左旋卡尼汀对犬心房急性电重构的影响

目的观察左旋卡尼汀（L-carn itine,L-CN）对犬心房颤动（房颤）所引发心房急性电重构的预防作用。方法12只犬随机分为L-CN组和生理盐水对照组。以800次/m in的频率快速起搏右心房1 s以诱发短阵房颤,在恢复窦性心律即刻重复发放刺激以维持房颤2 h。观察各组房颤前后不同时间段的右心房有效不应期（AERP）、AERP的频率适应性及右心房内传导速度（CV）的变化。结果房颤后盐水组AERP显著缩短（P<0.05）,L-CN组房颤前后AERP无显著缩短;盐水组的AERP的频率适应性显著下降（P<0.05）,L-CN组该指标无显著变化;房颤前后两组间右心房内CV无明显改变。结论L-CN能够有效防止房颤诱发的心房急性电重构。     

胡椒碱对兔心房电重构的影响

目的探讨回心草活性成分胡椒碱对心房快速起搏诱发的兔心房急性电重构的预防作用。方法选择新西兰白兔18只,随机分成对照组、心房快速起搏组和胡椒碱+心房快速起搏组(胡椒碱组),每组6只。对照组和心房快速起搏组术前生理盐水3ml/(kg.d)灌胃3d,胡椒碱组术前给予胡椒碱20mg/(kg.d)药物灌胃3d。对照组术中不行心房快速起搏,心房快速起搏组和胡椒碱组术中以最快能维持心房11起搏频率(500～600/min)行快速心房刺激3h,分别于起搏前和起搏后0.5、1.0、1.5、2.0、2.5和3.0h时,测定基础刺激周长分别为200ms和150ms的右心房有效不应期(atrial effective refractory period,AERP),分析AERP频率适应性的变化情况。结果对照组和胡椒碱组AERP200和AERP150随时间无明显变化。心房快速起搏组AERP200和AERP150与心房快速起搏持续时间呈负相关(r=-0.674,P<0.01;r=-0.543,P<0.01),分别在2.0h和2.5h达到最低值(P<0.05)。心房快速起搏组AERP频率适应性与心房快速起搏时间呈负相关(r=-0.307,P<0.05),对照组和胡椒碱组AERP频率适应性均无明显变化。仅在心房快速起搏组可诱发出阵发性心房颤动(房颤),房颤诱发率为50%,平均房颤持续时间为9.3min。结论胡椒碱能够预防心房快速起搏引起的心房电重构。     

心房电重构与房颤关系的基础研究

目的检查观测心房电生理改变与房颤（AF）发生和持续的关系,探讨心房电重构与房颤的内在联系。方法健康成年杂种犬14只（雌雄不拘,体重10．0～12．5kg）,随机分为2组：对照组（A组）和起搏组（B组）。右侧开胸将电极置于右心房,以400次／min的频率快速起搏右心房（A组只手术不起搏）,分别于实验开始及起搏6h后对每只犬进行电生理检查,测定心房有效不应期（AERP）。起搏开始及起搏后测定burst刺激诱发房颤的频率和持续时间。结果A组在整个时间内AERP无变化,B组心房快速起搏后,AERP明显缩短。A、B两组起搏前房颤的频率和持续时间差异无统计学意义。A组起搏前、后房颤的频率和持续时间无变化,B组心房快速起搏后房颤的频率增多,持续时间延长。结论快速心房起搏可以引起心房有效不应期缩短,即心房电重构。心房电重构造成的心房有效不应期等电生理变化促进了房颤的发生和维持,是心房电重构与房颤关系的基础。     

