艾司洛尔对大鼠心肌氧自由基代谢的干预效应

目的:探讨在心肺复苏时应用超短效β1受体阻滞剂艾司洛尔对复苏后心肌氧自由基代谢的影响。方法:实验于2002-01/2003-01在中国医科大学附属第二医院中心实验室完成。选用66只健康雄性Wistar大鼠随机分为3组:假手术组、肾上腺素组、肾上腺素+艾司洛尔组。采用窒息致大鼠再灌注损伤的复苏模型,监测心电图、心率、体温、平均动脉压。观察自主循环恢复后30,120,180min心肌超氧化物歧化酶(抗氧化酶)、丙二醛(脂质过氧化反应的最终产物)的变化。结果:进入结果分析实验动物54只,每组18只,每时点6只。①心肌超氧化物歧化酶活性:肾上腺素组、肾上腺素+艾司洛尔组各时点均低于假手术组犤复苏后30min,120min,180min各组:肾上腺素组为(104.06±6.11),(84.23±5.53),(69.08±8.76)NU/mg,肾上腺素+艾司洛尔组为(116.33±4.85),(99.33±7.93),(79.67±3.82)NU/mg,假手术组为(138.19±7.97),(135.48±6.43),(130.99±4.85)NU/mg,P<0.01犦,肾上腺素+艾司洛尔组高于肾上腺素组(P<0.05)。②心肌丙二醛含量:肾上腺素组、肾上腺素+艾司洛尔组各时点高于假手术组犤复苏后30min,120min,180min各组:肾上腺素组为(15.97±0.99),(21.48±2.84),(33.90±4.39)μmol/g,肾上腺素+艾司洛尔组为(12.88±1.12),(16.04±1.75),(23.59±1.85)μmol/g,假手术组为(10.80±1.43),(12.08±0.76),(12.22±1.84)μmol/g,P<0.01犦,肾上腺素+艾司洛尔组低于假手术组(P<0.01)。结论:艾司洛尔可能通过减轻超氧化物歧化酶活性的降低和丙二醛含量的升高而改善复苏后心肌氧自由基代谢的失衡。     

缺血预处理对高血脂大鼠心肌再灌注损伤和氧自由基代谢的影响

目的研究缺血预处理 (IP)对缺血再灌注 (I/R)高血脂大鼠离体心脏功能、心肌酶、氧自由基的影响。方法采用大鼠离体心脏灌注模型 ,以左室收缩峰压 (LVSP)和心室内瞬间最大变化速率 (dp/dtmax)估价心功能。以心肌酶 (CK)反应心肌损伤 ,以心肌组织丙二醛 (MDA)含量、超氧化物歧化酶 (SOD)活性、心肌细胞线粒体中谷胱甘肽过氧化酶 (GRH PX)活性反映心肌自由基代谢。将IP和I/R情况进行比较。结果IP使高血脂大鼠心脏再灌注后LVSP、dp/dtmax增高、CK降低、MDA减少、SOD和GSH PX增高 (均P <0 .0 5 ) ,且与正常大鼠无显著性差异 (均P >0 .0 5 )。结论IP对高血脂大鼠心肌缺血再灌注损伤有保护作用。高血脂可能不参与心肌缺血再灌注损伤的机制。     

1，6-二磷酸果糖对大鼠心肌再灌注损伤的干预效应

目的：探讨1，6-二磷酸果糖(fructose 1．6-diphosthate．FDP)的抗再灌注心肌损伤作用与脂质过氧化的关系。方法：实验于2003—06／07在大连医科大学中心实验室完成，选取健康SD大鼠60只，随机分成对照组、心肌缺血组、缺血再灌注组、缺血再灌注+FDP组和缺血再灌注+超氧化物歧化酶(superoxide dismutase，SOD)组。采用硫代巴比妥酸法和肌酸固定法，分别测定丙二醛及血清肌酸激酶(creatine kinase，CK)在大鼠心肌缺血和再灌注条件下的含量变化。结果：心肌缺血组SD大鼠CK含量明显升高，(4684．27&;#177;533．44)nkat／L；缺血组再灌注血清丙二醛和CK含量急剧上升，分别为(3．90&;#177;0．73)l,rmol／g，(5784．49&;#177;883．51)nkat／L；缺血再灌注+FDP组和缺血再灌注+SOD组丙二醛和CK含量均显著降低，分别为(2．82&;#177;0．4611,tmol／g，(3767，42．4&;#177;833．50)nkat／L；(3．22&;#177;0．72)μmol／g，(4234．18．4&;#177;766．82)nkat／L(P&;lt;0．01)。结论：再灌注心肌损伤加重；FDP对再灌注心肌损伤有明显的保护作用。     

