胺碘酮对低O_2、酸中毒及肾上腺素条件下豚鼠左心室流出道自律细胞电活动的影响

目的:研究胺碘酮对豚鼠左心室流出道自律细胞电活动的影响以及胺碘酮对低O2、酸中毒和肾上腺素(EPI)所致该部位自律性改变的影响。方法:采用标准玻璃微电极细胞内电位记录技术,分别观测胺碘酮对豚鼠左心室流出道自发慢反应电位的影响,以及胺碘酮对无糖低氧、pH6.8和EPI导致的该电位改变的影响。结果:(1)0.1μmol/L胺碘酮可使左心室流出道自发慢反应电位自发放电频率(RPF)减慢,最大舒张电位(MDP)绝对值减小,复极80%时间(APD80)延长(P0.05);1μmol/L胺碘酮可引起4相自动除极速度(VDD)和0相最大除极速度(Vmax)减慢,动作电位幅度(APA)减小,复极50%时间(APD50)延长(P0.05),RPF减慢,MDP减小和APD80延长(P0.01);10μmol/L胺碘酮可使VDD进一步减慢,APA进一步减小(P0.01),其它指标的改变维持1μmol/L胺碘酮灌流时的水平。(2)低O2可使VDD、RPF和Vmax减慢,MDP和APA减小,APD50缩短(P0.05);和低O2组相比,1μmol/L胺碘酮+低O2可使RPF和Vmax进一步减慢,MDP增大,APD80延长(P0.05),VDD进一步减慢,APD50延长(P0.01)。(3)pH6.8的灌流液可使VDD和RPF减慢,APD80缩短(P0.05),Vmax减慢,APA减小(P0.01);与pH6.8组相比,pH6.8的1μmol/L胺碘酮可使RPF进一步减慢,MDP和APA进一步减小,APD80延长(P0.05),VDD进一步减慢,APD50延长(P0.01)。(4)10μmol/LEPI可使VDD、RPF和Vmax加快,MDP增大,APD50和APD80缩短(P0.05),APA增大(P0.01);1μmol/L胺碘酮+10μmol/LEPI可使VDD和RPF减慢,MDP和APA减小,Vmax减慢,APD50和APD80延长(P0.05,P0.01)。结论:胺碘酮可降低豚鼠左心室流出道的自律性,同时对低O2、酸中毒和EPI所致的该部位自律性改变有一定的影响。     

腺苷对豚鼠左心室流出道自律细胞的电生理效应

目的 研究腺苷对豚鼠左心室流出道自律性电活动及其对肾上腺素、低氧和酸中毒电生理效应的影响.方法 采用玻璃微电极细胞内电位记录技术,分别观察腺苷对左心室流出道自发慢反应电位及对肾上腺素、低氧和酸中毒所致该电位改变的影响.结果 (1)10、50及100 μmol/L腺苷可呈剂量依赖性降低豚鼠左心室流出道自律细胞的电活动.(2)10 ixmol/L肾上腺素可明显提高左心室流出道的自律性,50μmol/L腺苷明显降低肾上腺素导致的该部位自律性升高.(3)低氧和酸中毒均可使该部位的自律性电活动明显降低,50μmol/L腺苷可使其自律性进一步降低.结论 腺苷对左心室流出道的自律性及肾上腺素、低氧和酸中毒导致的自律性异常有一定影响.     

一氧化氮对缺血再灌注豚鼠左心室流出道自律性电活动的影响

目的:研究一氧化氮(NO)对豚鼠左心室流出道自发电活动的影响及其对缺血/再灌注(I/R)时自发电活动改变的影响。方法:采用标准玻璃微电极细胞内电位记录技术观测外源性NO供体硝普钠(SNP)对豚鼠左心室流出道自发慢反应电位的影响及其对I/R时该电位改变的影响。结果:1、10、100μmol/L SNP呈浓度依赖性地导致4相自动除极速度(VDD)和自发放电频率(RPF)明显增加,但1 000μmol/L SNP的效应不明显。SNP呈浓度依赖性地导致最大舒张电位(MDP)绝对值和动作电位幅度(APA)增大,0相最大除极速度(Vmax)加快,复极50%和90%时间(APD50和APD90)缩短。缺血10 min组VDD和RPF明显减慢,APA和Vmax明显增大,APD50和APD90明显延长。与缺血10 min组相比,再灌注10 min组VDD和RPF明显加快,且常出现节律不齐,MDP绝对值和APA明显减小,APD50和APD90明显缩短。1、10、100μmol/L SNP再灌注时可明显改善缺血造成的VDD和RPF减慢以及再灌注造成的节律不齐,1 000μmol/L SNP的上述效应不明显。各浓度SNP再灌注时均可使缺血造成的APA和APD的改变恢复至对照组水平。结论:SNP可呈浓度依赖性地增加左心室流出道的自律性,并可明显改善I/R导致的自发慢反应电位的改变。     

