维生素丙对实验性急性心肌缺血性损伤的作用

1.维生素丙对实验性急性心肌缺血性损伤有预防作用,且只限于中剂量(0.2g/kg)时,小剂量和大剂量(0.4g/kg)时无效。2.维生素丙抗实验性急性心肌缺血性损伤的作用机制,可能是它对心肌营养性小血管血液灌流和代谢的改善,从而提高了心肌对缺血缺氧的耐受性。     

肾上腺素在心肺复苏中的作用机制分析

目的:探讨肾上腺素在心肺复苏中的作用机制,为开发新的复苏药物提供指导。方法:健康杂种犬36只,分为3组:4min闭胸复苏组(第1组)、4min开胸复苏组(第2组)、8min开胸复苏组(第3组)。复苏前后进行主动脉内压(AOP)、中心静脉压(CVP)的有创连续监测记录。观察比较各组在使用肾上腺素前、后所能产生的最大血流动力学效应。结果:静注肾上腺素前,3组主动脉收缩压(ASP)分别为66±14mmHg,79±20mmHg,69±13mmHg;舒张压(ADP)分别为25±2.2mmHg,36±15mmHg,16±7mmHg;冠脉灌注压(CPP)分别为2.8±3.8mmHg,30±15mmHg,11±5.8mmHg。静注肾上腺素后3组ASP分别为107±28mmHg,133±23mmHg,110±19mmHg。3组ADP分别为45±13mmHg,70±14mmHg,50±16mmHg。3组CPP分别为29±13mmHg,58±12mmHg,38±18mmHg。静注肾上腺素前后各血压值变化均有极显著性差异(P<0.001)。结论:肾上腺素可以显著提高各组的主动脉舒张压、冠脉灌注压。肾上腺素在复苏中的作用机制主要是其α1受体激动剂作用,增加了总外周阻力的结果。开发新的心肺复苏药物应以缩血管增加外周阻力而不影响心、脑血供的药物为主要方向。     

经食管左心房调搏终止心房扑动

近来,我们使用经食管左心房调搏(TEAP)的方法终止心房扑动(AF)6例,其中5例成功。现报告如下,并加以讨论。     

西安市院前急救疾病谱分析

为了解西安市院前急救病种构成梯次及其流行病学规律,笔者持对西安急救中心2001年1月1日至2003年12月31日所收治的急救患者进行回顾性的总结分析,现报道如下.     

神奇的电话Holter

患有心脏病的朋友,不妨多听一听来自Holter的忠告。     

实验性心肌梗塞时ST和异常Q波改变的规律及其与组织病理学的关系

<正> ST段移位和异常Q波的出现早已成为诊断心肌梗塞(MI)的主要指标。但随着心肌电生理的深入研究和临床与病理学的系统观察,愈来愈多的报告认为ST段移位和异常Q波的出现仪反映心肌电活动的改变,并不能完全反映心脏组织病理学的改变。本文实验的主要目的是给大鼠造成心肌梗塞后不同时间测定心电图,并给组织学检查结果作对比,从而观察ST段移位和异常Q波出现改变的规律以及与MI的发生、梗塞部位、梗塞范周和梗塞时间的关系。     

维生素丙对小鼠心肌营养性血流的影响

本实验用小鼠心肌摄取~(86)Rb的能力为指标,观察了维生素丙对小鼠心肌营养性血流的作用,根据初步结果认为:腹腔注射维生素丙可使小鼠心肌营养性血流增加18%(p<0.005),为探讨维生素丙改善心脏功能的作用机制提供了一定的实验依据;至于维生素丙对心肌代谢的作用,有待探讨。     

闭胸复苏犬的血流动力学特点的研究

目的 研究闭胸复苏犬的血流动力学特点,分析其机制.方法 健康杂种犬12只,采用电击致犬室颤的动物模型.心跳停止4 min后,按照国际心肺复苏指南2005标准开始心肺复苏.复苏2 min后,静注肾上腺素1 mg.致颤前及复苏过程中对主动脉内压、中心静脉压、心电图进行有创同步监测.方法 用Chart5Ch软件做统计图,计算冠脉灌注压,分析闭胸复苏犬的血流动力学特点.用配对t检验比较静注肾上腺素前后血流动力学变化,P＜0.05为差异具有统计学意义.结果 闭胸复苏犬的血流动力学效应表现为两种类型:8只犬(8/12)表现为主动脉内压(AOP)与中心静脉压(CVP)同步变化,而冠脉灌注压(CPP)几乎为0;4只犬(4/12)表现为主动脉内压升高而中心静脉压不变.静注肾上腺素后,AOP及CPP显著增大,其中,主动脉收缩压(ASP)[(66±14)mmHg和(107±28)mmHg,P＜0.01];主动脉舒张压(ADP)[(25±2.2)mmHg和(45±13)mmHg,P=0.001],CPP[(2.8±3.8)mmHg和(29±13)mmHg,P＜0.001];ASP,ADP及CPP增加值的95%可信区间分别是(21.1～59.1),(10.2～28.3)及(16.7～35.7).结论 胸泵机制是闭胸复苏的主要机制.肾上腺素可以打破心肺复苏时主动脉内压与中心静脉压的平衡,增加冠脉灌注压,可能增加复苏成功率.