1,6-二磷酸果糖对大鼠心肌再灌注损伤的干预效应

目的:探讨1,6-二磷酸果糖(fructose1,6-diphosthate,FDP)的抗再灌注心肌损伤作用与脂质过氧化的关系。方法:实验于2003-06/07在大连医科大学中心实验室完成,选取健康SD大鼠60只,随机分成对照组、心肌缺血组、缺血再灌注组、缺血再灌注+FDP组和缺血再灌注+超氧化物歧化酶(superoxidedismutase,SOD)组。采用硫代巴比妥酸法和肌酸固定法,分别测定丙二醛及血清肌酸激酶(creatinekinase,CK)在大鼠心肌缺血和再灌注条件下的含量变化。结果:心肌缺血组SD大鼠CK含量明显升高,(4684.27±533.44)nkat/L;缺血组再灌注血清丙二醛和CK含量急剧上升,分别为(3.90±0.73)μmol/g,(5784.49±883.51)nkat/L;缺血再灌注+FDP组和缺血再灌注+SOD组丙二醛和CK含量均显著降低,分别为(2.82±0.46)μmol/g,(3767.42±833.50)nkat/L;(3.22±0.72)μmol/g,(4234.18±766.82)nkat/L(P<0.01)。结论:再灌注心肌损伤加重;FDP对再灌注心肌损伤有明显的保护作用。     

心肺复苏中大鼠心肌细胞膜β1-肾上腺素能受体与心肌损伤研究

目的:探讨在心肺复苏中肾上腺素对自主循环恢复前大鼠心肌损伤与心肌细胞膜β1-肾上腺素能受体的关系.方法:健康雄性(SD)大鼠50只随机分为4组:空白对照组10只(O组)、复苏时照组10只(C组)、大剂量肾上腺素组15只(H组)、标准荆量肾上腺素组15只(S组).制备大鼠心肺复苏模型,窒息致心跳停止,再进行心肺复苏,心跳恢复立即取心肌标本,检测各组心肌组织Na+-K+-ATP酶和超氧化物歧化酶活力、环磷腺苷和丙二醛浓度并进行统计分析;电镜观察心肌细胞超微结构变化.结果:S组与H组心肌ATP酶和超氧化物歧化酶活力、丙二醛浓度比较差异有统计学意义(P<0.05或P<0.01);心肌环磷腺苷含量S组、H组比较差异无统计学意义(P>0.05),且与心肌损伤程度无相关性;电镜观察各组心肌细胞超微结构变化差异均有统计学意义(P<0.05).结论:心肺复苏中肾上腺素在自主循环恢复前已加重了心肌组织的损伤,而心肌细胞膜β1-肾上腺素能受体兴奋性增高可能不是主要的原因.     

心肺复苏中肾上腺素对大鼠心肌损伤机制的研究

目的:研究在心肺复苏中肾上腺素对自主循环恢复(ROSC)前大鼠心肌损伤情况及可能机制。方法:SD雄性大鼠50只,随机分为4组:空白对照组(O)、复苏对照组(C)、大剂量肾上腺素组(H)、标准剂量肾上腺素组(S)。采用大鼠心肺复苏模型,心跳恢复立即取心肌标本,检测各组心肌组织Na+-K+-ATP酶和SOD活力、cAMP和MDA浓度并进行统计分析;电镜观察心肌细胞超微结构变化。结果:S组与H组心肌ATP酶和SOD活力、MDA浓度有差异;心肌cAMP含量S组、H组无统计学差异,并与心肌损伤程度无相关性。结论:在心肺复苏中与标准剂量肾上腺素比较,大剂量肾上腺素在ROSC前已经加重了心肌组织的损伤,但心肌损伤可能与心肌β1-肾上腺素能受体(β1-AR)无关。     

纳络酮联合肾上腺素进行心肺复苏的疗效观察

目的：观察纳络酮与肾上腺素合用进行心肺复苏的疗效。方法：将66例心跳呼吸停止患者随机分两组,A组采用纳络酮联合肾上腺激素治疗,首剂静脉滴注肾上腺素3 mg,若无效,每5 min静脉滴注肾上腺素3 mg/次,每5 min一次;B组仅采用肾上腺素治疗。两组其他治疗方法相同。结果：A组在自主呼吸的恢复,意识的恢复方面明显优于B组。结论：在心肺复苏时,使用适量的肾上腺素联合纳络酮可提高心肺复苏的成功率。     

