氟中毒大鼠心肌细胞电生理变化及硒的影响

为观察氟中毒大鼠心肌生理变化及硒对变化的影响，两组Ｗｉｓｔａｒ大鼠饮１．５８、２．６３ｍｍｏｌ／Ｌ高氟水，两组大鼠饮高水加饲２．０ｍｇ／ｋｇ硒饲料。实验进行４个月、８个月时服硒鼠尿硒、氟升高；８个月时血硒上升，血氟下降。心民生理参数显示氟中毒大鼠ＲＰ、ＡＰＡ、Ｖｍａｘ降低，ＡＰＤ５０、ＡＰＤ９０缩短。投硒则使ＲＰ、ＡＰＡ、Ａｍａｘ程度不同 的恢复，ＡＰＤ５０、ＡＰＤ９０达到对照组水平。表明氟中毒大     

肾上腺紧张素与高血压

目的观察实验性高血压大鼠及原发性高血压病（ＥＨ）患者的血浆肾上腺紧张素（ＡＤＴ）水平变化。方法用特异性放射免疫法测定血浆ＡＤＴ含量。结果两组实验性高血压大鼠平均动脉压（ＭＡＰ）及左室指数（ＬＶＩ）明显高于对照大鼠，而血浆ＡＤＴ水平则低于对照大鼠；５９例ＥＨ患者血浆ＡＤＴ水平（１０１．４３±４．１８ｎｇ／Ｌ）亦明显低于对照组（１６６．９３±５．０７ｎｇ／Ｌ，Ｐ＜０．００１），随着病期的加重，降低更显著，组间有显著差异（Ｆ＝７４．２９，Ｐ＜０．００１），两两比较Ｐ值均＜０．０１。结论ＡＤＴ的这种变化是维持机体自稳态调节的一种代偿机制     

氟硒对豚鼠心室肌细胞动作电位的影响

应用灌流方法和细胞内微电极技术观察Ｆ－、Ｓｅ及Ｆ－加Ｓｅ对豚鼠心肌细胞电生理影响。结果用５．２６×１０－６ｍｏｌ／ＬＦ－灌流，随时间延长ＲＰ降低，ＡＰＤ５０、ＡＰＤ９０缩短，Ｖｍａｘ有下降趋势。用９．５０×１０－６ｍｏｌ／ＬＳｅ灌流，ＡＰＤ５０、ＡＰＤ９０明显延长。上述浓度的Ｆ－和Ｓｅ同时应用则灌流前后心肌电生理各参数无明显改变。此表明Ｆ－灌流可使心肌细胞膜电位降低，兴奋性降低，复极时间缩短，Ｓｅ可桔抗Ｆ－所致的此种心肌电生理异常。     

不同浓度的金属硫蛋白对离体豚鼠乳头肌缺氧,…

为探讨金属硫蛋白（ＭＴ）对豚鼠乳头肌缺血再灌注损伤所致心律失常的影响，利用标准玻璃微电极技术，采用缺氧及复氧豚鼠乳头肌模型，模拟体内缺血再灌注损伤，观察不同浓度ＭＴ对豚鼠乳头肌电生理特性的影响。结果显示低浓度的ＭＴ（０．００２ｍｍｏｌ／Ｌ）对正常及缺氧和复氧 鼠乳头肌的动作电位（ＡＰ）有关参数及自律性均无影响；中等浓度的ＭＴ（０．０２ｍｍｏｌ／Ｌ）仅使正常乳头肌的ＡＰ复极达５０％时程（ＡＰＤ５０）     