Abstract：

Objective To study the hemodynamics during closed chest cardiopulmonary resuscitation (CCCPR) in dogs in order to unravel the mechanism. Method Twelve healthy mongrel dogs were selected to make animal model of ventricular fibrillation induced by electric shock on the chest wall. Closed-chest cardiopulmonary resuscitation (CCCPR) was initiated four minutes after ventricular fibrillation appeared according to American Heart Guidelines in 2005 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Rescue. After CPR for 2 minutes, 1mg epinephrine was injected intravenously. The central venous pressure (CVP), the aortic pressure (AOP)and the invasive electrocardiogram (ECG) were used to monitor continuously before ventricular fibrillation and the entire course of CPR. The coronary perfusion pressure (CPP) was calculated. The changes in aortic diastolic pressure (ADP) and CPP produced by chest compression or the injection of epinephrine were analyzed. The aortic pressure and the central venous pressure were recorded simultaneously during CPR. A chart was made and the CPP was calculated with the software Chart5Ch. The hemodynamic changes produced by the administration of epinephrine were studied. Data were analyzed with paired Student t test. P ＜ 0.05 was considered as a significant difference. Results Two kinds of hemodynamic effects of CPR were observed. In 8 dogs (8/12) , the aortic pressure changed synchronously with the CVP, and the CPP was almost zero, and in other 4 dogs (4/12), the aortic pressure increased and the CVP remained unchanged with presence of the CPP. After the administration of epinephrine, the AOP and the CPP increased significantly. The Aortic systolic pressure(ASP) increased from (66± 14) mmHg to(107 ± 28) mmHg, (P = 0. 001). The Aortic diastolic pressure (ADP) increased from (25 ±2.2) mmHg to(45 ± 13) mmHg (P =0.001). And the coronary perfusion pressure (CPP) increased from (2.8± 3.8) mmHg to (29 ± 13) mmHg (P ＜ 0.001). The 95 % confidential interval of the added value of the ASP,ADP and CPPwere (21.1-59.1), (10.2-28.3) and (16.7-35.7), respectively. Conclusions The thoracic pump mechanism is the primary role in the closed chest Cardiopulmonary resuscitation. Epinephrine can increase ADP and CPP and has the capability to break the balance between aortic pressure and central venous pressure, increasing the rate of successful cardiopulmonary resuscitation.     

射频消融术治疗室上性心动过速56例

56例室上性心动过速行射频消融术58例次(其中2例复发行2次消融术),其中35例为房室旁路折返性心动过速(AVRT);左侧旁路消融成功率95.4％,平均放电次数5.6±2.1次,操作时间78±51min;右侧旁路消融成功率92.6％,平均放电次数15±12次,操作时间136±68min;房室结折返性心动过速(AVNRT)21例,采用后位法消融成功率78.6％,平均放电次数4±5次,放电时间4.6±2.9min,出现交界区心律时成功率96.9％。     

胸痛患者多巴酚丁胺负荷超声心动图的左心功能变化

目的　探讨胸痛患者在多巴酚丁胺负荷超声心动图 (DSE)情况下的左心功能变化。方法　采用二维、脉冲式多普勒超声检测DSE患者左室收缩和舒张功能。结果　 18名胸痛患者 ,经DSE后 ,出现左室壁局部运动异常 8例 (DSE阳性患者 ) ,左室壁普遍性运动增强 10例 (DSE阴性患者 )。DSE阴性患者的每搏量 (SV)、心输出量 (CO)明显高于DSE阳性患者 (P <0 .0 5 ) ;多巴酚丁胺峰值剂量时E/A比值两组患者均 <1。结论　DSE可作为胸痛患者左室局部、整体收缩功能的较好评估方法 ,而对左室舒张功能的判定尚缺乏合适的指标