Explore the vast range of titles available.

目的观察不同参数的低频脉冲电刺激对B16-F10黑色素瘤小鼠的抑瘤效应,评估其对心脏结构及功能的影响。方法将由B16F10细胞接种产生的荷瘤BALB/c小鼠随机分为4组。治疗组选择场强20V/cm,脉宽1ms,频率分别为10Hz（10Hz组）、20Hz（20Hz组）和25Hz（25Hz组）的脉冲电刺激作用于荷瘤小鼠30min/d,以不用电刺激为对照组（每组10只）,治疗时监测各小鼠心电图变化情况。脉冲电刺激荷瘤小鼠7d后比较各组肿瘤体积及生存期的变化,HE染色观察肿瘤及心脏组织形态学变化,免疫组化法比较各组小鼠肿瘤组织中S-100B蛋白的表达变化,ELISA法检测小鼠血清肌钙蛋白T（c Tn T）及肌酸激酶同工酶（CK-MB）的水平变化。结果低频脉冲电刺激治疗15d后,10Hz组、20Hz组和25Hz组的肿瘤体积分别为463.0±33.0、248.6±34.6和229.9±15.9mm^3,显著小于对照组（2027.0±133.4mm^3,P〈0.05）,且20Hz组生存率延长率（67.4%）明显高于10Hz组（15.5%）和25Hz组（8.8%）;随着频率增加,S-100B蛋白表达依次减少;25Hz组小鼠心律失常评分及血清c Tn T、CK-MB水平显著高于对照组（P〈0.05）;10Hz组和20Hz组小鼠心律失常评分及血清c Tn T、CK-MB表达与对照组比较差异无统计学意义（P〉0.05）。结论低频脉冲电刺激对小鼠黑色素瘤具有抑瘤作用,在20V/cm、20Hz时抑制作用最强,且不影响小鼠正常的心电活动。

目的 探讨舒芬太尼预处理对大鼠心肌缺血再灌注损伤的影响以及JAK2-STAT3信号通路的作用.方法 雄性SD大鼠60只,体质量250～300 g,随机均分为假手术组（S组）、缺血再灌注组（I/R组）、舒芬太尼预处理组（SPC组）、舒芬太尼预处理联合JAK2激酶抑制剂组（S＋A组）及JAK2激酶抑制剂组（A组）.采用结扎冠状动脉左前降支的方法制作心肌缺血再灌注模型.SPC组于心肌缺血前股静脉泵注舒芬太尼1μg/kg,泵注5 min,间隔5 min,重复处理3次,总量共3 μg/kg;S＋A组：舒芬太尼预处理前5 min给予JAK2激酶抑制剂AG490（1 mg/kg）,缺血前30min舒芬太尼预处理;A组：缺血前35 min给予JAK2激酶抑制剂AG490（1 mg/kg）.心肌缺血前30min（T0）、缺血前即刻（T1）、缺血30 min（T2）、再灌注30 min（T3）和再灌注120 min（T4）时记录心率（HR）和平均动脉压（MAP）.再灌注120 min抽取动脉血,离心取血清测定肌酸激酶同工酶（CK-MB）和乳酸脱氢酶（LDH）.实验结束时,各组取6只大鼠心脏测算心肌梗死面积,其余6只大鼠采用Western blot测定心肌组织磷酸化STAT3 （P-STAT3）的表达.结果 比较各组间不同时点HR的差异无统计学意义（P＞0.05）.与S组相比,其余各组T2～T4时MAP降低（P＜0.05或P＜0.01）;血清CK-MB和LDH活性明显增高（P＜o.01）.与I/R组相比,SPC组MAP数值稍高,但差异无统计学意义;CK-MB和LDH活性降低（P＜0.01）;心肌梗死范围减小（P＜0.01）.与S组比较,I/R组和SPC组P-STAT3表达上调（P＜0.01）,且SPC组上调高于I/R组（P＜0.01）.结论 舒芬太尼预处理减轻大鼠心肌缺血再灌注损伤的机制可能与激活JAK2-STAT3信号通路、上调P-STAT3的表达有关.