艾司洛尔对围术期窦性心动过速的疗效观察

目的 :观察不同剂量艾司洛尔 (esmolol)对围术期窦性心动过速的疗效。方法 :对 86例窦性心动过速者行麻醉 ,随机分为两组 ,Ⅰ组 (n =43)艾司洛尔 1mg/kg静注 ;Ⅱ组 (n =43)艾司洛尔 2mg/kg静注 ,监测心电图 ,心率及血压。记录用药前 ,用药后 1,3,5 ,10 ,2 0min测定指标变化并行统计学处理。结果 :Ⅰ组有效 2 6例 ,无效 17例 ,Ⅱ组有效 40例 ,无效 3例。结论 :艾司洛尔适合麻醉期间心动过速的治疗     

梗塞后左室重构及β阻断剂治疗对心肌重构的影响

心肌梗塞后左室重构是指急性心肌梗塞 (AMI)后发生的左室结构和功能的重建 ,其结果引起左室明显扩张和几何形状变化 ,导致收缩、舒张功能障碍并发生慢性心功能不全(CHF) [1 - 3]。这一过程对预后极为不利 ,但可用药物延缓和预防。已证实 ,用 ACEI治疗的患者患 AMI,左室重构少见且发生更缓慢 [4 ,5] 。许多作者认为 ,β阻断剂同样有能力影响重构过程 [6 ]。然而 ,这个问题尚处于研究阶段。1　心肌梗塞后心肌重构的机理AMI最初 72 h心脏结构即可发生变化 ,表现为梗塞区心肌伸展、室壁变薄 [1 ] ,扩张部分的形状首先取决于梗塞的大小和…     

山莨菪碱对心肺复苏大鼠心脏结构和心肌微血管血流量变化的影响

目的探讨山莨菪碱(Ani)对心脏停搏大鼠心脏结构和心肌血流量变化的影响。方法采用电击致大鼠心脏停搏模型,将实验动物随机分为三组,每组20只。心脏停搏后4min行呼吸机辅助呼吸、胸外心脏按压,4min后静脉给药,生理盐水对照组不用复苏药物;肾上腺素组(Epi组)静脉注射肾上腺素200μg/kg;山莨菪碱组(Ani组)静脉注射肾上腺素200μg/kg并Ani10mg/kg。计算自主循环恢复率和复苏成功率;测量左心室容积(LVV)和心室间隔厚度(VST);利用激光多普勒血流量图像仪测量心肌组织血流量。结果 Ani组大鼠自主循环恢复率和复苏成功率(90%,80%)>Epi组(75%,50%)>对照组(50%,30%),三组相比有统计学差异(P<0.05)。Ani组LVV的变化较Epi组轻;Ani组心肌组织血液灌注量在自主循环恢复(ROSC)后30min、45min、60min均明显高于对照组和Epi组,差异有统计学意义(P<0.05)。结论复苏早期应用Ani干预可望减轻Epi引起的负面影响,提高组织灌注量,从而改善复苏后的器官功能,可能会提高复苏的成功率。     

The role of oxygen-derived free radicals in burn-induced myocardial contractile depression