左旋卡尼汀对犬心房急性缺血诱发电生理变化的影响

目的观察左旋卡尼汀(L-CN)对犬心房急性缺血时心房肌电生理改变及心房颤动(房颤)诱发率的影响。方法2003～2005年将解放军总医院的12只健康杂种犬随机分为L-CN用药组和生理盐水对照组。结扎右冠状动脉心房分支,造成心房肌局部缺血。观察各组缺血前后右心房不同部位的有效不应期(AERP)、右心房内传导速度(CV)的变化,计算右心房内心房激动波波长(WL)和房颤的诱发率并行心房肌病理学检查。结果(1)结扎右冠脉后盐水组缺血区心肌AERP均明显缩短;L-CN组右冠脉结扎后AERP无显著缩短。(2)冠脉结扎前后,两组右心房内CV均无明显改变。(3)结扎冠脉后,盐水组右心房内WL明显缩短;L-CN组的WL无显著变化。(4)盐水组结扎右冠脉后在不同时间段测量时均诱发房颤,L-CN组结扎冠脉后均未诱发房颤。(5)盐水组可见不同程度的心肌缺血,以冠脉结扎处近端为显著;L-CN组不同部位心肌均未见缺血变化。结论L-CN能够有效防止心肌缺血诱发的电生理变化,从而有效减少房颤的发作。     

犬急性心房颤动电重构现象的实验研究

目的 观察短阵心房颤动(房颤)的电重构现象及其恢复过程，探讨电重构与房颤再发及维持的关系。方法 15只健康成年犬于左、右心房外膜7个部位缝合双极记录电极，自心耳给予600次／min起搏诱发2h房颤，其中5只犬每间隔10min测量左、右心耳的心房有效不应期(AERP)，观察其恢复过程；另10只犬在房颤前后分别测量在起搏周长350ms、250ms、200ms时7个部位的AERP并记录电生理检查时房颤的诱发率及其持续时间。结果 2h房颤后心房各点AERP显著缩短，对心率适应不良，AERP离散度增高，继发性房颤诱发率增高、持续时间延长。AERP缩短可持续30min，60-80min后恢复。左心耳AERP恢复过程慢于右心耳。可诱发房颤的部位AERP更短，与继发性房颤的平均持续时间呈显著性负相关。可诱发房颤的心房其AERP离散度明显增高，但与继发性房颤的持续时间无关。AERP心率适应不良部位继发性房颤的诱发率高于生理性AERP心率适应性部位。低位右心房及左心耳部位的期前兴奋易于诱发房颤。结论 2h诱发的房颤足以使健康心房发生类似持续性房颤的电重构，电重构使房颤易于再发。AERP离散度与房颤的诱发有关，AERP缩短与房颤的持续性有关，房性早搏的发生部位与房颤的易患性有关。     

迷走神经活动对心房电重构的影响

目的 研究迷走神经干预对心房电重构的影响.方法 24只杂种犬随机分为3组,为排除交感神经对心房电重构的影响,3组犬均应用美托洛尔阻断交感神经效应.A组10只犬快速心房起搏过程中无迷走神经干预,B组8只犬应用阿托品阻断迷走神经效应,C组6只犬在快速心房起搏过程中同时进行迷走神经刺激.在右心房(RA)、冠状静脉窦(CS)和右心室(RV)放置多极导管.通过RA电极导管进行600次/min心房起搏30 min构建急性心房电重构模型.在右心房快速起搏前后测量基础状态(无迷走神经刺激)和迷走神经刺激下的心房有效不应期(AERP)和心房颤动(房颤)易感窗口(VW).结果 A组犬右心房快速起搏后基础状态下及迷走神经刺激时的AERP较起搏前明显缩短(P＜0.05).B组犬右心房快速起搏后基础状态下及迷走神经刺激时的AERP较起搏前无明显变化(P＞0.05).C组犬右心房快速起搏后基础状态下及迷走神经刺激时的AERP较起搏前明显缩短(P＜0.05).A组及C组右心房快速起搏后AERP缩短值明显大于B组(P＜0.05),但A组及C组AERP缩短值差异无统计学意义(P＞0.05).迷走神经刺激下,B组犬在右心房快速起搏前后均较难诱发房颤(VW接近0),A组及C组犬右心房快速起搏后较起搏前容易诱发房颤(P＜0.05).结论 短期右心房快速起搏导致的心房电重构过程中伴随着迷走神经兴奋性增强.迷走神经兴奋性增强及迷走神经刺激加重心房电重构,导致房颤易感性增加.迷走神经阻滞能减轻心房电重构,降低房颤易感性.     

