肾上腺素无效的心脏停搏患者应用氨茶碱复苏方法的探讨

目的 :探讨在肾上腺素无效的心脏停搏患者中应用腺苷受体拮抗剂氨茶碱的方法。方法 :对 32例心跳骤停后肾上腺素无效者 ,给予静脉注射氨茶碱 (0 .2 5 g,3～ 5 min重复注射 ) ,观察心律、血压、呼吸等的变化。结果 :随着氨茶碱剂量的递增 ,心脏停搏患者中出现心律反应所占比例明显增加 ;最终有 16例 (5 0 .0 % )患者恢复窦性心律或室上性节律及自主循环和呼吸。有 2例 (6 .3% )患者在氨茶碱用至 0 .5 g时 ,出现心室颤动。氨茶碱的用量与心率、复苏开始时间、肾上腺素用量和 QRS间期均呈中度正相关 (P <0 .0 5 )。结论 :应用氨茶碱重复注射的方法治疗心脏停搏是可选择的方法。     

心肺复苏中氨茶碱与肾上腺素联合应用的疗效

目的探讨联合应用肾上腺素和氨茶碱在心肺复苏早期的临床疗效。方法观察120例在该院急诊科、老年病科、ICU病房进行心肺复苏患者的临床资料,其中40例患者在心肺复苏中使用标准剂量的肾上腺素抢救为标准剂量组,40例使用大剂量肾上腺素抢救为大剂量组,40例应用肾上腺素联合氨茶碱抢救为联合组。比较三组复苏疗效、自主循环恢复时间和格拉斯哥昏迷评分结果。结果联合组自主循环恢复率、24 h存活率、出院存活率均显著高于大剂量组和标准组(P0.05);并且自主循环及自主呼吸恢复时间短于大剂量组和标准计量组(P0.05)。结论在抢救心脏停搏病人流程中应用肾上腺素联合氨茶碱能明显提高患者心肺复苏的自主循环恢复率及提高存活率并能维持其稳定性。     

高原地区老年慢性肺心病重度急性加重期患者糖皮质激素的应用

目的　探讨高原老年慢性肺心病因呼吸道感染致重度急性加重期患者应用肾上腺糖皮质激素 3d和 10d对减轻气道阻塞、改善气体交换和症状的效果。　方法　 78例患者随机分为 2组 ,Ⅰ组 (3 9例 )仅前 3d静脉滴注地塞米松 0 2mg/kg ,1次 / 12h ,随后 7d改用生理盐水 ,Ⅱ组 (3 9例 )前 3d静脉滴注地塞米松 0 2mg/kg ,1次 / 12h ,随后 3d为0 1mg/kg ,1次 / 12h ,最后 4d为0 1mg/kg,1次 /d。治疗期间 2组患者均口服相同剂量的舒喘灵、氨茶碱、必嗽平和西咪替丁 10d ,选用敏感抗生素。治疗前、治疗 3d、10d后分别测定肺功能、动脉血气 ,并观察呼吸困难、咳嗽、咳痰的变化。　结果　治疗 3d ,Ⅰ组 1s用力呼气容积占预计值百分比 (FEV1% )、动脉血氧分压 (PaO2 )、动脉血二氧化碳分压 (PaCO2 )分别为 (3 5 9± 7 6) %、(44 4± 5 8)mmHg、(46 1± 5 8)mmHg ,Ⅱ组分别为 (3 4 8± 7 3 ) %、(45 0± 5 7)mmHg、(46 9± 5 0 )mmHg ;治疗 10d后 ,Ⅰ组 3项指标分别为(3 6 7± 7 6) %、(45 6± 6 1)mmHg、(44 8± 5 2 )mmHg ,Ⅱ组分别为 (42 0± 7 1) %、(49 7± 6 3 )mmHg、(41 7± 4 2 )mmHg ,与治疗前比较均为P <0 0 1。治疗 3d时 ,两组患者的症状评分、FEV1%、FEV1/用力肺活量 (FVC)比值、PaO2 、PaC     

