短APD;提高细胞外液Ca²⁺浓度可使其抑制作用逆转。结果提示NI具有钙通道阻滞作用。     

莲心碱对大鼠血流动力学及兔心房特性的影响

iv莲心碱(Lien)3mg/kg可一过性地抑制麻醉或毁脊髓大鼠血流动力学诸指标,对麻醉大鼠LVP,+dp/dt_max及SAP的抑制较奎尼丁(Qui)3mg/kg为强;Lien 1～30 mg/kg可依量性地产生上述效应,12mg/kg的Lien和Qui分别使LVP,+dp/dt_max,SAP下降33%,37%,29%和9%,12%,9%,而二者对其它血流动力学参数的抑制程度却相近。Lien 12 mg/kg对血流动力学诸指标的抑制强度与维拉帕米(Ver)1 mg/kg相似。Lien 1～100μmol/L可浓度依赖性地抑制左房收缩力和右房频率。提示其对血流动力学影响的特性与Ver更相似而与Qui有别。     

Class III Antiarrhythmic Action and Inotropy: Effects of Almokalant in Acute Ischaemic Heart Failure in Dogs

Abstract: We studied the haemodynamic and metabolic effects of the novel class III antiarrhythmic agent almokalant (H 234/09) in acute ischaemic heart failure at a dose prolonging ventricular repolarization. In pentobarbital anaesthetized dogs, heart failure was induced by microembolization of the area supplied by the main left coronary artery until a stable left ventricular end-diastolic pressure (LVEDP) of 32 ± 2 mmHg was achieved. Embolization depressed LV dP/dt_max, LV dP/dt_min, left ventricular systolic pressure (LVSP) and cardiac output. After intravenous infusion of almokalant (0.35 μg/kg) LV dP/dt_max and LV dP/dt_min were not significantly changed at paced cycle length of 300 msec, whereas LVSP and aortic pressure decreased both at spontaneous and paced cycle length of 300 msec. LVEDP remained unchanged. Heart rate decreased from 185 ± 7 to 167 ± 5 beats/min., and corrected QT-time (QT_c) increased from 9.5 ± 0.3 to 10.4 ± 0.5 msec. Arterial concentration and net myocardial uptake of glucose, lactate and free fatty acids were not significantly influenced by almokalant. In conclusion, almokalant at a dose prolonging ventricular repolarization had no negative inotropic effect in acute ischaemic heart failure.     

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。     

Influence of intravenous infusion of ethanol on regional blood flow in conscious rats

Abstract— The effects of intravenous infusions of ethanol and saline (0·9% NaCl) on mean arterial pressure (MAP), heart rate (HR), total peripheral resistance (TPR), cardiac contractility (dP/dt_max) and systemic haemodynamics were studied in conscious, unrestrained rats by the radioactive microsphere technique. Saline (0·03 and 0·06 mL min^?1 kg^?1 for 12 min each dose) in the time-control group did not affect MAP, HR, TPR, dP/dt_max or vascular conductances in any organs or beds. While the low dose ethanol (2·4 mg min^?1 kg^?1) did not alter MAP, HR, TPR, systemic haemodynamics or dP/dt_max, the high dose (4·8 mg min^?1 kg^?1) slightly reduced MAP and TPR but did not affect HR, cardiac output or dP/dt_max. Both doses of ethanol vasodilated the intestine and spleen, but vasoconstricted the skin. The high dose caused additional vasodilatation in the heart and testes and the low dose also constricted the skeletal muscle bed. Our results show that ethanol, at non-hypotensive or slightly hypotensive doses, has marked vasodilator effects in the heart, intestine, spleen and testes.     

KP-102 (growth hormone-releasing peptide-2) attenuates ischemia/reperfusion injury in isolated rat hearts

KP-102, a synthetic growth hormone (GH)-releasing peptide, exerts a variety of effects on cardiac function. In the present study, we investigated the direct cardiac effects of KP-102 with regard to ischemia/reperfusion injury by using isolated rat hearts. Isolated Wistar rat hearts were mounted on a Langendorff apparatus and subjected to 30 min of ischemia followed by 40 min of reperfusion. The rat hearts were treated with 0.1–10 nmol/l KP-102 beginning from 15 min before ischemia until the end of the experiment, with the exception of the ischemia period. Cardiac parameters such as the left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), maximum dP/dt (+dP/dt_max), minimum dP/dt (−dP/dt_max), and heart rate (HR) were measured. The following ischemia/reperfusion-induced cardiac dysfunctions were observed: increased LVEDP and decreased LVDP, +dP/dt_max, and −dP/dt_max. KP-102 at a dose of 0.1 nmol/l or more induced lower LVEDP and higher LVDP and gave higher +dP/dt_max and −dP/dt_max values during the reperfusion as compared with the control groups. In particular, KP-102 at 10 nmol/l clearly suppressed the increase in the LVEDP after reperfusion; eventually, the LVEDP was restored to the preischemia level. At 40 min of reperfusion, 10 nmol/l KP-102 noticeably increased the LVDP, +dP/dt_max, and −dP/dt_max, as compared with the control. KP-102 had no effect on the HR throughout the experiment. In conclusion, KP-102 improved cardiac function in rat isolated hearts subjected to ischemia/reperfusion injury, which is independent of GH secretion.     