硒对氟致机体损伤保护作用的实验研究

目的 研究硒对氟致机体损伤的保护作用及探讨其保护机理。方法 Wistar大鼠饮30mg／L和50mg／L高氟水造成慢性氟中毒，同时另外两组大鼠饮高氟水、饲2mg／kg加硒饲料。1年内每月测饮水摄食和排尿量，测尿氟含量；每2月摄X线片。喂养4、8、14个月分批处死大鼠，测硒氟含量、骨形态计量学参数、自由基含量、抗氧化酶类、甲状腺激素、心电图、心肌电生理参数等。结果 对氟中毒大鼠投硒可改善饮食、增加体重；促进尿氟排泄，降低体氟；延迟X线异常改变和氟骨症的发生同时减少骨量对骨矿化障碍产生抑制作用；恢复抗氧化酶类活性；调整甲状腺激素水平；拮抗氟中毒所致的心电图和心肌电生理异常。结论 一定浓度范围内的硒具有拮抗高氟作用，促进尿氟排泄、保护骨骼系统、调整自由基代谢及对肝、肾、心脏的作用是硒拮抗高氟的重要机制。     

急性冠状动脉综合征合并糖耐量减低对纤溶系统的影响

目 的：分析急性冠状动脉综合征（ＡＣＳ）患者合并糖耐量异常对Ｄ－二聚 体（ＤＤ）含量 的 影 响。方 法：选 择１３５例住 院 治 疗 的ＡＣＳ患者。根据糖代谢情况,患者被分为单纯ＡＣＳ组（４８例）,２型糖 尿 病（Ｔ２ＤＭ）＋ＡＣＳ组（４６例）和糖 耐 量 减 低（ＩＧＴ）＋ＡＣＳ组（４１例）;同期住院健康体检者３５例作为正常对照组。测定 比 较 各 组 的浆ＤＤ水平。结 果：与正常对照组和单纯ＡＣＳ组比 较,Ｔ２ＤＭ＋ＡＣＳ组和ＩＧＴ＋ＡＣＳ组的甘油三酯水平［（１．１２±０．３９）ｍｍｏｌ／Ｌ,（１．５２±０．９２）ｍｍｏｌ／Ｌ比（２．５７±１．１７）ｍｍｏｌ／Ｌ,（２．３２±０．９６）ｍｍｏｌ／Ｌ］显著 升 高（Ｐ均＜０．０１）;与正常对照组比较,单纯ＡＣＳ组、Ｔ２ＤＭ＋ＡＣＳ组和ＩＧＴ＋ＡＣＳ组患 者 血 浆ＤＤ水平［（３６０．５０±７４）ｎｇ／ｍｌ比（７９５．２４±１３４．１０）ｎｇ／ｍｌ比（６６３．３１±１１６．０６）ｎｇ／ｍｌ,（７０２．４０±１２６．６４）ｎｇ／ｍｌ］均显 著 升 高（Ｐ均＜０．０１）;而Ｔ２ＤＭ＋ＡＣＳ组和ＩＧＴ＋ＡＣＳ组的 血 浆ＤＤ水平显著低于单纯ＡＣＳ组（Ｐ均＜０．０５）。结论：急 性 冠 状动脉综合征合并糖耐量减低患者纤溶系统功能较单纯ＡＣＳ患者 减 退。     

老年男性冠心病患者血清硫酸脱氢表雄酮含量变化的临床意义

目的观察老年男性冠心病患者血清硫酸脱氢表雄酮（ＤＨＥＡ－Ｓ）含量变化，探讨其与睾酮（Ｔ）、胰岛素（ＩＮＳ）、血糖（Ｇｌｕ）、甘油三酯（ＴＧ）、总胆固醇（ＴＣ）、载脂蛋白Ｂ（ａｐｏＢ）及年龄的相关性。方法用放免法测定６９例老年男性冠心病患者血清ＤＨＥＡ－Ｓ含量，并与３５例年龄匹配的男性健康人对照。结果冠心病组ＤＨＥＡ－Ｓ含量（２．９６±１．８０μｍｏｌ／Ｌ）显著低于对照组（４．０６±１．７６μｍｏｌ／Ｌ，Ｐ＜０．０１），病情重组（２．４４±１．３６μｍｏｌ／Ｌ）又明显低于病情轻组（３．３２±２．１２μｍｏｌ／Ｌ，Ｐ＜０．０５）；冠心病组ＤＨＥＡ－Ｓ含量与年龄呈负相关（ｒ＝－０．３０５４，Ｐ＜０．０１），对照组两者也呈负相关（ｒ＝－０．３６１５，Ｐ＜０．０５）；冠心病患者ＤＨＥＡ－Ｓ降低与空腹血清ＩＮＳ、ＴＧ及ａｐｏＢ增高均呈负相关（分别为ｒ＝－０．３２９７、－０．２５１９及－０．２４１３，Ｐ＜０．０１或０．０５）。结论老年男性冠心病患者血清ＤＨＥＡ－Ｓ含量降低，并与冠心病某些危险因素如老年、高胰岛素血症、高甘油三酯血症、血清ａｐｏＢ高值相关，但其确切的发病机理有待深入研究。     