目的探讨糖尿病对缺血预适应（IPC）大鼠心肌缺血再灌注（I/R）的影响及其可能机制。方法取糖尿病SD大鼠及非糖尿病SD大鼠各30只,建立冠状动脉阻断的在体心肌I/R模型,各分为3组（n=10）：假手术（Sham）组开胸后穿线做套环,但不收紧结扎线,持续155min,全程旷置作为基础水平对照;I/R组手术穿线平衡35min后,持续收紧结扎冠状动脉主干造成缺血30min,放松后行再灌注90min;IPC组手术穿线平衡35min后,缺血5min,再灌注5min,反复3次,而后重复I/R组操作。测定各组缺血前及实验结束后的血清肌酸激酶（CK）、乳酸脱氢酶（LDH）水平,心肌组织丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性,心肌梗死范围以及心肌葡萄糖摄取率。结果非糖尿病大鼠中,I/R组和IPC组CK、LDH活性及MDA含量显著高于Sham组（P〈0.01或P〈0.05）,且I/R组显著高于IPC组（P〈0.05或P〈0.01）;I/R组及IPC组SOD活性显著低于Sham组（P〈0.01）,且I/R组显著低于IPC组（P〈0.05）;IPC组心肌梗死面积显著低于I/R组（P〈0.05）,而心肌葡萄糖摄取率显著高于I/R组（P〈0.05）。在糖尿病大鼠中,IPC组与I/R组的上述指标比较均无统计学差异（P〉0.05）。结论糖尿病可抑制IPC对在体大鼠缺血再灌注心肌的保护作用,其机制可能与心肌胰岛素抵抗有关。

目的观察香椿子总多酚预处理对大鼠心肌缺血再灌注损伤是否具有干预作用。方法 50只SD大鼠随机均分成5组（n=10）：假手术组,模型组,香椿子总多酚预处理低、中、高剂量组,后3组分别给予香椿子总多酚50、100、200mg/kg,假手术组和模型组分别给予等体积5‰羧甲基纤维素钠,各组均灌胃给药7d。灌胃结束后,模型组和香椿子总多酚预处理组采用左冠状动脉前降支结扎30min再灌120min的方法复制大鼠心肌缺血再灌注损伤模型,假手术组只穿线不结扎。记录冠脉结扎前、结扎后30min及再灌注30、60、90min心电图,比较各组大鼠心电图J点抬高的程度。再灌注结束时腹主动脉取血,测定血清中磷酸肌酸激酶（CK）活力,肌钙蛋白I（cTnI）、血栓素B2（TXB2）和6-酮-前列腺素F1α（6-keto-PGF1α）含量。最后,取出心脏,自结扎线以下平行均匀切成5片,用1%氯化三苯基四氮唑（TTC）染色15min,测定心肌梗死程度。结果与假手术组比较,模型组大鼠的心电图J点显著抬高,血清中CK活力和cTnI、TXB2含量显著升高,6-keto-PGF1α水平显著下降（P〈0.05）,出现了明显的心肌梗死。与模型组相比,香椿子总多酚各预处理能显著降低心肌缺血再灌注大鼠心电图J点抬高的程度,降低血清中CK活力及cTnI、TXB2含量,升高血清中6-keto-PGF1α水平,减轻心肌梗死程度,差异具有统计学意义（P〈0.05）。结论香椿子总多酚预处理对大鼠心肌缺血再灌注损伤具有干预作用。