The release of oxygen free radicals from ischemic myocardium has been implicated as a causative factor of cardiac dysfunction after thermal injury. In this study, isolated coronary perfused guinea pig hearts were used to determine if free radical scavengers improve left ventricular (LV) intrinsic contractile response to burn shock. Parameters measured included peak isovolumic LV pressure (LVP) and maximal rate of LVP rise (+dP/dtmax) and fall (-dP/dtmax) at a constant preload. Control animals were immersed in body temperature water and divided into four groups: Group 1, untreated N = 10; Group 2, control animals treated with unbound superoxide dismutase (SOD), N = 5; Group 3, control animals treated with ficoll-SOD, N = 5; and Group 4, control animals treated with PEG-SOD, N = 5. Scald burn equivalent to 45% of total body surface area was produced in 64 animals. Fluid resuscitation was initiated immediately after burn in all animals, and animals were then divided into seven burn experimental groups. In Group 5, 10 animals were treated with fluid alone, lactated Ringer's, 4 mL/kg/% burn. Burned animals in Group 6 (N = 10) received a reduced volume of Ringer's 2 mL/kg/% burn plus unbound-SOD, 50 mg/kg; 10 animals in Group 7 received this volume of Ringer's plus ficoll-SOD, 50 mg/kg. In groups 8, 9, and 10 animals were given fluid, lactated Ringer's, 2 mL/kg/% burn plus varying doses of PEG-SOD (Group 8: N = 9, 1,000 U; Group 9: N = 10, 6,000 U; Group 10: N = 5, 12,000 U). In Group 11 (N = 10), animals received SOD-PEG, 6,000 U, plus catalase, CAT-PEG, 6,000 U, given with 4 mL/kg/% burn lactated Ringer's solution. Hypotension, hypothermia, and hemoconcentration were similar in all animals after thermal injury, regardless of treatment regimen. Burn hearts showed significantly lower LVP, +dP/dt max, and -dP/dt max than control hearts (P less than 0.05). Compared to controls, coronary pressure and coronary vascular resistance were significantly higher in all treated burn groups. There was no significant difference in heart rate or time to peak pressure or time to maximal contraction or relaxation among the groups. Left ventricular function curves for burned hearts were shifted downward and to the right of curves obtained from control hearts (P less than 0.01), regardless of scavenger treatment. PEG-SOD, 6,000 U, improved left ventricular contractility (+dP/dt) at maximal levels of end-diastolic pressure but deficits in left ventricular pressure and relaxation persisted.(ABSTRACT TRUNCATED AT 400 WORDS)     

依那普利对急性心肌梗死患者脂蛋白(a)和氧自由基的影响

背景许多研究已表明血管紧张素转换酶抑制剂具有独立于降压以外抗动脉粥样硬化的血管保护作用,但其机制未完全明确.目的研究血管紧张素转换酶抑制剂对急性心肌梗死患者脂蛋白(a)和氧自由基的影响,探讨血管紧张素转换酶抑制剂抗动脉粥样硬化的机制.设计以急性心肌梗死患者为研究对象的观察对比研究.单位解放军总医院南二科.对象选择2001-04/2002-08在天津港口医院心内科住院的急性心肌梗死患者35例,男19例,女16例,年龄42～75岁,平均(62±9)岁.随机分为两组,治疗组20例,对照组15例.纳入标准符合世界卫生组织的急性心肌梗死诊断标准者;排除标准肾功能不全、休克、低血压者及曾服血管紧张素转换酶抑制剂有过敏及明显咳嗽史者.所有患者于发病前2周未服用过血管紧张素转换酶抑制剂并且同意参加本研究.方法治疗组于心梗后第3天晨起予依那普利5 mg口服1次,若无首剂低血压反应,于心梗后第4天开始口服依那普利5 mg/次,2次/d,连续2周,再予10 mg/次,2次/d,连续2周.对照组不用依那普利.分别于服药前、服药后2周和4周时两组同时取血,检测血清中的脂蛋白(a)、氧自由基、三酰甘油、总胆固醇、高密度脂蛋白胆固醇和载脂蛋白(a).主要观察指标两组患者用药前后三酰甘油、总胆固醇、高密度脂蛋白胆固醇、载脂蛋白(a)及血清中的脂蛋白(a)、氧自由基水平的比较.结果依那普利能明显降低急性心肌梗死患者氧自由基水平,用药前、用药2周和用药4周的氧自由基水平分别为(1 423.14±216.23),(1 076.62±287.12)和(566.57±138.02)U/mL(t=2.937,3.571,P＜0.01),但不影响脂蛋白(a)和血脂水平(P＞0.05).结论依那普利通过抗氧化作用来抑制急性心肌梗死患者动脉粥样硬化的进程,改善其预后,但不降低血脂水平,为依那普利抑制急性心肌梗死患者动脉粥样硬化的机制提供了理论参考.     

Effects of oxygen-derived free radicals on type II pneumocytes in primary culture

After a brief review of oxygen-derived free radicals formation, cellular antioxidant equipment, and in vivo oxidant lung injury, the model of type II pneumocytes in primary culture is described with its characteristics and limitations. This model has been used to study either the in vivo or the in vitro effects of free radicals: the resistance of type II cells isolated from animals exposed to oxidants may be explained by their higher level of anti-oxidant enzymes. In contrast, type II cells isolated from control animals do not develop a resistance to the toxic effects on an in vitro exposure to free radicals. This discrepancy might be the result of a possible interaction of alveolar macrophages or fibroblasts with type II cells, which remains to be explored.     