氨茶碱联用大剂量肾上腺素对老年人心肺复苏的影响

目的 探讨氨茶碱联用大剂量肾上腺素对老年人心肺复苏的影响.方法 选择老年心搏骤停患者126例,随机分为A组40例、B组43例、C组43例,分别给予肾上腺素1 mg、肾上腺素5 mg、氨茶碱0.5g+肾上腺素5mg静脉推注.观察各组临床疗效、股动脉压和血浆TNF-α、IL-6浓度变化.结果 与A组、B组比较,C组自主循环恢复率、24 h存活率明显增高,自主循环持续时间明显延长,自主循环和自主呼吸恢复时间明显缩短,主动脉舒张压明显增高,血浆TNF-α、IL-6浓度明显降低,以上差异均有统计学意义(P均＜0.05).结论 心肺复苏早期氨茶碱联用大剂量肾上腺素能促进自主循环和自主呼吸的恢复与稳定.     

卡维地洛对抗乌头碱诱发的大鼠心律失常作用的研究

评价卡维地洛抗大鼠实验性心律失常的作用 ,探讨其抗心律失常作用的离子通道机理 ,为临床用药提供理论依据。采用乌头碱诱发大鼠心律失常模型 ;采用膜片钳技术 ,观察乌头碱、卡维地洛对急性分离的大鼠心室肌细胞钠通道电流 (INa)的影响。结果 :诱发大鼠出现室性早搏、室性心动过速、心室颤动及心脏停搏时 ,对照组及卡维地洛组所用乌头碱的量 (μg)分别为 :室性早搏 :2 1.75± 3.4 7vs 31.81± 2 .0 4 ;室性心动过速 :2 3.5 2± 4 .13vs 36 .0 6± 3.79;心室颤动 :37.6 3± 7.94vs 6 4 .13± 1.4 0 ;心脏停搏 :6 9.31± 1.85vs 84 .6 5± 5 .2 5。利用膜片钳技术观察到 :对照组INa密度为 :5 8.6 3± 11.6 5 pA/pF ;卡维地洛组加入乌头碱后以及再加入卡维地洛后的INa密度分别为73.35± 12 .80 (pA/pF) ;10 .19± 0 .0 2 (pA/pF) ,与自身加药前相比P <0 .0 5。乌头碱及卡维地洛使INaI V曲线分别向下方及向上方移位。结论 :卡维地洛具有抗乌头碱诱发的大鼠心律失常的作用 ,其抗心律失常作用机制之一可能与Ⅰ类抗心律失常药类似 ,即抑制INa。     

甲泼尼龙琥珀酸钠对窒息型大鼠复苏后早期的心功能影响

目的:探讨甲泼尼龙琥珀酸钠(甲强龙)对窒息大鼠模型心肺复苏后早期心功能的影响及机制。方法:45只SD大鼠,雌雄不拘,分为对照组、常规复苏组(常规复苏+肾上腺素10μg/kg)和甲强龙组(常规复苏+肾上腺素10μg/kg+甲强龙1.8 mg/kg)。对窒息大鼠模型进行心肺复苏,记录平均动脉压(MAP)、左心室收缩压(LVSP)和左心室舒张末压(LVEDP)的变化,ELISA法检测大鼠心脏组织中肾上腺素能α1受体和β1受体水平。结果:在心肺复苏自主循环恢复(ROSC)30 min后,与对照组比较,常规复苏组及甲强龙组大鼠的MAP和LVSP均有明显下降(P均0.05);在ROSE后0、15 min时,常规复苏组及甲强龙组LVEDP与对照组相比有显著性差异(P均0.05)。甲强龙组MAP在ROSC后60、120 min时,LVSP在ROSC后30、60、120 min时均显著高于常规复苏组(P均0.05)。心肺复苏后,甲强龙组与对照组、常规复苏组比较,心脏组织中肾上腺素能α1受体和β1受体水平均明显升高(P均0.05)。结论:甲强龙可提高心肺复苏后心脏组织内肾上腺素能α1受体和β1受体含量,有利于心肺复苏后MAP和LVSP的稳定。     