苦参碱对异丙肾上腺素致豚鼠心律失常的保护作用

<正>目的:研究苦参碱对异丙肾上腺素诱发豚鼠心律失常的电生理影响及苦参碱抗心律失常作用。方法:采用常规玻璃微电极细胞内记录技术,观察正常灌流液、异丙肾上腺素灌流液和异丙肾上腺素+苦参碱(50μmol/L)灌流液对豚鼠左心室流出道慢反应自律细胞动作电位0相幅值(APA)、50%复极化时间     

异丙肾上腺素对心肌细胞电活动的影响及丹参的保护作用

本实验在大鼠右心室乳头肌细胞上,观察丹参在预防异丙肾所致心肌损伤中对心肌细胞电活动的影响。异丙肾可影响心肌细胞去极化和复极化,使APA、OS和RP降低、APD延长、Vmax下降。丹参可减弱异丙肾对心肌细胞的损伤效应,使APD缩短、Vmax和OS增大,使其被控制在接近对照组水平,特别是APD_(50)的缩短尤为明显。实验结果表明,阻滞细胞膜慢通道、减少细胞内钙负荷,可能为丹参对心肌保护作用的重要途径。     

炙甘草汤对豚鼠离体心肌细胞电生理效应的影响

<正>目的:观察炙甘草汤对缺氧心肌电生理活动的影响,从细胞跨膜电位角度探讨炙甘草汤抗心律失常的作用机制。方法:采用常规玻璃微电极细胞内记录的方法,观察正常灌流液、缺氧灌流液和缺氧+炙甘草汤(40mg/ml)     

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。     

平喘固本方对哮喘豚鼠肺组织β-肾上腺素能受体、腺苷酸环化酶及环磷酸腺苷的影响

本文介绍了平喘固本方对致敏哮喘豚鼠肺组织β－肾上腺素能受体（β－AR）、腺苷酸环化酶(AC)活性及环磷酸腺苷(cAMP)含量的影响。豚鼠随机分成四组：对照组、平喘固本方组、酮替芬（西药对照）组和固本咳喘（中药对照）组，豚鼠肺中β－AR结合容量分别为22．68±6．19、29．77±5．84、24.64±2.64和26．13±6．52fmol／mg蛋白，平喘固本方组β－AR的结合位点（Rt值）大于对照组及酮替芬组，P＜0．05。肺组织中AC活性分别为9．66±2．36、13．1±2.4、8．4±2.4和9.02±2．81pmol·min－1／mg蛋白，平喘固本方组明显高于对照组、西药组和中药组，差异显著（P＜0．05）。cAMP含量分别为0．070±0．014、0096±0．027、0．098±0．029和0．097±0．015pmol／mg组织，用药各组均高于对照组，差异显著（P＜0．05）。提示平喘固本方可以提高哮喘豚鼠脑组织中β－AR功能，激活AC，使细胞中cAMP含量增加，使致敏哮喘豚鼠症状得以改善。     

肾动脉狭窄对心肌内去甲肾上腺素的含量及血压的影响

本文研究了35只京都种大白鼠(WKY)肾动脉狭窄手术后对心肌内去甲肾上腺素(NA)含量及血压的影响,发现左肾动脉狭窄(2K1C)型与右肾切除后再作左肾动脉狭窄(1K1C)型心肌内NA含量在实验组都低于对照组,而血压则高于对照组,两者有统计学意义。实验组(或对照组)心肌内NA含量在2K1C型都高于1K1C型,两者有显著性差异,但血压则2K1C型低于1K1C型。     

实验性哮喘豚鼠肺组织β-肾上腺素能受体的量变及电针刺激对其影响

本文采用放射配基结合法,观察了实验性哮喘豚鼠肺组织β-肾上腺素能受体的变化,并与正常动物作了比较。结果表明,哮喘豚鼠肺组织的β-受体结合~3H-DHA的最大结合量(BmAX)比对照组者低38%(P<0.01)。首次观察到随哮喘发作次数的增多,豚鼠肺组织β-受体的减少趋于明显;电针刺激可使哮喘豚鼠肺组织的β-受体数量恢复至对照动物水平。电针刺激对正常动物的β-受体数量未见有影响。     

Resting values of left ventricular work to coronary blood flow ratio in rats exposed to intermittent high altitude hypoxia and swimming

Summary Total hemodynamic values and left ventricular blood flow were studied using Sapirstein's method of ⁸⁶Rb uptake in female rats 24 h after a last exposure to high altitude. A simulated altitude of 1350 m was used, initial exposure being for 30 min, gradually increased by 30 min daily up to 330 min daily for 5 days a week; the total number of exposures was 32. In another animal group the hypobaric exposure was combined with swimming in water at 37 C.In both experimental groups the cardiac output and stroke volume increased, and in rats undergoing swimming the total peripheral resistance decreased as well.In the rats exposed to intermittent hypoxia only, left ventricular blood flow increased by about the same proportion as the cardiac output. The ratio of left ventricular work to coronary blood flow was significantly increased.In rats exposed to the combined influence of hypoxia and swimming, the increase in left ventricular blood flow did not match either the increase in cardiac output, or the weight gain of the left ventricle. The ventricular work to coronary blod flow ratio was the same as in controls.     