大豆低聚糖对高脂大鼠脂质过氧化的影响

大豆低聚糖对实验性大鼠高脂血症的防治研究结果证明：能降低血清总胆固醇（ＴＣ）（Ｐ＜０．０５），提高血清高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）（Ｐ＜０．００１），提高ＨＤＬ－Ｃ／ＴＣ比值（Ｐ＜０．００１），降低血清甘油三酯（ＴＧ）水平（Ｐ＜０．００１）；降低心肌组织过氧化脂质（ＬＰＯ）水平（Ｐ＜０．０１），提高心肌组织超氧化物歧化酶（ＳＯＤ）活性（Ｐ＜０．０１），有抑制脑组织过氧化损伤的趋势。结果提示：大豆低聚糖具有降低高脂大鼠血脂水平，拮抗过氧化损伤的作用。     

氟中毒大鼠心电图改变及其硒的影响

为观察氟中毒大鼠心电图变化及其Ｓｅ的影响，两组Ｗｉｓｔａｒ大鼠饮用１．５８、２．６３ｍｇ／Ｌ高Ｆ＾－水，另两组鼠饮高Ｆ＾－水加饲０．０２５ｍｇ／ｋｇＳｅ饲料，在实验前及实验４、８、１２个月进描记心电图。结果两组大鼠随摄氟时间延长Ｔ波降低，Ｑ－Ｔ间期缩短。     

氟中毒大鼠服硒对体内氟及抗氧化酶和脂类影响的实验研究

目的研究硒对氟中毒大鼠体内氟、抗氧化酶和脂类代谢的影响作用。方法Ｗｉｓｔａｒ大鼠饮２．６３ｍｍｏｌ／Ｌ高氟水１０个月后分为氟、氟加２．０ｍｇ／ｋｇ硒、改饮正常水、改正常水加硒４组,再喂养１０个月。观察尿氟动态变化,测定骨、组织、血清氟和硒,同时测血ＧＳＨ－ｐｘ、ＳＯＤ、ＬＰＯ及血ＴＣ、ＴＧ、ＨＤＬ－Ｃ、ＬＤＬ－Ｃ等。结果氟加硒组较氟中毒组尿氟排泄增高,骨、组织氟降低,酶和脂代谢改善;改正常水加硒组,排尿氟和降体氟作用优于单纯改水组,酶和脂类指标水平更趋正常。结论一定浓度范围内的硒对氟中毒大鼠具有排高氟和调整自由基、脂类代谢紊乱作用。改正常水加硒则有促进氟中毒恢复的作用。     

