血管紧张素Ⅱ引起心肌重构的分子机制

目的采用结扎冠脉模型探讨血管紧张素Ⅱ（ANGⅡ）引起心肌重构的分子机制。方法将Wistar大鼠分为梗塞组和假手术组，梗塞组结扎左冠脉，测两心肌组织中ANGH含量，用原位杂交和组化方法了解c－fosmRNA及其蛋白表达。结果与假手术组比较，梗塞组ANGⅡ上升，c－fosmRNA原位杂交信号及蛋白表达的免疫组化信号增强。结论心肌重构与上升的ANGⅡ引起的c－fos表达增强有关。     

牛磺酸对离体肝星状细胞增殖及凋亡的影响

目的　观察牛磺酸对肝星状细胞增殖及凋亡的影响 ,并探讨其作用的可能机制。方法　用噻唑蓝 (MTT)法检测细胞增殖 ,流式细胞仪检测细胞周期及凋亡 ,丫啶噔活体染色观察细胞凋亡形态 ,免疫细胞化学结合计算机图像分析系统检测c jun、c fos表达。 结果　在 5～ 5 0mmol/L浓度范围内 ,牛磺酸能剂量依赖性地抑制肝星状细胞增殖 ,可使G0 /G1期细胞增多 ,S期细胞减少 ,并能明显抑制c jun、c fos的表达 (P <0 .0 1)。此外 ,牛磺酸尚可抑制血小板源生长因子BB对肝星状细胞的促增殖作用 ,而牛磺酸对肝星状细胞凋亡无诱导作用。结论　牛磺酸可显著抑制肝星状细胞增殖 ,使肝星状细胞阻滞于G0 ～G1期 ;牛磺酸对肝星状细胞增殖的抑制作用与其抑制c jun、c fos的表达有关 ;牛磺酸不能诱导肝星状细胞凋亡。     

实验性脑缺血再灌注中TGF-β_1免疫组化及分子生物学研究

目的　探讨脑缺血再灌注损伤中 TGF-β1 对神经细胞凋亡的调控。方法　在缺血及再灌注不同时间点用免疫组化及 RT- PCR方法观察缺血中心区及半影区 TGF-β1 蛋白及 m RNA表达的动态变化。结果　缺血中心区 TGF-β1 蛋白及 m RNA表达略有增强 ,而缺血半影区 TGF-β1蛋白及 m RNA表达明显增强 ,且在缺血再灌注 2 4 h及 48h达到高峰 ,与神经细胞凋亡趋势相符。结论　脑缺血时 ,TGF-β1 表达随梗塞区凋亡细胞的多少而变化 ,通过对神经细胞凋亡的调控 ,参与缺血后神经细胞的修复     

实验性脑缺血再灌注中TGF—β1免疫组化及分子生物学研究

目的 探讨脑缺再灌注损伤中TGF－β1对神经细胞凋亡的调控。方法 在缺血及再灌注不同时间点用免疫组化及RT－PCR方法观察缺血中心区及半影区TGF－β1蛋白及mRNA表达的动态变化。结果 缺血中心区TGF－β1蛋白及mRNA表达有增强，而缺血半影区TGF－β1蛋白及mRNA表达明显增强，且在缺血再灌注24h及48h达到高峰，与神经细胞凋亡趋势相符。结论 脑缺血时，TGF－β1表达随梗塞区凋亡细胞的多少而变化，通过对神经细胞凋亡的调控，参与缺血后神经细胞的修复。     