腺苷预处理和缺血预处理心肌保护效果对比研究

目的探讨心肌腺苷预处理和缺血预处理对离体大鼠心脏缺血/再灌注后心肌功能的影响。方法采用离体大白鼠工作心脏模型,比较腺苷预处理和缺血预处理对心肌缺血再灌前、后左室收缩压(LVSP)、左室舒张末期压(LVDEP)、左心室内压上升及下降最大速率(±dp/dtmax)、主动脉压(AP)、冠脉流量(CF)、心输出量(CO)、每搏心输出量(SV)和冠脉流出液乳酸脱氢酶(LDH),心肌三磷酸腺苷(ATP)含量、超氧化物歧化酶(SOD)活性、脂质过氧化物(LPO)含量及自灌注停搏液至完全停搏的时间(AT)。结果3组大鼠AT间差异有显著性意义(P<0.05),且Control组与其他两组间差异均有显著性意义(P<0.05)。3组大鼠停搏前、复跳后30minAP、LVSP、LVDEP、±dp/dtmax、SV、CF、Co间差异均有显著性意义(P<0.05)。3组大鼠ATP、SOP、LPO、LDH间差异亦均有显著性意义(P<0.05)。结论腺苷预处理和缺血预处理后产生相似的心肌保护作用,明显促进心肌缺血再灌后心肌功能的恢复,增进心脏的收缩功能、心肌ATP含量和SOD活性的恢复,减少LDH的漏出。腺苷预处理对心脏模拟体外循环的缺血再灌注损伤具有保护作用,具有临床应用价值。     

西沙比利通过一氧化氮影响大鼠胃HCO_3~-分泌的实验研究

本文研究了西沙比利对大鼠胃粘膜损伤的影响和对胃粘膜—氧化氮含量分泌的影响 ,结果表明 :加入无水乙醇后 ,西沙比利 1mg/kg组胃粘膜溃疡面积及溃疡深度显著低于空白对照组 ( 10 .2± 6.9mm2 vs 2 6.1± 13.5mm2 )( 18%± 3%vs 5 0 %± 2 7% ) (P <0 .0 5 ) ,西沙比利 0 .5mg/kg组溃疡深度 ( 39%± 11% )和 2mg/kg组溃疡深度 ( 18%±7% )亦显著低于空白对照组 (P <0 .0 5 )。给予西沙比利 1mg/kg后 ,其大鼠一氧化氮 ( 2 3.32± 7.40 μmol/mg)显著高于空白对照组 ( 16.93± 3.87μmol/mg) (P <0 .0 5 )。加入西沙比利 2mg/kg后 ,大鼠胃粘膜一氧化氮含量 ( 4.35± 1.5 2μmol/mg)显著低于空白对照组 (P <0 .0 5 )。西沙比利 0 .5mg/kg组一氧化氮含量与空白对照组间差异无显著意义( 16.76± 1.0 6μmol/mg) (P >0 .0 5 )。西沙比利 1mg/kg组胃HCO3-分泌率显著升高 ( 2 0 2 %± 60 %vs 119%± 40 % )。空白对照组和西沙比利 0 .5mg/kg组无此变化。西沙比利 1mg/kg组加入无水乙醇 30分钟后HCO3-恢复率为 810 %± 2 2 0 % ,与加入无水乙醇 15分钟比较 ( 12 0 0 %± 40 0 % )差异有显著意义 (P <0 .0 5 )。西沙比利 2mg/kg组HCO3-分泌率显著降低 ( 68%± 37%vs 12 7%± 2 7% ) (P <0 .0 5 ) ,加入无水乙醇 30     

大剂量肾上腺素改善小儿心脏停搏的转归

已有动物实验提示,心肺复苏目前应用的肾上腺素标准剂量可能太小。本文比较小儿顽固性心脏停博用标准剂量肾上腺素(SDE)和大剂量肾上腺素(HDE)治疗的疗效和转归。观察组和对照组各由20例心脏停搏的患儿组成,平均年龄分别为2.5岁和3岁,停搏至心肺复苏开始的时间分别为2.5岁和3岁,停搏至心肺复苏开始的时间分别是3.4±1.7分和3.4±1.6分,差别均无显著意义(P>0.05)。二组病例均按高级心肺复苏的标准方案进行急救,包括心脏按压,气管插管和100%O:吸入,所有     