Effect of scavengers of oxygen-derived free radicals on mortality in endotoxin-challenged mice

Oxygen-derived free radicals have been implicated as mediators of cellular injury in several model systems. Recently, a role for free radicals has been proposed in the mortality associated with Gram-negative bacterial sepsis. To determine if pretreatment with free radical scavengers can prevent endotoxin-induced mortality, mice rendered sensitive to endotoxin with actinomycin D were treated with either superoxide dismutase (SOD), N-acetylcysteine (NAC) or saline and were then challenged with a dose of endotoxin calculated to cause a mortality of greater than 80%. Mortality was assessed at 12-h intervals after challenge. Increased survival was seen in the SOD-treated group compared to the control group (p less than or equal to .05). In contrast, survival in mice treated with NAC, another potential scavenger, was not significantly different from the control group. These results support the hypothesis that superoxide and hydroxyl radicals contribute to mortality in Gram-negative bacterial sepsis.     

The measurement of oxygen-derived free radicals and related substances in medicine

Due to the high reactivity of the chemical species and the presence of multiple potentially interfering substances, the measurement of oxygen-derived free radicals in biological material requires highly developed techniques. The currently employed methods are reviewed according to the reactions upon which they are based, the assays, possible interferences and their use in medical research. Detection of the emission of light is a very popular method. Although it is in principle unspecific, there are modifications to measure individual radical species. The only direct way to detect radicals is electron spin resonance spectroscopy. Among the specific assays for O2- the reductions of nitroblue tetrazolium or cytochrome c are predominant. For the detection of H2O2 different techniques are employed for either intracellular or extracellular determination. An array of substances has been used for the measurement of OH. Which of them is the most useful depends on the question to be answered. There are also indirect methods that determine free radicals based on chemical modifications caused by them; the most important assays of this kind quantify lipid peroxides. In addition, assays for thiobarbituric acid-reactive substances and DNA strand breaks and interstrand crosslinks are used.     

丹菟注射液对创伤性关节炎大鼠血清氧自由基的影响

背景创伤性关节炎的治疗目前仍是临床上一个棘手的问题,传统中医药治疗对创伤性关节炎有独到的优势,但其机制有待探究.目的探讨丹菟注射液对创伤性关节炎动物模型血液中一氧化氮(NO)、超氧化物歧化酶(SOD)及丙二醛水平的影响.地点和对象实验在暨南大学医学院第六附属医院内完成,对象为Wistar大鼠36只,雌雄各半,体质量(250±49)g,由湖南中医学院动物实验中心提供.设计随机对照实验.干预将36只大鼠随机分为3组丹菟注射液组、生理盐水组及正常对照组.丹菟注射液组及生理盐水组建立创伤性关节炎模型.3组动物分别予丹菟注射液和生理盐水皮下注射及不做任何处理.于第8周处死动物,采集标本.主要观察指标大鼠血一氧化氮,SOD,丙二醛水平.结果骨关节炎大鼠血中一氧化氮,SOD,丙二醛的变化结果生理盐水组分别为(63.11±20.01)mmol/L,(2023±321)nkat,(5.19±0.85)mmol/L,丹菟注射液组分别为(48.79±16.89)mmol/L,(2315±248)nkat,(4.02±1.38)mmol/L.与生理盐水组比较,丹菟注射液能降低动物血清中一氧化氮(t=2.118,P＜0.05)和丙二醛(t=2.782,P＜O.05)的水平、提升SOD(t=2.796,P＜0.05)的含量.结论丹菟注射液可通过抑制一氧化氮的表达,激活SOD,清除氧自由基,降低脂质过氧化程度,从而达到保护关节软骨,防治骨关节炎的目的.     

不同强度运动对大鼠自由基代谢影响的研究

目的：研究不同强度运动对大鼠血清、骨骼肌、心肌、肝脏中自由基代谢的变化。方法：18只雄性Wistar大鼠随机分为安静对照组（CG）、适度运动组（MG）和运动性低血色素组（SG）,每组6只。5周递增负荷跑台运动后测定血清、腓肠肌、心肌、肝脏丙二醛（MDA）、总抗氧化能力（T-AOC）。结果：经5周递增负荷跑台运动后,MG组T-AOC活性在血清、腓肠肌、肝脏中显著高于CG组（P<0.01）;SG大鼠各组织中MDA含量明显高于CG和MG（P<0.01）,T-AOC活性（除心肌外）明显低于MG（P<0.01）。结论：①适度运动可提高大鼠各组织总抗氧化能力,增强机体清除自由基的能力。②长时间大强度递增负荷跑台运动导致的总抗氧化能力下降,脂质过氧化反应增强是引起运动性低血色素的重要原因之一。