硒对大鼠心电图及心肌细胞动作电位的影响

目的　探讨硒对大鼠心电图及心肌细胞动作电位的影响。方法　对Ｗ ｉｓｔａｒ雄性大鼠腹腔内注射亚硒酸钠（２ｍ ｇ·ｋｇ－１·ｄ－１）,连续９ 周,应用心电图和细胞内玻璃微电极技术,观察正常大鼠和阿霉素致心肌损伤大鼠心电图及心肌细胞动作电位的变化。结果　硒组心电图较实验前及对照组无变化（ Ｐ ＞ ０．０５ ）,心肌细胞复极达峰值电位５０％ 所需时间（ＡＰＤ５０）延长（ Ｐ ＜ ０．０５ ）。ＡＤＭ 组和硒＋ ＡＤＭ 组心电图Ｑ－Ｔ 间期及心肌细胞ＡＰＤ５０、ＡＰＤ９０较对照组及试验前均延长（ Ｐ＜ ０．０１）。心率、静息电位（ＲＰ）、动作电位幅度（ＡＰＡ）及动作电位０ 相最大去极化速率（Ｖｍ ａｘ）无变化（ Ｐ ＞ ０．０５）。结论　硒能延长正常大鼠心肌细胞ＡＰＤ５０,不能逆转阿霉素心肌损伤大鼠ＡＰＤ５０、ＡＰＤ９０及Ｑ—Ｔ 间期延长。此结果对于心肌病的防治具有重要意义。     

松属素阻断核转录因子κB信号通路降低心肌梗死大鼠室性心律失常

目的探讨松属素(pinocembrin,Pino)对心肌梗死(MI)后室性心律失常诱发率的影响及其可能的机制。方法随机将大鼠分为假手术组(Sham组),MI组和Pino组,每组20只,后2组结扎左前降支血管建立MI模型,且Pino组于建MI前30 min大鼠尾静脉注射Pino 5 mg/kg,建MI后连续给药5 d。灌流体外心脏,检测各组大鼠心室肌电生理指标,采用酶联免疫吸附法检测血清TNF-α和白细胞介素(IL-1β)水平,用马松染色检测心肌纤维化水平,用免疫印迹法检测心室NF-κB表达量。结果与Sham组比较,MI组大鼠心室肌有效不应期(ERP)明显降低(P<0.05),动作电位时程(APD)、APD电交替及室性心律失常的诱发率明显增加(P<0.05);与MI组比较,Pino组大鼠ERP、APD50、APD90、APD电交替及室性心律失常的诱发率均显著改善[(59.0±6.6)ms vs(41.5±3.4)ms,(38.0±2.3)ms vs(54.0±1.0)ms,(74.8±8.8)ms vs(116.0±7.7)ms,(92.5±7.1)ms vs(106.3±5.2)ms,30.0%vs 80.0%,P<0.05]。Pino组大鼠TNF-α和IL-1β表达较MI组明显降低[(59.99±1.26)ng/L vs(70.46±2.13)ng/L,(40.94±1.74)ng/L vs(61.15±0.81)ng/L,P<0.05]。马松染色显示,Pino组大鼠心肌纤维化较MI组明显改善[(23.24±2.40)%vs(31.95±1.99)%,P<0.05]。Pino组大鼠NF-κB p65蛋白表达较MI组明显降低,差异有统计学意义(0.37±0.04 vs 0.57±0.09,P<0.05)。结论 Pino可显著降低MI后室性心律失常的诱发率,其机制可能与抑制NF-κB信号通路,减轻炎性反应有关。     

缺血后处理对大鼠心室肌细胞内向整流钾电流和动作电位的影响

目的探讨缺血后处理(IPC)对大鼠心室肌细胞内向整流钾电流(IK1)和动作电位的影响及机制。方法实验分IPC组、缺血/再灌注(I/R)组、单纯灌流(SP)组,利用大鼠心脏建立离体灌注模型,采用胶原酶酶解法分离得到大鼠单心室肌细胞,采用膜片钳全细胞技术分别记录三组心室肌细胞电流和动作电位的变化。结果在-120mV和-30mV刺激电压水平,IK1电流密度:IPC组低于I/R组,I/R组高于SP组(P均<0.05),IPC组同SP组无差异(P>0.05)。与SP组和IPC组比较,I/R组静息电位明显升高(P<0.05);而动作电位幅度、20%动作电位时程、50%动作电位时程、90%动作电位时程均明显下降(P<0.05)。而IPC组各值与SP组无差异(P>0.05)。结论IPC可以降低大鼠缺血/再灌注心肌细胞IK1,延长缺血/再灌注心肌细胞APD。     