交感神经对犬快速右心房起搏诱发阵发性心房颤动的影响

目的研究交感神经对犬快速右心房起搏所诱发的心房颤动(房颤)中的作用。方法选择杂种犬28只,随机分为4组:交感刺激组、交感离断组、异丙肾上腺素组(Iso组)、美托洛尔组(Met组),每组7只。各组分别于交感神经干预前后检测心房有效不应期(AERP)及快速右心房起搏的房颤诱发情况,观察各组交感神经干预对其的影响。结果与基础状态比较,交感刺激组和Iso组干预后AERP明显缩短(P<0.05),交感离断组和Met组AERP明显延长(P<0.01);Iso组房颤诱发率明显升高(P<0.01)。与交感刺激组和Met组比较,Iso组房颤诱发率明显升高(P<0.01)。随着AERP时程延长,房颤的诱发率逐渐下降,呈负相关线性趋势(r=-0.728,P=0.003)。结论交感神经活性与心房电重构有一定的联系,单纯刺激交感神经不能改变房颤的诱发频率,但交感神经递质可使房颤更易于诱发。     

热休克蛋白70 mRNA表达上调对兔心房快速起搏电重构的影响

目的：探讨热应激诱导心肌热休克蛋白70（HSP70）mRNA表达上调后,对兔快速心房起搏电重构的影响。方法：将24只新西兰大白兔随机分成热应激＋起搏组（n=8）、起搏组（n=8）和假手术组（n=8）。热应激造模：将新西兰大白兔麻醉后,放入恒温箱中加热,肛温达41℃后持续15 min,再放入室温恢复24 h。起搏：以600次/min行右心房起搏,测量0 h、2 h、4 h、6 h的右房有效不应期（AERP200、AERP150）,AERP频率适应性,心房颤动（AF）诱发率。起搏组对未造模的兔起搏。假手术组只测量不起搏。用逆转录聚合酶链式反应（RT-PCR）检测各组心肌HSP70 mRNA含量。结果：（1）快速心房起搏后,起搏组AERP200和AERP150立即缩短,起搏2h接近最小值[AERP200（79.38±6.23）ms,AERP150（71.25±6.94）ms],较起搏前[AERP200（100.00±6.55）ms,AERP150（89.38±6.78）ms]显著缩短（P〈0.01）;热应激＋起搏组起搏前后AERP无显著变化;（2）0 h时,起搏组右心房处（AERP200-AERP150）/50 ms为（0.21±0.10）ms,起搏2 h、4 h、6 h后分别为（0.16±0.07）、（0.14±0.05）、（0.13±0.05）ms,较起搏前非常显著缩短（P〈0.001）;（3）快速心房起搏前,予以程序性刺激和猝发刺激,各组AF诱发率均为0,起搏后2 h、4 h、6 h AF诱发率：起搏组分别为50.0%、75.0%、87.5%;热应激＋起搏组分别为25.0%、25.0%、37.5%;较起搏组显著减少（P〈0.05）;（4）热应激＋起搏组心脏各部位HSP70 mRNA表达较起搏组和假手术组明显增高（P〈0.05）,起搏组和假手术组间无显著差异。结论：心脏热休克蛋白70 mRNA表达上调后可抑制右心房快速起搏引起的心房电重构。     