银杏内酯B对大鼠心肌缺血再灌注损伤后细胞凋亡及凋亡相关蛋白表达的影响

目的探讨银杏内酯B对大鼠心肌缺血再灌注损伤后细胞凋亡及相关蛋白表达的影响。方法将100只SD大鼠随机分为假手术组、模型组及银杏内酯B低剂量组(15mg/kg)、中剂量组(30mg/kg)、高剂量组(60mg/kg),每组20只。通过夹闭左冠状动脉前降支制作心肌缺血再灌注大鼠模型。监测各组大鼠心电图波动变化;红四氮唑(TTC)染色法测量心肌梗死体积;苏木精-伊红(HE)染色法观察心肌组织病理变化;末端标记法(TUNEL)观察细胞凋亡状况;免疫蛋白印记法测定凋亡相关蛋白(Bcl-2、Bax、激活型Caspase-3)表达。结果与模型组比较,银杏内酯B各剂量组心电图明显改善,其中银杏内酯B高剂量组基本恢复正常;银杏内酯B中剂量组、高剂量组心肌梗死体积显著降低(P<0.05或P<0.01),心肌组织病变明显改善,心肌细胞凋亡指数(AI)显著降低(P<0.01),Bcl-2蛋白表达显著上调(P<0.05或P<0.01),Bax和激活型Caspase-3蛋白表达显著下调(P<0.05或P<0.01),Bcl-2/Bax比值显著升高(P<0.01)。结论银杏内酯B通过调节凋亡相关蛋白表达从而抑制再灌注性损伤后心肌细胞凋亡。     

心肌重塑中AT1受体β1受体与PKC和MAPKs信号转导通路间关系的探讨

目的　探讨心肌重塑中AT1受体、β1受体与PKC和MAPKs信号转导通路间的关系 ,以进一步探讨心肌重塑的分子机制。方法　Wistar大鼠 2 4只 ,随机分为 4组 ,分别为假手术组、单纯心肌梗死组、氯沙坦组和倍他乐克组 ,结扎左冠状动脉前降支建立大鼠心肌梗死后心肌重塑模型 ,均观察 2 1d ,其中假手术组不结扎冠状动脉。心肌I型、III型胶原、纤维连接蛋白、c fos、细胞外信号调节激酶 (ERK)和蛋白激酶C(PKC)表达的变化均用免疫组织化学染色法和计算机图像分析进行检测分析。用RT PCR方法检测c fos受体mRNA表达的变化。结果　单纯梗死组心肌I型、III型胶原、纤维连接蛋白 (FN)、c fos、ERK1和PKC蛋白表达增强 ,与假手术组比较均有显著性差异 (P <0 0 5或P <0 0 1) ,且c fosmRNA表达增强 ;氯沙坦组心肌Ⅰ型、Ⅲ型胶原、FN、c fos、ERK1和PKC蛋白表达均比单纯梗死组显著减少 (P <0 0 5或P <0 0 1) ,c fosmRNA表达减弱 ,而倍他乐克组对PKC和ERK1表达无明显影响。结论　PKC和MAPK信号转导通路与心肌梗死后心肌重塑相关 ,其中心脏AT1受体与PKC和MAPK信号转导通路有关 ,而 β1受体与PKC和MAPK信号转导通路可能无关 ,其参与心肌重塑的信号转导通路有待进一步研究     

银杏叶提取物对大鼠脑缺血再灌注损伤热休克蛋白70表达的影响

目的探讨银杏叶提取物对大鼠缺血再灌注损伤热休克蛋白70表达的影响。方法42只大鼠随机分为3组:假手术组、单纯缺血再灌注组、缺血再灌注+银杏叶提取物组,每组14只。通过免疫组织化学方法和原位末端标记法(TUNEL)检测热休克蛋白70表达及凋亡细胞数,TTC染色观察梗死体积。结果3组均可检测到热休克蛋白70的表达,单纯缺血再灌注组热休克蛋白70的表达较假手术组增强(P<0.01),缺血再灌注+银杏叶提取物组较缺血再灌注组表达增强(P<0.05)。缺血再灌注+银杏叶提取物组梗死体积及凋亡细胞数明显少于缺血再灌注组(P<0.01)。结论银杏叶提取物可能通过上调缺血缺氧后热休克蛋白70的表达减少神经细胞凋亡。     