BMP4 is required in the anterior heart field and its derivatives for endocardial cushion remodeling, outflow tract septation, and semilunar valve development

The endocardial cushions play a critical role in septation of the four-chambered mammalian heart and in the formation of the valve leaflets that control blood flow through the heart. Within the outflow tract (OFT), both cardiac neural crest and endocardial-derived mesenchymal cells contribute to the endocardial cushions. Bone morphogenetic protein 4 (BMP4) is required for endocardial cushion development and for normal septation of the OFT. In the present study, we show that anterior heart field (AHF)-derived myocardium is an essential source of BMP4 required for normal endocardial cushion expansion and remodeling. Loss of BMP4 from the AHF in mice results in an insufficient number of cells in the developing OFT endocardial cushions, defective cushion remodeling, ventricular septal defects, persistent truncus arteriosus, and abnormal semilunar valve formation.     

Short-term effects of electrically induced tachycardia on antioxidant defenses in the normal and hypertrophied rat left ventricle

Increased oxidative stress resulting from enhanced production of reactive oxygen species and/or inadequate mechanisms of antioxidant defenses has been recognized as an important factor contributing to the initiation and progression of cardiac dysfunction under a wide variety of pathophysiological conditions. The main objective of this study was to examine the effect of electrically induced tachycardia on oxidative stress and the capacity of antioxidant defenses in the normal and hypertrophied left ventricle (LV) in the rat. Left ventricular hypertrophy (LVH) was produced by banding the descending abdominal aorta. The activities of antioxidant enzymes, concentrations of non-enzymatic antioxidants, and biomarkers of oxidative stress were measured in the LV of aortic-banded animals (LVH), untreated or banded rats subjected to short-term (45 min) atrial pacing [(CTR + S) and (LVH + S), respectively], and untreated (CTR) or sham-operated (SHAM) controls. The results indicate that the increase in heart rate in vivo as a result of atrial pacing to a maximum level, independent of sympathetic nerve activity, leads to a substantial increase in oxidative stress and a marked decline in the activities of antioxidant enzymes in both the normal and hypertrophied left ventricle of the rat. The accompanying increase in tissue content of α- and γ-tocopherols seem to contribute to attenuation of the oxidant stress-related loss of thiol stores in the LV. Stable left ventricular hypertrophy induced by aortic banding for six weeks has a minor impact on the capacity of the endogenous antioxidant defense system in the LV, but significantly and negatively affects the ability of the heart LV to tolerate the stress of tachycardia.     

Computer modeling of the effects of aortic valve stenosis and arterial system afterload on left ventricular hypertrophy

The degree of left ventricular hypertrophy is generally thought to reflect the severity of aortic stenosis. However, the compounded influence of arterial system load is poorly understood. We developed a computer model to investigate the effects of aortic valve stenosis in combination with various systemic arterial parameters in the development of left ventricular hypertrophy. Data show that an increased peripheral resistance and/or aortic valve resistance, results in an increase in left ventricular wall thickness and mass, while peak systolic wall stress remains constant. Changing arterial compliance to above normal level would not induce significant changes in wall thickness, while reduction in arterial compliance below normal would cause an increase in ventricular wall thickness. When a double load is imposed on the left ventricle by way of a stenotic valve and an increased arterial afterload, a greater and an aggregated increase in wall thickness results, hastening the hypertrophic process.     

应用二尖瓣环运动速度和时间指标评价冠心病患者左室整体舒张功能

目的：应用脉冲多普勒组织成像（DTI）定量分析并比较心绞痛与心肌梗死（心梗）患者二尖瓣环长轴方向上舒张运动速度和时间变化，探讨其评价左室整体舒张功能异常的价值。方法：冠心病心绞痛组16例、心梗组34例、对照组16例。记录二尖瓣环侧壁、间隔、前壁和下壁的运动频谱。测量舒张早、晚期峰值运动速度及其比值，舒张早期波开始时间、达峰时间和局部等容舒张时间，并计算4个位点的均值，分别以Em、Am、Em/Am、QEm、TEm和IVRTm表示。结果：心绞痛组和心梗组Em和Em/Am显著低于对照组（P<0.01），心梗组Em又低于心绞痛组（P<0.01）；心绞痛组和心梗组QEm、TEm及IVRTm显著长于对照组（P<0.01或P<0.05），心梗组IVRTm又长于心绞痛组（P<0.01）；IVRTm与Em呈显著负相关（r=-0.64, P<0.01）。结论：脉冲DTI所测Em、Em/Am、QEm、TEm及IVRTm均可反映冠心病患者左室整体舒张功能异常，Em和IVRTm尚可反映心肌缺血损害的严重程度。