夹竹桃麻素对兔心房电重构的影响

目的探讨烟酰胺腺嘌呤二核苷酸磷酸氧化酶抑制剂夹竹桃麻素对兔心房急性电重构的预防作用。方法选择新西兰白兔18只,随机分为对照组、心房快速起搏组和夹竹桃麻素+心房快速起搏组(夹竹桃麻素组),每组6只。对照组和心房快速起搏组术前生理盐水3 ml/(kg·d)灌胃3 d,夹竹桃麻素组予30 mg/(kg·d)药物灌胃3d。对照组术中不行心房快速起搏,心房快速起搏组与夹竹桃麻素组术中以最快的能维持心房1:1起搏的频率(500～600/min)给予快速刺激。分别在0、0.5、1.0、1.5、2.0、2.5和3.0 h时,测量基础刺激周长分别为200 ms和1 50 ms的右心房有效不应期(atrial effective rcfractory period,AERP),分析AERP频率适应性的变化,并记录心房颤动(房颤)的诱发情况。结果对照组和夹竹桃麻素组AERP_(200)和AERP_(150)无明显变化,心房快速起搏组AERP_(200)和AERP_(150)与心房快速起搏时间呈负相关(r=—0.650,P<0.01;r=—0.498,P<0.01);对照组和夹竹桃麻素组AERP频率适应性指标无明显变化,心房快速起搏组AERP频率适应性与心房快速起搏时间呈负相关(r=一0.341,P<0.05);心房快速起搏组和夹竹桃麻素组的房颤诱发率分别为66.67%和16.67%,平均房颤持续时间分别为37.75 min和0.67 min,差异有统计学意义(P<0.05)。结论夹竹桃麻素能够减缓心房电重构的发生、发展,降低房颤的持续时间。     

血管紧张素-(1-7)及其信号转导途径拮抗剂对犬急性心房电重构的影响

目的观察血管紧张素-(1-7)[Ang-(1-7)]及其信号转导途径拮抗剂对心房电重构的影响。方法以普通杂种犬56只建立心房快速起搏(600次/分)模型,分为AS组(假手术)、AC组(起搏对照)、AA组[起搏+Ang-(1-7)]、AN组[起搏+Ang-(1-7)+Mas受体特异拮抗剂A-779]、AP组[起搏+Ang-(1-7)+Akt抑制剂API-2]、AW组[起搏+Ang-(1-7)+PI3K抑制剂Wort]、AL组[起搏+Ang-(1-7)+NO合酶抑制剂L-NAME],每组8只。各组药物于起搏开始前5 min静脉点滴至起搏结束。右心耳起搏2 h后,以心脏程序期前刺激法(S1S2),分别测量基础起搏周长为300、250和200 ms时高位左、右心房和低位左、右心房以及左、右心耳部位的心房有效不应期(AERP)、AERP对心率适应性、心房颤动(简称房颤)诱发率及房颤持续时间。结果与AS组比较,AC组的AERP显著缩短、频率适应性不良、房颤诱发率增高且持续时间延长(P0.05);AA组与AS组相比,上述各指标无差异(P0.05);AA组与AC组比较,AERP明显延长,频率适应性不良发生率、房颤诱发率明显减小,房颤持续时间明显缩短(P0.05);AN组、AP组、AW组、AL组AERP及其频率适应性、房颤诱发率及持续时间与AC组无差异(P0.05)。结论在急性心房快速起搏犬模型,Ang-(1-7)对心房电重构有抑制作用,Ang-(1-7)信号途径拮抗剂可阻断其对心房电重构的预防作用。     

Protective effect of N2-mercaptopropionylglycine on rats and dogs liver during ischemia/reperfusion process

BACKGROUND: N2-mercaptopropionylglycine is a powerful super oxide synthesis inhibitor and has been tested as a preventive agent of metabolic and structural hepatic damage in the ischemia/reperfusion process. AIM: To analyze some effects of N2-mercaptopropionylglycine administration to animals of two species submitted to normothermic liver ischemia/reperfusion. MATERIAL AND METHODS: Twenty-two rats and 22 dogs were divided into four groups: group I: rats that received intravenous saline 0.9%; group II: rats that received 100 mg/kg of N2-mercaptopropionylglycine; group III: dogs that received saline intravenous 0.9% and group IV: dogs that received 100 mg/kg N2-mercaptopropionylglycine. RESULTS: Ten minutes after the saline or drug administration, each group was submitted to left lobe liver ischemia for 25 minutes followed by reperfusion. Biochemical studies 24 hours after reperfusion revealed a significantly lower elevation of transaminases in animals of groups II (AST = 271 +/- 182; ALT = 261 +/- 161 ) and IV (AST = 101 +/- 45; ALT = 123 +/- 89) when compared to the controls group: I (AST = 2144 +/- 966; ALT = 1869 +/- 1040 00) and III (AST = 182 +/- 76.51; ALT = 277 +/- 219), respectively. Histology study demonstrated a significantly minor aggression to animals of groups II and IV when compared to groups I and III, respectively. CONCLUSION: These results suggest a significant release of free radicals of oxygen in the process and that N2-mercaptopropionylglycine may have a significant protective effect on liver parenchyma when submitted to ischemia/reperfusion.     