CDc25c在肝脏缺血再灌注损伤中的保护作用

目的探讨Cdc25c对肝脏缺血再灌注半脘氨酸蛋白酶(Caspase)-3蛋白表达的影响及与肝细胞凋亡的内在联系。方法健康30只SD大鼠随机分为空白对照组(S组);缺血再灌注+生理盐水组(I/R组);pAdEasy-Cdc25c+缺血再灌注组(C组),每组10只。Western印迹方法检测CDc25c、Caspase-3在肝脏组织中的表达;TUNEL法检测肝细胞凋亡。结果 I/R组中Caspase-3的蛋白表达及肝细胞凋亡明显多于S组(P<0.05);S和C组中Cdc25c的蛋白表达高于I/R组,而细胞凋亡低于I/R组(P<0.05)。结论 Cdc25c的表达降低Caspase-3蛋白的表达,抑制肝细胞凋亡,保护缺血再灌注肝损伤。     

大鼠肝脏缺血再灌注时肝细胞凋亡与Bcl-2蛋白表达的关系

目的 探讨肝脏缺血再灌注时肝细胞凋亡与Bcl—2蛋白表达的关系。方法 建立大鼠局部肝脏缺血再灌注模型，将72只健康雄性Wistar大鼠随机分为正常组、假手术组和缺血再灌注组，采用免疫组织化学法测定再灌注后不同时相中肝组织Bcl—2蛋白含量，用末端脱氧核苷酸转移酶介导的三磷酸脱氧尿苷(dUTP)缺口末端标记(TUNEL)法和透射电镜观察肝细胞凋亡状态。结果 再灌注后1、3、6、24h肝组织Bcl—2蛋白含量明显低于正常组及假手术组，并于3～6h达到其最低值；再灌注后1、3、6、24h肝细胞凋亡指数(HAI)则明显高于正常组和假手术组，并于3～6h达到高峰。再灌注后各时相中Bcl—2蛋白水平与HAI呈明显负相关。结论 在肝脏缺血再灌注时，Bcl—2蛋白表达水平异常下调，其抑制细胞凋亡的效能减弱，促使肝实质细胞凋亡增加，加重肝脏缺血再灌注损伤。     

菟丝子黄酮对缺血再灌注大鼠心肌细胞凋亡的影响

目的观察菟丝子黄酮对缺血再灌注大鼠心肌细胞凋亡及相关基因表达的影响。方法结扎大鼠冠状动脉左前降支30 min,再灌注2 h建立心肌缺血再灌注模型。将50只SD大鼠随机分为假手术组、缺血再灌注组及菟丝子黄酮低、高剂量组和消心痛组。再灌注结束后检测血清肌酸激酶和乳酸脱氢酶,DNA末端标记法计算凋亡指数,免疫组织化学法和Western Blotting法检测心肌Bcl-2和Bax蛋白表达,计算Bcl-2/Bax值。结果与假手术组比较,缺血再灌注组心肌酶肌酸激酶、乳酸脱氢酶和凋亡指数显著增高(P<0.01),Bcl-2和Bax蛋白表达增强(P<0.01);与缺血再灌注组比较,菟丝子黄酮低、高剂量组及消心痛组能降低血清肌酸激酶、乳酸脱氢酶含量和凋亡指数(P<0.01),增加Bcl-2而减少Bax的表达(P<0.01)。结论菟丝子黄酮能够抑制缺血再灌注损伤大鼠的心肌细胞凋亡,与消心痛效果相近。     