目的探讨5-脂氧合酶（5-CO）选择性抑制剂齐留通（zileuton）对缺血再灌注心肌的保护作用及其可能机制。方法健康成年雌性SD大鼠30只，随机分为假手术组（s组，g／=10）、缺血再灌注组（I／R组，n=10）、齐留通组（Z组，n=10），采用结扎前降支造成缺血45min、松开结扎线灌注120min的方法建立缺血再灌注模型。Z组于手术前15min给予3mg／kg齐留通。再灌注结束后处死动物，HE染色观察心肌的病理损伤情况，TUNEL法检测心肌细胞凋亡率，ELISA法检测血浆中白三烯B4（LTB4）、IL-1p、TNF-a的含量，Westernblotting和免疫荧光法检测中性粒细胞中的5-LO分布变化。结果与I／R组比较，齐留通处理可以明显减轻缺血再灌注所致的心肌病理损伤，降低心肌细胞凋亡率，降低血浆中炎症因子LTB4、IL-1p和TNF-d的水平，抑Ns-LO的激活转位，差异有统计学意义（P〈0．05），但各组5-LO表达总量无明显差异（P〉0．05）。结论齐留通对缺血再灌注心肌具有一定的保护作用，其机制可能与抑制5-LO转位激活，进而减轻炎症损伤、抑制心肌凋亡有关。

目的探讨磷酸肌酸（PCr）对糖尿病大鼠心肌缺血再灌注损伤（MIRI）心功能的影响。方珐建立糖尿病8周大鼠模型，随机分为4组：假手术组（I）、MIRI＋生理盐水组（Ⅱ）、MIRI＋PCr单次注射组（Ⅲ）、MIRI＋PCr多次注射组（Ⅳ），测定各组的左室收缩压（LVSP）、左室压上升最大速率（＋dp／dtmax）、左室压下降最大速率（-dp／dtmax）和左室舒张末压（LVEDP）来评价心功能的变化。结果与Ⅰ组相比，Ⅱ、Ⅲ、Ⅳ组的LVSP和＋dp／dtmax均呈下降趋势，Ⅱ组数值下降明显（P〈O．01），Ⅲ、Ⅳ组数值下降较缓（P〈0．05）；与Ⅱ组相比，Ⅲ、Ⅳ组数值较大（P〈0．05）；UI组和Ⅳ组比较无统计学差异（P〉0．05）。与I组相比，Ⅱ、Ⅲ、Ⅳ组dp／dtmax和LVEDP均呈上升趋势，Ⅱ组上升明显（P〈O．01），Ⅲ、Ⅳ组上升较缓（P〈0．05）；与Ⅱ组相比，Ⅲ、Ⅳ组数值均较小（P〈O．05）；且Ⅲ、Ⅳ组之间也有差异（P〈0．05）。结论PCr能够改善糖尿病大鼠MIRI的心功能，多次给药作用更优。

Overload-exercise （OE） causes myocardial injury through inducing autophagy and apoptosis. In this study we examined whether an autophagy inhibitor 3-methyladenine （3-MA） could alleviate OE-induced cardiac injury. Rats were injected with 3-MA （15 mg/kg, iv） or saline before subjected to various intensities of OE, including no swim （control）, 2 h swim （mild-intensity exercise, MIE）, 2 h swim with 2.5% body weight overload （moderate OE; MOE）, 5% overload （intensive OE; IOE） or 2.5% overload until exhausted （exhaustive OE; EOE）. After OE, the hearts were harvested for morphological and biochemiacal analysis. The cardiac morphology, autophagosomes and apoptosis were examined with H＆E staining, transmission electron microscopy and TUNEL analysis, respectively. Autophagyrelated proteins to （LC3-Ⅱ/Ⅰ and Beclin-1） and apoptosis-related proteins （Bci-2/Bax） were assessed using Western blotting. Our results showed that compared with the control, MIE did not change the morphological structures of the heart tissues that exhibited intact myocardial fibers and neatly arranged cardiomyocytes. However, IOE resulted in irregular arrangement of cardiomyocytes and significantly increased width of cardiomyocytes, whereas EOE caused more swollen and even disrupted cardiomyocytes. In parallel with the increased OE intensity （MOE, IOE, EOE）, cardiomyocyte autophagy and apoptosis became more and more prominent, evidenced by the increasing number of autophagosomes and expression levels of LC3-Ⅱ/Ⅰ and Beclin-1 as well as the increasing apoptotic cells and decreasing Bcl-2/Bax ratio. 3-MA administration significantly attenuated OE-induced morphological changes of cardiomyocytes as well as all the autophagy- and apoptosis-related abnormalities in MOE, IOE and EOE rats. Thus, the autophagy inhibitor 3-MA could alleviate OE-induced heart injury in rats.