1780例先天性心脏病心内畸形的外科治疗

目的 :回顾分析 1780例先天性心脏病心内畸形的外科治疗疗效 ,并比较二种心脏停搏液灌注心脏停跳和不停跳心内直视手术的疗效。方法 :1780例患者均在全麻体外循环下进行手术 ,其中采用冷晶体心脏停搏液灌注心脏停跳下手术 (冷晶体组 ) 6 4 3例 ,冷血心脏停搏液灌注心脏停跳下手术(冷血组 ) 2 31例 ,心脏不停跳手术 (不停跳组 ) 90 6例。心脏不停跳心内直视手术仍常规建立体外循环 ,置左心房引流管 ,降温至 (32± 1)℃并维持 ,仅阻断上下腔静脉 ,不阻断主动脉 ,维持灌注压在 6 0mmHg(1mmHg =0 133kPa) ,心脏跳动下进行畸形矫正 ,方法同停跳下手术。结果 :手术早期死亡 73例 (死亡率3 8% ) ,其中冷晶体组手术死亡 4 2例 (死亡率 6 5 % ) ,残余室间隔缺损 6例 (发生率 0 9% ) ;冷血组手术死亡 7例 (死亡率 3 0 % ) ;不停跳组手术死亡 2 4例 (死亡率 2 6 % ) ,其余均痊愈出院 ,随访 6个月～ 10年 ,恢复良好。结论 :先天性心脏病外科治疗有较好疗效 ,心脏不停跳心内直视手术 ,是一种可行而有效的心肌保护方法 ,并可简化操作 ,提高手术成功率。     

Repeated administration of vasopressin but not epinephrine maintains coronary perfusion pressure after early and late administration during prolonged cardiopulmonary resuscitation in pigs

BACKGROUND: It is unknown whether repeated dosages of vasopressin or epinephrine given early or late during basic life support cardiopulmonary resuscitation (CPR) may be able to increase coronary perfusion pressure above a threshold between 20 and 30 mm Hg that renders defibrillation successful. METHODS AND RESULTS: After 4 minutes of cardiac arrest, followed by 3 minutes of basic life support CPR, 12 animals were randomly assigned to receive, every 5 minutes, either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 U/kg, respectively; n=6) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively; n=6). Another 12 animals were randomly allocated after 4 minutes of cardiac arrest, followed by 8 minutes of basic life support CPR, to receive, every 5 minutes, either vasopressin (late vasopressin: 0.4 and 0.8 U/kg, respectively; n=6), or epinephrine (late epinephrine: 45 and 200 microg/kg, respectively; n=6). Defibrillation was attempted after 22 minutes of cardiac arrest. Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after early vasopressin compared with early epinephrine (50+/-4 versus 34+/-3 mm Hg, P<0.02; 42+/-5 versus 15+/-3 mm Hg, P<0.0008; and 37+/-5 versus 11+/-3 mm Hg, P<0. 002, respectively). Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after late vasopressin compared with late epinephrine (40+/-3 versus 22+/-4 mm Hg, P<0.004, and 32+/-4 versus 15+/-4 mm Hg, P<0.01, respectively). All vasopressin animals survived 60 minutes, whereas no epinephrine pig had return of spontaneous circulation (P<0.05). CONCLUSIONS: Repeated administration of vasopressin but only the first epinephrine dose given early and late during basic life support CPR maintained coronary perfusion pressure above the threshold that is needed for successful defibrillation.     

氨茶碱和肾上腺素联用在心肺复苏早期的应用研究

目的探讨心肺复苏早期联用氨茶碱和肾上腺素的临床效果。方法心搏骤停患者69例,随机分为研究组和对照组。研究组早期联用氨茶碱和肾上腺素,对照组应用肾上腺素治疗。结果与对照组比较,研究组自主循环恢复率和24 h存活率增高（P〈0.01）,自主循环和自主呼吸恢复时间明显缩短、持续时间明显延长（P〈0.01）。结论心肺复苏早期联用氨茶碱和肾上腺素明显促进自主循环和自主呼吸的恢复,并能维持其稳定。     

Is a pressor necessary during aortic perfusion and oxygenation therapy of cardiac arrest?