银丹心脑通软胶囊对垂体后叶素致心肌缺血大鼠心电图的影响

目的 观察银丹心脑通软胶囊对垂体后叶素(pituitrin,Pit)致心肌缺血大鼠心电图的影响.方法 采用大鼠舌下静脉注射Pit造成急性心肌缺血模型,观察各给药组在注射Pit后不同时间点Ⅱ导联心电图T波变化百分率和心率的变化.结果 银丹心脑通软胶囊低、高剂量组与模型组比较,均能明显降低心肌缺血大鼠心电图T波峰值变化百分率(P<0.05),与注射Pit前比较,能对抗Pit致心率减慢的损伤(P<0.05).结论 银丹心脑通软胶囊具有抗Pit引起的大鼠急性心肌缺血的作用.     

Electrophysiological and antiarrhythmic effects of lidocaine in canine acute myocardial ischemia.

The electrophysiologic effects of temporary (15 minute) ligations of the left anterior descending coronary artery were examined in 16 dogs. Monophasic action potential duration (APD) and effective refractory period (ERP) were determined in the ischemic and normal zones. Intervals (Q-EG) were measured from the onset of the QRS in a standard ECG lead to the major deflection of electrograms recorded in these zones. Control ligations were compared to those in which a 2 mg./Kg. intravenous bolus of lidocaine was administered immediately after ligation followed by a constant rate intravenous infusion of 70 μg/Kg./minute. Lidocaine reduced the number of ventricular beats per minute (17 to 8) (p < .01) and at the same time it prolonged ERP only in the ischemic zone (14 msec.; p < .01), shortened APD only in the normal zone (8 msec.; p < .05), reduced $\text{APD}\text{ERP}$ in the ischemic zone (1.12 to 1.01; p < .01), and to a lesser extent in the normal zone (1.17 to 1.12; p < .05), and it prolonged conduction only in the ischemic zone (10 msec. at peak effect; p < .01). During the control ligation, APD in the ischemic zone was 8 msec. shorter than in the normal zone (p < .05), while with lidocaine the difference was reduced to 3 msec. (N.S.). The effects of lidocaine reducing the disparity in APD between ischemic and normal zones in prolonging conduction and refractoriness in the ischemic zone and in reducing $\text{APD}\text{ERP}$ may explain the demonstrated antiarrhythmic properties in acute myocardial ischemia.     

慢性缺血性心力衰竭模型制备方法的对比研究

目的探讨冷冻左心室前壁与结扎前降支两种方法诱导大鼠心肌梗死后制作慢性心力衰竭模型的对比研究。方法选择8～10周龄SD健康大鼠120只,随机分为冷冻组(50只),结扎组(50只)、假手术组(20只)。手术后4周行心电图、心功能检查,取心脏组织行TTC、HE染色并观察其死亡率。结果手术后4周冷冻组大鼠死亡率为32%低于结扎组48%。与假手术组比较,冷冻组、结扎组大鼠心电图显示为心肌梗死,LVEF、左心室短轴缩短率明显降低,左心室舒张末直径明显升高,差异有统计学意义(P<0.01),冷冻组和结扎组大鼠心肌切片、TTC染色可见100%梗死区;梗死区HE染色主要为瘢痕组织,假手术组未见心肌梗死。结论冷冻法诱导的心力衰竭模型在心功能、心肌梗死面积等方面等同于结扎法,且死亡率明显减低,冷冻左心室前壁诱导大鼠心肌梗死后慢性心力衰竭模型较结扎法更好。     

Nitric oxide activates the sarcolemmal K(ATP) channel in normoxic and chronically hypoxic hearts by a cyclic GMP-dependent mechanism