Effect of technique of administration on plasma lidocaine levels

There are many clinical situations in which IV access is unavailable, and the endotracheal route is a valuable alternative route for drug therapy. The optimal technique of endotracheal drug administration, however, has not been determined. Twenty-nine dogs were divided into five groups and given endotracheal lidocaine at two doses, 2 mg/kg and 4 mg/kg, by differing techniques: control, undiluted lidocaine in a syringe was given as a bolus; needle, the drug was given through a needle attached to the syringe; dilution, lidocaine was diluted approximately 1:1 with normal saline and the entire dilution was given as a bolus; normal saline (NS) followup, lidocaine in a syringe was given as a bolus, followed immediately by an equal bolus of normal saline; and catheter, the drug was given through a catheter that was placed inside and extended just beyond the endotracheal tube. Mean plasma lidocaine levels (microgram/mL) at five minutes were as follows (at a 2-mg/kg endotracheal lidocaine dose): control, 0.64; needle, 0.0; dilution, 3.1; and (at a 4-mg/kg endotracheal lidocaine dose) control, 1.0; needle, 0.6; dilution, 6.2; NS followup, 1.9; and catheter, 1.9. At all time periods with either dose of lidocaine (2 or 4 mg/kg), the highest plasma lidocaine levels occurred with dilution and the lowest with the needle method. These results were highly significant (P less than .001). The highest plasma lidocaine levels may be attained by diluting the drug with normal saline. Higher levels were achieved when the drug was given through a catheter or when the drug was followed with a bolus of normal saline.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of the Cardioselective, Sarcolemmal KATP Channel Blocker HMR 1098 on Atrial Electrical Remodeling During Pacing-Induced Atrial Fibrillation in Dogs

PURPOSE: The progressive shortening of the atrial effective refractory period (ERP) during atrial fibrillation (AF) might be due to the activation of the KATP channels by rapid atrial rates. We tested the hypothesis that the cardioselective, sarcolemmal KATP channel blocker HMR 1098 would prevent atrial ERP shortening during AF. METHODS AND RESULTS: Nine dogs were treated with HMR 1098 (3 mg/kg bolus injection followed by a continuous intravenous (i.v.) infusion at 17 microg/kg/min rate maintained throughout the study) and 7 dogs served as controls receiving i.v. saline. Pharmacological autonomic blockade was induced by i.v. administration of atropine (0.04 mg/kg) and propranolol (0.2 mg/kg) and maintained throughout the study by continuous i.v. infusion of atropine (0.007 mg/kg/h) and propranolol (0.04 mg/kg/h). Rapid right atrial pacing at 50 msec cycle length (CL) was initiated and maintained for 6 hours. High right atrial ERP (HRA-ERP) and corrected sinus node recovery time (HRA-cSNRT), coronary sinus ERP (CS-ERP) and corrected SNRT (CS-cSNRT) at three (400, 300, 200 msec) CLs were measured before and after pacing at different time points. Baseline values were not different between control and treated dogs. In the control group the HRA-ERP progressively shortened (from 179 +/- 21 msec at baseline to 161 +/- 23 msec at 360 min at 400 msec CL) ( p = 0.002), with a gradual decrease, loss or inversion of ERP rate adaptation at shorter (300, 200 msec) CLs. HMR 1098 treatment did not prevent the shortening of HRA-ERP during the first 2 to 3 hours of rapid atrial pacing. However, beginning at 180-240 min, HMR 1098 increased the HRA-ERP ( p = 0.01) to baseline by 360 min. HMR 1098 treatment did not prevent another feature of atrial electrical remodeling, the flattening or inversion of ERP rate adaptation. In neither group did CS-ERP shortening occur. The maximum cSNRT at 360 min prolonged significantly in both groups during HRA and CS pacing as well compared with baseline. CONCLUSIONS: HMR 1098 treatment did not prevent the shortening of HRA-ERP, the salient feature of atrial electrical remodeling in the first 2 to 3 hours of rapid atrial rates, but did prevent it thereafter. Another characteristic feature of atrial electrical remodeling, the flattening or inversion of physiological ERP rate adaptation was not prevented by HMR 1098 treatment. Sinus node depression was detectable after short-term (6 hours) rapid atrial pacing and was not affected by HMR 1098.     