STUDY OBJECTIVE: Occlusion of the descending aorta and infusion of oxygenated ultrapurified polymerized bovine hemoglobin may improve the efficacy of advanced cardiac life support (ACLS). Because selective aortic perfusion and oxygenation (SAPO) directly increases coronary perfusion pressure, exogenous epinephrine may not be required. The purpose of this study was to determine whether exogenous epinephrine is necessary during SAPO by comparing the rate of return of spontaneous circulation and aortic and coronary perfusion pressures during ACLS-SAPO in animals treated with either intra-aortic epinephrine or saline solution. METHODS: A prospective, randomized, interventional before-after trial with a canine model of ventricular fibrillation cardiac arrest and ACLS based on external chest compression was performed. The ECG, right atrial, aortic arch, and esophageal pulse pressures were measured continuously. A descending aortic occlusion balloon catheter was placed through the femoral artery. Ventricular fibrillation was induced, and no therapy was given during the 10-minute arrest time. Basic life support was then initiated and normalized by standardization of esophageal pulse pressure and central aortic blood gases. After 3 minutes of basic life support, the aortic occlusion balloon was inflated, and 0.01 mg/kg epinephrine or saline solution was administered through the aortic catheter followed by 450 mL of ultrapurified polymerized bovine hemoglobin over 2 minutes. Defibrillation was then attempted. The outcomes and changes in intravascular pressures were compared. RESULTS: Aortic pressures were higher during infusions in animals treated with epinephrine. During infusion, the mean aortic relaxation pressure increased by 58+/-5 mm Hg in animals that had received epinephrine versus 20+/-11 mm Hg in those that had received saline placebo. The coronary perfusion pressure during infusion increased by 52+/-8 mm Hg in animals that had received epinephrine versus 26+/-10 mm Hg in those that had received saline. Only 2 of 7 animals in the placebo group had return of spontaneous circulation versus 7 of 8 in the epinephrine group. CONCLUSION: The addition of epinephrine to ACLS-SAPO increases vital organ perfusion pressures and improves outcome from cardiac arrest. There appears to be a profound loss of arterial vasomotor tone after prolonged arrest. This loss of vasomotor tone may make exogenous pressors necessary for resuscitation after prolonged cardiac arrest.     

Survival with full neurologic recovery and no cerebral pathology after prolonged cardiopulmonary resuscitation with vasopressin in pigs

OBJECTIVES: We sought to determine the effects of vasopressin and saline placebo in comparison with epinephrine on neurologic recovery and possible cerebral pathology in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). BACKGROUND: It is unknown whether increased cerebral blood flow during CPR with vasopressin is beneficial with regard to neurologic recovery or detrimental owing to complications such as cerebral edema after return of spontaneous circulation. METHODS: After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive every 5 min either vasopressin (0.4, 0.4 and 0.8 U/kg; n = 6), epinephrine (45, 45 and 200 microg/kg; n = 6) or saline placebo (n = 5). The mean value +/- SEM of aortic diastolic pressure was significantly (p < 0.05) higher 90 s after each of three vasopressin versus epinephrine versus saline placebo injections (60 +/- 3 vs. 45 +/- 3 vs. 29 +/- 2 mm Hg; 49 +/- 5 vs. 27 +/- 3 vs. 23 +/- 1 mm Hg; and 50 +/- 6 vs. 21 +/- 3 vs. 16 +/- 3 mm Hg, respectively). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve return of spontaneous circulation. RESULTS: All the pigs that received epinephrine and saline placebo died, whereas all pigs on vasopressin survived (p < 0.05). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait in all vasopressin-treated animals; after 96 h, magnetic resonance imaging revealed no cerebral pathology. CONCLUSIONS: During prolonged CPR, repeated vasopressin administration, but not epinephrine or saline placebo, ensured long-term survival with full neurologic recovery and no cerebral pathology in this porcine CPR model.     

Comparison of standard versus high-dose epinephrine in the resuscitation of cardiac arrest in dogs