Chronic myocardial hypoxia results in elevated nitric oxide (NO) production and increased current through the sarcolemmal K(ATP) channel. We hypothesized these two processes are related and determined whether NO alters the electrophysiology of Purkinje fibers obtained from rabbits (n=12/group) raised in a normoxic (F(I)O2=0.21) or hypoxic (F(I)O2=0.12) environment from birth to 9 days of age. Action potential duration (APD)(90) was shorter (112+/-3 ms v 126+/-3 ms) and maximum diastolic potential (MDP) was more negative (-84+/-2 mV v-80+/-1 mV) in hypoxic hearts compared with normoxic controls. In normoxic hearts the NO donors, S-nitrosoglutathione (GSNO) 50 microM and spermine NONOate (50 microM) shortened APD(90) and increased MDP to levels present in chronically hypoxic hearts. This effect was completely abolished by the K(ATP) channel blocker glibenclamide (3 microM) and by a nitric oxide trap, Carboxy-PTIO (100 microM). The NO carrier glutathione (50 microM) and decomposed spermine NONOate had no effect on APD(90) or MDP. GSNO had no effect in hypoxic hearts; however, when GSNO was combined with glibenclamide APD(90) increased, and MDP decreased to normoxic values. 8-Bromo cGMP (100 microM) shortened APD(90) and increased MDP to levels present in chronically hypoxic hearts. This effect was abolished by glibenclamide. A soluble guanylyl cyclase inhibitor, ODQ (10 microM), had no effect on action potentials in normoxic hearts but in hypoxic hearts resulted in an increase in APD(90) to levels present in normoxic hearts and a decrease in MDP. The effect of ODQ could not be reversed by GSNO. We conclude that NO activates the sarcolemmal K(ATP) channel in normoxic and chronically hypoxic hearts by a cyclic GMP-dependent mechanism.     

盐酸咪达普利对扩张型心肌病跨室壁复极不均一性的影响

目的 :探讨咪达普利 (IMI)对扩张型心肌病 (DCM )心室肌跨室壁复极不均一性的影响及其与抑制室性心律失常的关系。方法 :32只家兔 ,随机分为DCM加IMI组、DCM组、IMI组及正常对照组 ,每组 8只。然后测定其心室颤动阈值 (VFT)以及心外膜、中层心肌和心内膜心肌细胞的单相动作电位复极 90 %时程 (APD90 )、跨室壁复极离散度 (TDR)。结果 :DCM加IMI组与DCM组相比 ,前组VFT升高 ,三层心肌APD90 均缩短 ,以中层心肌APD90 缩短更为明显 ,TDR减小。IMI组与正常对照组相比 ,VFT、三层心肌的APD90 、TDR差异均无显著性意义。结论 :IMI能抑制DCM室性心律失常的发生 ,间接地减小三层心肌跨室壁复极不均一性是重要机制     

Secondary and primary repolarization changes in left ventricular hypertrophy: a model study

The contributions of reduced conduction velocity (CV) and prolonged action potential duration (APD) to QT interval prolongation and T wave and T vector loop morphology in left ventricular hypertrophy (LVH) were studied using an analytical computer model. Three types of anatomic LVH were simulated: concentric and eccentric hypertrophy, and left ventricular dilatation. In each LVH type, depolarization changes were simulated by CV slowing and primary repolarization changes by APD prolongation. Both CV slowing and APD prolongation prolonged the QT interval; however, the secondary and primary repolarization changes differed in additional electrocardiogram (ECG) characteristics creating specific vectorcardiographic/ECG patterns. The secondary repolarization changes were characterized by prolonged QT interval, accompanied by pronounced QRS changes, including increased maximum spatial QRS vector magnitude, prolonged QRS duration, QRS morphology consistent with intraventricular conduction delay, lower values of the T/QRS duration ratio, increased maximum spatial T vector magnitude, narrow and prolonged discordant T vector loops, and discordant tall T waves creating a pattern of ST strain in the precordial ECG leads. QT prolongation in primary repolarization changes was accompanied with inconsiderable changes of QRS amplitude and duration, higher values of the T/QRS duration ratio, widened rounded T loops, and notched or bifid T waves in left precordial leads of the 12-lead ECG. These simulation data are consistent with the accumulated evidence suggesting that LVH induces changes in CV and APD. Our results emphasize the need for simultaneous consideration of morphologic QRS and T wave patterns together with QT prolongation in clinical evaluation of LVH.