Amiodarone as a first-choice drug for restoring sinus rhythm in patients with atrial fibrillation: a randomized, controlled study

STUDY OBJECTIVES: To investigate the efficacy and safety of amiodarone administered as the drug of first choice in the conversion of atrial fibrillation, regardless of its duration. DESIGN:: Prospective, randomized, controlled clinical study. SETTING:: Tertiary cardiac referral center. PATIENTS: Two-hundred eight consecutive patients (102 men; mean [+/- SD] age, 65 +/- 10 years) with atrial fibrillation. INTERVENTIONS: One-hundred eight patients received amiodarone, and 100 patients received placebo treatment. Patients randomized to amiodarone received 300 mg IV for 1 h, and then 20 mg/kg for 24 h. They were also given 600 mg/d orally, divided into three doses, for 1 week, and thereafter 400 mg/d for 3 weeks. Patients randomized to placebo treatment received an identical amount of saline solution IV over 24 h, and oral placebo treatment for 1 month. MEASUREMENTS AND RESULTS: Baseline clinical characteristics were similar in the two groups. Conversion to sinus rhythm was achieved in 87 of 108 patients (80.05%) who received amiodarone, and in 40 of 100 patients (40%) in the placebo group (p < 0.0001). Statistical analysis showed that the duration of the arrhythmia and the size of the left atrium affected both the likelihood of conversion to sinus rhythm and the time to conversion in both groups. No side effects requiring discontinuation of treatment were observed in either group. CONCLUSIONS: Amiodarone appears to be safe and effective in the termination of atrial fibrillation. However, extreme cases with a large left atrium and long-lasting arrhythmia need long-term therapy.     

左旋卡尼丁对急性心肌梗死患者肌钙蛋白T和C-反应蛋白的影响及意义

目的探讨左旋卡尼丁(L-CN)对急性心肌梗死患者肌钙蛋白T(cTnT)和C-反应蛋白(CRP)含量的影响。方法2004年1~12月在沈阳医学院附属沈洲医院住院治疗的急性心肌梗死(AMI)患者25例,为试验组,给予L-CN4.0g/d,共用7d;另选AMI患者25例作为对照组。所有患者于用药前、用药第3天后,用药结束后检测cTnT和CRP。并于用药前和用药结束后行超声心动图检查及心肌灌注显像分析。结果用药前cTnT和CRP含量两组间差异无显著性意义(P>0.05)。用药第3天后试验组cTnT和CRP较对照组下降但差异无显著性意义;用药结束后试验组cTnT和CRP较对照组显著减低(P<0.05)。试验组在用药后左心室射血分数(LVEF)较对照组明显改善(P<0.05),心肌缺损面积缩小(P<0.05)。结论心肌梗死时给予L-CN治疗可降低血循环中cTnT和CRP含量,有利于心肌修复,缩小梗死面积。     

Late administration of methylprednisolone does not enhance naloxone effect in hypovolemic shock