A prospective, randomized, blinded study was conducted to evaluate the efficacy of standard compared with high-dose epinephrine in cardiac arrest in dogs. Twenty-five mongrel dogs were anesthetized and monitored by central venous catheter, intra-arterial catheter, and ECG. A left lateral thoracotomy was performed, and the proximal left anterior descending artery was ligated. After ten minutes of myocardial ischemia, ventricular fibrillation was obtained by application of 6-V AC. Mechanical ventilation was stopped. Total arrest time was ten minutes. All animals were randomized into one of five resuscitation protocols; each protocol was identical except for the dose and route of epinephrine administration. Group 1 animals comprised the control group and received normal saline. Group 2 and 3 animals received epinephrine in doses of 0.014 mg/kg by central venous and intracardiac injection, respectively. Group 4 and 5 animals received epinephrine in doses of 0.071 mg/kg by central venous and intracardiac injection, respectively. None of the dogs receiving normal saline had a return of spontaneous circulation, defined as a spontaneous systolic blood pressure of more than 50 mm Hg. Nine of the ten animals from groups 2 and 3 and all of the ten animals from groups 4 and 5 had a return of spontaneous circulation. However, animals receiving the standard dose of epinephrine had a significantly longer resuscitation time compared with the high-dose group (P = .05) and required more doses of epinephrine for successful resuscitation than did animals receiving high doses (P less than .02).(ABSTRACT TRUNCATED AT 250 WORDS)     

High-dose epinephrine improves outcome from pediatric cardiac arrest

STUDY OBJECTIVE: Animal studies suggest that the standard dose of epinephrine (SDE) for treatment of cardiac arrest in human beings may be too low. We compared the outcome after SDE with that after high-dose epinephrine (HDE) in children with refractory cardiac arrest. DESIGN: Prospective intervention versus historic control groups. TYPE OF PARTICIPANTS: Two similar groups of 20 consecutive patients each (median ages, 2.5 and 3 years) with witnessed cardiac arrest who remained in arrest after at least two SDEs (0.01 mg/kg). INTERVENTIONS: Treatment with an additional SDE versus HDE (0.2 mg/kg). MEASUREMENTS AND MAIN RESULTS: The rates of return of spontaneous circulation and long-term survival were compared. Fourteen of the HDE group (70%) had return of spontaneous circulation, whereas none of the SDE group did (P less than .001). Eight children survived to discharge after HDE, and three were neurologically intact at follow-up. No significant toxicity from HDE was observed. CONCLUSION: HDE provided a higher return of spontaneous circulation rate and a better long-term outcome than SDE in our series of pediatric cardiac arrest. HDE may warrant incorporation into standard resuscitation protocols at an early enough point to prevent irreversible brain injury.     

限食对衰老大鼠心功能的保护作用及其机制

目的研究限食对衰老大鼠心功能的保护作用及其机制。方法选择2月龄SD大鼠10只,随机分为衰老组和限食组(60%进食量),每组5只。2组大鼠每天皮下注射D-半乳糖100mg/kg,连续给药42d建立衰老动物模型;衰老模型建立后另选5只2月龄SD大鼠设为青年组。3组行心功能检测,包括左心室内压(LVSP)、左心室舒张末压(LVEDP)、左心室压力最大上升速率(+dp/dtmax),以及血浆丙二醛水平、超氧化物歧化酶活性和左心室心肌脂褐素水平测定。结果与青年组比较,衰老组大鼠LVSP、+dp/dtmax、超氧化物歧化酶活性明显降低,LVEDP、丙二醛、脂褐素水平明显升高,差异有统计学意义(P<0.05,P<0.01);与衰老组比较,限食组LVSP[(110.88±7.35)mm Hg(1mm Hg=0.133kPa)vs(70.18±19.27)mm Hg]、+dp/dtmax[(2827.60±237.88)mm Hg/s vs(2365.66±99.81)mm Hg/s]和超氧化物歧化酶[(115.77±10.17)U/ml vs(90.10±17.11)U/ml]活性明显升高,LVEDP[(7.12±2.51)mm Hg vs(14.05±2.01)mm Hg]、丙二醛[(12.54±1.66)nmol/ml vs(15.83±2.51)nmol/ml]和脂褐素[(348.82±27.29)ng/mg vs(400.12±31.89)ng/mg]水平明显降低,差异有统计学意义(P<0.05,P<0.01)。结论衰老大鼠心功能有所降低,限食可能通过降低机体氧化应激水平,使脂褐素形成减少,从而改善衰老大鼠心功能。     

Immediate Hemodynamic Changes Produced by Urapidil in Normotensive and Spontaneously Hypertensive Rats