Korean Red Ginseng Induced Cardioprotection against Myocardial Ischemia in Guinea Pig

This study was designed to evaluate the protective effect of Korean red ginseng (KRG) against ischemia/reperfusion (I/R) injury in isolated guinea pig heart. KRG has been shown to possess various ginsenosides, which are the major components of Panax ginseng. These components are known naturally occurring compounds with beneficial effects and free radical scavenging activity. The heart was induced to ischemia for 60 min, followed by 120 min reperfusion. The hearts were randomly allocated into five groups (n=8 for each group): normal control (N/C), KRG control, I/R control, 250 mg/kg KRG group and 500 mg/kg KRG group. KRG significantly increased hemodynamics parameters such as aortic flow, coronary flow and cardiac output. Moreover, KRG significantly increased left ventricular systolic pressure (LVSP), the maximal rate of contraction (+dP/dt_max) and maximal rate of relaxation (-dP/dt_max). Also, treatment of KRG ameliorated electrocardiographic index such as the QRS, QT and RR intervals. Moreover, KRG significantly suppressed the lactate dehydrogenase, creatine kinase-MB fraction and cardiac troponin I and ameliorated the oxidative stress markers such as malondialdehyde and glutathione. KRG was standardized through ultra performance liquid chromatograph analysis for its major ginsenosides. Taken together, KRG has been shown to prevent cardiac injury by normalizing the biochemical and oxidative stress.     

Cardioprotective effect of matrine on isoproterenol‐induced cardiotoxicity in rats

Objectives This study was designed to explore the effect and mechanism of matrine, an active component of Chinese traditional medicine, on isoproterenol‐induced acute cardiotoxicity in rats. Methods Acute myocardial injury was induced in rats by daily subcutaneous injection of isoproterenol (85 mg/kg) for two days. Haemodynamic and biochemical parameters were measured and histopathological examination was performed. Key findings Chronic oral administration of matrine (50, 100 or 200 mg/kg per day for 10 days) significantly reduced the release of lactic dehydrogenase, glutamic oxaloacetic transaminase and creatine kinase after isoproterenol‐induced myocardial ischaemic injury, improved the left ventricular (LV) dysfunction, including increased LV systolic pressure (LVSP), maximum rate of developed LV pressure (LV dP/dt_max) and minimum rate of developed LV pressure (LV dP/dt_min), increased the activity of superoxide dismutase, catalase and glutathione peroxidase, and also decreased the content of the lipid peroxidation product malondialdehyde in plasma and myocardial tissues in rats. Acute oral administration of matrine at a dose of 100 or 200 mg/kg for two days also had a cardioprotective effect on this rat model. The protective role of matrine on isoproterenol‐induced myocardial damage was further confirmed by histopathological examination. There were no significant changes in heart rate and blood pressure in all experimental groups. Conclusions Our results suggest that matrine has a significant cardioprotection against isoproterenol‐induced cardiotoxicity through its antioxidant property.     

黄花夹竹桃次甙甲和次甙乙的强心作用与毒性

本实验用在体猫和豚鼠的衰竭心脏、离体豚鼠心脏和左心房条观察了次甙甲和次甙乙的强心作用与毒性,并与已知强心甙哇巴因和毒毛旋花子甙K进行比较。结果表明,次甙甲和次甙乙都可使猫和豚鼠的衰心泵血功能部分或完全恢复,给药后LV-dp/dt max,LVSP和BP升高,LVEDP和CVP下降,其作用性质与哇巴因和毒毛旋花子甙K相似,安全范围以次甙甲较大,等毒性剂量的次甙甲和次甙乙对离体豚鼠心脏的强心作用均比哇巴因强,给药后2—3分钟差异显著,但三者对离体豚鼠左心房条的正性肌力作用则相似。     

Changes in haemodynamics and left ventricular function during intravenous nifedipine infusion with and without additional propranolol in patients with coronary artery disease. A randomized,placebo controlled trial

Summary The haemodynamic effects of a combined intravenous treatment of nifedipine and propranolol in ten patients with coronary artery disease compared to a single treatment with nifedipine or placebo were investigated.Nifedipine infusion resulted in a reduction of left ventricular (LV) afterload and LV volumes with an increase in heart rate and EF and no change of the double product, coronary sinus flow, LV diastolic parameters and dp/dt_max. Addition of propranolol lowers myocardial oxygen demand by reducing heart rate and dp/dt_max together with a sustained afterload reduction with no change in LV volumes and EF.The vasodilatatory action of nifedipine pretreatment balanced the negative effects of acute beta-receptor blockade on LV function and allows the reduction of myocardial oxygen demand without a deterioration of LV function.