Aim： We have shown that low-dose gadolinium chloride （GdCI3） abolishes arachidonic acid （AA）-induced increase of cytoplasmic Ca2＋, which is known to play a crucial role in myocardial ischemia/reperfusion （I/R） injury. The present study sought to determine whether low-dose GdCI3 pretreatment protected rat myocardium against I/R injury in vitro and in vivo. Methods： Cultured neonatal rat ventricular myocytes （NRVMs） were treated with GdCI3 or nifedipine, followed by exposure to anoxia/ reoxygenation （A/R）. Cell apoptosis was detected; the levels of related signaling molecules were assessed. SD rats were intravenously injected with GdCI3 or nifedipine. Thirty min after the administration the rats were subjected to LAD coronary artery ligation followed by reperfusion. Infarction size, the release of serum myocardial injury markers and AA were measured; cell apoptosis and related molecules were assessed. Results： In A/R-treated NRVMs, pretreatment with GdCl3 （2.5, 5, 10 pmoVL） dose-dependently inhibited caspase-3 activation, death receptor-related molecules DR5/Fas/FADD/caspase-8 expression, cytochrome c release, AA release and sustained cytoplasmic Ca2＋ increases induced by exogenous AA. In I/R-treated rats, pre-administration of GdCl3 （10 mg/kg） significantly reduced the infarct size, and the serum levels of CK-MB, cardiac troponin-I, LDH and AA. Pre-administration of GdCl3 also significantly decreased the number of apoptotic cells, caspase-3 activity, death receptor-related molecules （DR5/Fas/FADD） expression and cytochrome c release in heart tissues. The positive control drug nifedipine produced comparable cardioprotective effects in vitro and in vivo. Conclusion： Pretreatment with low-dose GdCl3 significantly attenuates I/R-induced myocardial apoptosis in rats by suppressing activation of both death receptor and mitochondria-mediated pathways.

To the Editor： In a single-center, prospective randomized clinical study including 122 elderly patients undergoing the carotid endarterectomy （CEA）, Wang et al. showed that compared with propofol-based total intravenous anesthesia, low-dose sevoflurane inhalation along with propofol reduced the incidence of postoperative myocardial injury.

Aim： To evaluate the effects of aldosterone with or without high sodium intake on blood pressure, myocardial structure and left ven- tricular function in rats, and to investigate the mechanisms underlying the effects. Methods： Eight-week-old male Sprague-Dawley rats were randomly divided into 3 groups： （1） control （CON） group fed a normal sodium diet, （2） aldosterone （ALD） group receiving aldosterone infusion and a normal sodium diet, and （3） high sodium plus aldosterone （HS- ALD） group receiving 1% NaCI diet in conjunction with aldosterone infusion. Aldosterone was administered through continuously sub- cutaneous infusion with osmotic minipump at the rate of 0.75 pg/h for 8 weeks. The myocardium structure was observed using transt- horacic echocardiography and transmission electron microscopy. The collagen deposition in left ventricle was evaluated with Masson＇s trichrome staining. The expression of IL-18, p22phox, and p47phox proteins was examined using Western blot analysis. Results： The systolic blood pressure in the ALD and HS-ALD groups was significantly higher than that in the CON group after 2-week treatment. But the blood pressure showed no significant difference between the HS-ALD and ALD groups. The left ventricular hyper- trophy, myocardial collagen deposition and oxidative stress were predominantly found in the HS-ALD and ALD group. Furthermore, the breakdown of myocardial structure and oxidative stress were more apparent in the HS-ALD group as compared with tho~e in the ALD group. Conclusion： Long-term infusion of aldosterone results in hypertension and profibrotic cardiovascular responsesin rats fed a normal sodium diet, which were mediated by oxidative stress. High-sodium intake could aggravate myocardial injuries induced by aldosterone.