The immediate effects on regional and systemic hemodynamics of urapidil (1 mg/kg IV), a recently synthesized vasodilator with a possible combined central and peripheral action, were studied in spontaneously hypertensive (SHR) and normotensive (WKY) rats. Maximal decrease in mean arterial pressure was achieved within the first minute after injection (154 ± 4 vs 113 ± 6 mm Hg in SHR and 111 ± 4 vs 82 ± 4 mm Hg in WKY, p < 0.01). This effect was accompanied by a transient (10 min) significant increase in heart rate in both strains. There was a significant fall in total peripheral resistance (0.43 ± 0.02 vs 0.30 ± 0.02 U/kg in WKY and 0.62 ± 0.03 vs 0.43 ± 0.03 U/kg in SHR, p < 0.01) and rise in cardiac index 15 min after drug injection (371 ± 9 vs 425 ± 12 m1/min/kg in WKY and 395 ± 8 vs 432 ± 12 ml/min/kg in SHR, p < 0.01). Organ vascular resistance decreased significantly in all the organs of WKY and most of the organs of SHR rats. However, a significant increase in blood flow was observed only in skeletal muscle. The data indicate that urapidil is a potent hypotensive agent. The pressure fall is mediated through a decreased total peripheral resistance that is distributed through all circulations. The increased cardiac output and heart rate are most likely reflexly induced.     

Effects of dichloroacetate following canine asphyxial arrest

Sodium dichloroacetate (DCA) has been shown to lower elevated serum lactate levels produced by hypoxia, exercise, and phenformin. We conducted a study to investigate the effect of DCA treatment on lactic acidosis following resuscitation from asphyxial cardiac arrest. Conditioned dogs were anesthetized with pentobarbital (30 mg/kg), endotracheally intubated, and mechanically ventilated to maintain an arterial pCO2 of 30 to 40 mm Hg. Asphyxial cardiac arrest was produced by endotracheal tube occlusion for six to eight minutes. After five minutes of cardiac arrest, the endotracheal tube was unclamped and closed-chest CPR was begun. Six animals received DCA 100 mg/kg IV push after one minute of CPR. Control animals (n = 6) received an equal volume of saline. CPR was continued until the return of a spontaneous pulse, when mechanical ventilation was resumed. Arterial and venous blood gases, glucose, and lactate levels were obtained at baseline and 15, 30, 45, 60, 90, and 120 minutes after resuscitation. Mean arterial blood pressure, pulse, and glucose, and venous and arterial blood gases were similar in both groups throughout the study. By 45 minutes after resuscitation, the DCA-treated group showed a significantly faster rate of decline in lactate levels that continued to the final sampling period. By 90 minutes, arterial lactate in DCA animals was not significantly different from baseline (pre-arrest) values. DCA given during cardiac arrest will cause a more rapid normalization of arterial lactate after successful resuscitation. Further studies are needed to evaluate the effects of lowered lactic acid on survival and neurological outcome following cardiac arrest.     

A comparison of myocardial function after primary cardiac and primary asphyxial cardiac arrest.

Although myocardial dysfunction after resuscitation from ventricular fibrillation (VF) has been extensively investigated, less is known of the function of the myocardium after asphyxial cardiac arrest. The present experimental study was designed to compare postresuscitation left ventricular (LV) function after cardiac arrest caused by asphyxia with that of cardiac arrest induced by dysrhythmia. Four groups of Sprague-Dawley rats, which included eight animals in each group, were investigated. In the first two groups, cardiac arrest followed asphyxia produced by neuromuscular blockade with and without airway obstruction. In a third group, cardiac arrest was induced by electrical fibrillation of the ventricle. The fourth group represented animals in which the duration of asphyxial cardiac arrest was maintained for a time interval corresponding to that of the VF group. The fourth group received approximately the same number of electrical shocks as the third (VF) group. All animals were successfully resuscitated with precordial compression and mechanical ventilation. Postresuscitation measurements, including cardiac output, LV end-diastolic pressure (LVEDP), rate of pressure rise at LV pressure of 40 mm Hg (LV dP/dt40), and negative LV dP/dt, demonstrated decreased myocardial function in each group. No differences in cardiac function were observed between the animals with primary respiratory arrest whether or not the airway was obstructed. However, disproportionate and consistently greater impairment in myocardial function followed primary cardiac arrest due to VF when compared with equal duration of asphyxial cardiac arrest. We conclude that in this healthy animal model, asphyxial cardiac arrest resulted in significantly lesser impairment of postresuscitation myocardial function when compared with cardiac arrest caused by VF.