Studies on the mechanism of action of the bipyridine milrinone on the heart

Summary Milrinone is a positive inotropic and vasodilator agent when tested in experimental animals and in human heart-failure patients. It is generally believed that milrinone acts by inhibiting phosphodiesterase IV, thus increasing cyclic AMP, [Ca^{+ +}]_i and cardiac contractile force and relaxation. Maximal force produced by milrinone is greater when single-dose response curves are compared to cumulative dose-response curves. In vitro, milrinone produces a tachyphylaxis, the extent of which is both dose- and time-dependent. Recovery of tachyphylaxis is both dose- and time-dependent and is not influenced by inhibitors of protein or RNA synthesis. There is a specific cross-tachyphylaxis between milrinone and amrinone, theophylline, papaverine, and Bay K8644. This tachyphylaxis may explain the low maximal contractile response of the cumulative dose-response observed in isolated tissues. Milrinone increased cyclic AMP in dog and guinea pig cardiac muscle. As previously shown by Endoh et al. [17], milrinone in low doses produced a biphasic effect on cyclic AMP. The early increase (first 60–70 s) in cyclic AMP shows a good correlation with contractile force changes. If cyclic AMP is determined at maximal contractile force this correlation was poor. Here we also present instances where the increase in cyclic AMP after milrinone (determined at maximal effect) does not correlate with the contractile response. The cross-tachyphylaxis of milrinone with Bay K8644 suggests that milrinone has an action on the sarcolemmal Ca⁺⁺ channels. Bay K8644 suppresses the positive inotropic effect of catecholamines by 50%, but not the cyclic AMP response. The inotropic effect of milrinone, in contrast to norepinephrine is highly sensitive to [Ca⁺⁺]₀, stimulation rate, and [K⁺]₀. In this respect milrinone behaves more like Bay K8644. We postulate that the main inotropic action of milrinone is due to a sarcolemmal effect. The early cyclic AMP production described could be in the sarcolemmal compartment and this may explain some of the similarities of milrinone’s actions with those of Bay K8644. The tachyphylaxis observed with the inotropic effect of milrinone does not extend to the decreases in relaxation time. This and other findings to be discussed suggest that the positive inotropic and reduction in relaxation time by milrinone depend on different mechanisms, possibly through differential compartmentalization of cyclic AMP.     

锌对心肌保护作用机理的探讨

应用电镜、电子示踪技术和立体计量测试法，从形态学上观察异丙基肾上腺素对心肌膜系统的影响及锌的保护作用，同时应用标准玻璃微电极技术和微机实时分析方法，研究异丙基肾上腺素致心肌损伤及锌对心肌保护作用的机理。实验结果表明：异丙基肾上腺素可引起心肌细胞膜系统损伤，此时心肌细胞的去极化和复极化过程均发生改变；经锌前处理后，心肌损伤程度明显减轻，心肌细胞的复极化过程得到明显改善。锌对心肌的保护作用，主要是通过阻断心肌细胞膜慢通道、减少平台期钙离子内流、防止细胞内钙超载来实现。     

丙硫咪唑对囊尾蚴糖原作用的观察

猪囊尾蚴于体外经驱虫药丙硫味唑在0,20,50,100μg/ml和96小时作用后,进行了组织化学观察。对照组囊尾蚴的糖原分布在头颈部和外囊壁上,颈部区糖原分布较均匀,外囊壁糖原较多。实验各组头颈部糖原均有减少,而外囊壁糖原无显著变化。     

Data on the spread of Culex pipiens on the territory of the USSR]

A map of Culex pipiens molestus distribution over the USSR was made using data of sanitary epidemiological stations of various regions of the country, literature and the authors' own data. It was shown that during the last decades (1978-1990) the Cx. p. molestus breeding occurring predominantly in flooded basements of comfortable houses, especially in new built towns and cities, was recorded throughout the European part of the USSR including some subarctic regions. Cx. p. molestus is also widespread in the Asiatic part of the country including Western and Eastern Siberia, southern regions of Far East and the Sakhalin Island and Kamchatka. In the permafrost areas, most of new houses are built on piles without basements and cellars, and it prevents Cx. p. molestus breeding. The dates of appearance of these mosquitos in various parts of the country due to the development of transportation are discussed.     

Comments on the effect of variations in the size of the heart on the magnitude of ECG potentials

Utilizing a mathematical model of the inhomogeneous torso, the effect of variations in the size of the heart on the amplitude of the surface potential is studied. The results show that incases of congestive heart failure, low potentials may result in spite of the cardiomegaly. This can be explained by the increased lung conductivity due to edema.