The late addition of methylprednisolone (MP) in our canine hypovolemic shock protocol was evaluated to determine whether any hemodynamic enhancement of the naloxone (NAL) effect might be present. Thirty-four dogs were bled to a mean arterial pressure (MAP) of 40-45 mm Hg and held there for 45 minutes. All animals were then treated (T = 0) with 0.9% NaCl (NS) or NAL. In two groups of animals, MP (30 mg/kg) was given as an IV bolus 30 minutes after initiating NS or NAL therapy. At 60 minutes, the infusions were stopped and the shed blood was returned. Animals treated with NAL with or without MP showed improvement in MAP, maximal left ventricular contractility (LVdP/dt max), and cardiac output (CO) compared to NS. We found little hemodynamic improvement with the addition of MP at T = 30 for either the NAL or NS. Plasma endorphinlike activity (PELA) values decreased during treatment in the groups receiving NAL. Survival was improved in all groups except those receiving NS, but survival was statistically better only in the group that received NAL.     

左旋卡尼汀对老年腹部术后心力衰竭患者的疗效分析

目的观察左旋卡尼汀治疗老年腹部术后心力衰竭患者的临床疗效。方法选择腹部手术后并发心力衰竭老年患者57例,随机分为2组,对照组25例予洋地黄、利尿剂、血管扩张剂、血管紧张素转换酶抑制剂等常规药物治疗,卡尼汀组32例,在常规治疗的基础上加用国产左旋卡尼汀5.0g治疗15d。结果两组治疗后临床症状和射血分数（EF）较治疗前均有改善,但卡尼汀组心功能改善的临床显效率（44%）和总有效率（94%）均较对照组（36%和80%）显著提高（分别为P<0.05和P<0.01）,治疗后卡尼汀组EF（0.52±0.03）与对照组（0.50±0.04）和治疗前（0.48±0.05）相比,差别均有显著性意义（均P<0.01）,且无药物不良反应。结论左旋卡尼汀辅助治疗老年腹部术后心力衰竭患者有较好疗效。     

Prevention of alpha-naphthylthiourea-induced pulmonary edema with fructose-1,6-diphosphate

Neutrophil-derived oxygen free radicals have been implicated in the pathogenesis of noncardiogenic pulmonary edema. Fructose-1,6-diphosphate (FDP) has been shown to inhibit oxygen free radicals production by activated neutrophils. Thus, we investigated whether FDP would attenuate formation of pulmonary edema in anesthetized dogs injected with alpha-naphthylthiourea (ANTU). Hemodynamic studies involved measurements of left ventricular systolic and end-diasystolic pressures (LVSP and LVEDP), pulmonary artery pressure (PaP), heart rate (HR), and cardiac output (CO). Mean wet weight to dry weight ratios of lung tissue samples were calculated. Following baseline measurements, dogs were injected intravenously (IV) with ANTU 5 mg / kg (n = 16) and 10 mg / kg (n = 8) and half of the dogs were randomly selected to receive 75 mg / kg FDP (10%) and subsequent infusion of 7 mg / kg / min. The rest were given 0.9% NaCl in the same manner. Four hours after ANTU administration, the animals were euthanatized. Except for decline in the CO (nonsignificant), no significant changes in systemic hemodynamics within and between the groups were noted. In the FDP group, PaP and pulmonary arteriolar resistance (PaR) remained unchanged. In the saline group, PaP increased from 12.5 +/- 2.44 to 21.8 +/- 3.14 mm Hg (P < .001) and PaR from 166 +/- 29 to 468 +/- 74 dynes. cm / sec(5) (P < .005). During the study LVDEP, PaO(2), PaCO(2), and hematocrit did not change significantly within and between the groups. The lungs mean wet weight to dry weight ratios for the sham-operated dogs were 4.20 +/- 0.41, for the FDP group 4.32 +/- 0.59 and 6.22 +/- 1.37 for the saline group (P < .0005). These data indicate that FDP protected the lung from ANTU-induced injury.