稳心颗粒对心肌梗死大鼠血管内皮细胞超微结构的影响

目的观察稳心颗粒对心肌梗死大鼠内皮细胞超微结构的影响。方法将30只SD大鼠随机分为对照组,心肌梗死模型组,心肌梗死模型+稳心颗粒组,每组10只大鼠。测定大鼠血浆NO及ET-1含量变化,观察血管内皮细胞超微结构的改变。结果与对照组比较,心肌梗死模型组大鼠血浆ET-1含量明显增加(P<0.01),血浆NO含量明显减少(P<0.01),线粒体肿胀,肌浆网扩张,内皮脱落。与心肌梗死模型组比较,心肌梗死模型+稳心颗粒组大鼠血浆ET-1的含量明显降低(P<0.01),血浆NO的含量明显增加(P<0.01),内皮细胞出现线粒体肿胀和内质网扩张明显减少,无内皮脱落。结论稳心颗粒对心肌梗死大鼠血管内皮细胞超微结构具有保护作用,这种保护作用与稳心颗粒使NO及ET-1的含量发生变化有关。     

甲亢和甲减患者血浆NO、ET水平与心功能相关性研究

目的 探讨甲状腺功能亢进症（甲亢）和甲状腺功能减退症（甲减）患者血浆一氧化氮（NO）、血管内皮索（ET）水平及其与心功能的相关性。方法 分别用比色法、放射免疫法测定甲亢患者（甲亢组）和甲减患者（甲减组）及正常人（对照组）血浆NO、ET和血清游离三碘甲状腺原氨酸（FT3）、游离甲状腺索（FT4）和超敏促甲状腺激素（sTSH）浓度；同时采用多普勒元创心排量检测心功能指标：每搏输出量（SV）、心输出量（CO）、射血分数（EF）、心指数（CI）。结果 甲亢组和甲减组患者血浆NO浓度均比对照组明显升高（P〈0．01）；甲亢组血浆ET浓度比对照组明显升高（P〈0．01），甲减组比对照组明显降低（P〈0．01）；甲亢组各心功能指标比对照组高（P〈0．01），而甲减组比对照组低（P〈0．01）。经相关分析显示，甲亢组NO与CI呈正相关，ET与EF、CI呈正相关；甲减组NO与CI呈负相关。结论 血浆NO和ET浓度变化参与自身免疫性甲状腺疾病的病理生理机制：不同的甲状腺功能状态下血浆NO和ET浓度对心功能产生不同影响。     

MBMC 移植对扩张型心肌病慢性心力衰竭大鼠血中 NO、ET-1 和 CEC 的影响

目的：研究骨髓单个核细胞（MBMC）移植对实验性扩张型心肌病慢性心力衰竭大鼠血一氧化氮（NO）、内皮素-1（ET-1）和循环内皮细胞（CEC）的影响。方法：建立扩张型心肌病慢性心力衰竭大鼠模型。实验组直接心肌注射DAPI标记过的MBMC。于造模后即刻、移植后4和12周,行血NO、ET-1、CEC检测。结果：实验组移植前血浆NO、ET-1及CEC水平与对照组比较无显著性差异（P〉0.05）。造模成功大鼠血浆NO水平明显降低,ET-1及CEC水平明显升高,与移植前比较有显著性差异（P〈0.05）。MBMC移植术后4周、12周时,大鼠血浆NO水平继续升高,ET-1及CEC水平持续下降,与移植前、造模成功后4周时比较有显著性差异（P〈0.05）。结论：①该大鼠模型有严重的血管内皮损伤;②MBMC移植对其血管内皮损伤具有明显的修复作用;③血中NO、ET-1、CEC水平检测,可作为判断血管内皮损伤程度、评价疗效、判断预后的指标。     

大鼠慢性肾缺血时心肌组织ET-1、CGRP、NO含量与心功能关系的研究

目的研究肾动脉狭窄时心肌组织ET-1、CGRP和NO含量与心功能变化的关系。方法将Wistar大鼠随机分为狭窄组（n=30）和假手术组（n=10）,其中狭窄组在左右肾动脉之间结扎腹主动脉（狭窄程度50％）。于术后16周测定大鼠血液动力学指标,分析心肌组织中ET-1、CGRP和NO含量变化以及与心功能的关系。结果大鼠左右肾动脉之间结扎腹主动脉使狭窄组单侧肾脏萎缩、血压持续升高,左室收缩及舒张功能下降、左室重量指数增加。术后16周时,与假手术组相比,狭窄组心肌组织ET-1含量明显增高（P〈0．01）,CGRP含量明显下降（P〈0．01）,NO含量略下降（P〉0．05）;心肌组织ET-1含量与左室＋dp／d．t max呈负相关（r=-0．37,P〈0．05）。结论大鼠腹主动脉狭窄导致的慢性肾缺血,可使心肌组织ET-1含量增高、CGRP和NO含量下降,其中ET-1含量与大鼠左室收缩呈负相关。     

扩张型心肌病患者内皮功能与抗氧化功能变化的研究

目的观察扩张型心肌病（DCM）患者内皮功能与抗氧化功能变化，探讨二者变化在DCM发生发展中的相互作用。方法选择DCM64例，并以32例健康人做对照。取空腹静脉血，测定红细胞谷胱甘肽过氧化物酶（RBCGSH—Px）、红细胞超氧化物岐化酶（RBCSOD）活性及血清一氧化氮合成酶（NOS、iNOS、cNOS）活性；测定血浆内皮素（ET）及血清一氧化氮（NO）、脂质过氧化物（LPO）含量。结果DCM患者ET及NO含量明显高于对照组（P〈0．01），心衰组高于无心衰组（P〈0．05）。NOS、iNOS和cNOS活性明显高于对照组（P〈0．05），NOS和iNOS活性心衰组高于无心衰组（P〈0．05）。RBCGSH．Px及RBCSOD活性比对照组明显降低（P〈0．01），LPO含量比对照组明显升高（P〈0．01），RBCGSH—Px／LPO及RBCSOD／LPO比值比对照组明显变小（P〈0.01）。结论内皮功能失调与抗氧化功能降低以及两者间的相互作用与DCM发生发展有密切关系。     

尿激酶溶栓治疗急性脑梗死患者血浆NO、ET和D-二聚体含量变化及临床意义

目的 探讨急性脑梗死患者尿激酶溶栓治疗前后血浆一氧化氮（NO）、内皮素（ET）和D-二聚体含量动态变化及临床意义。方法 测定38例急性脑梗死患者溶栓前及溶栓后2h、4h、24h、48h血标本NO、ET和D-二聚体含量，并与正常对照组33例进行比较。结果 脑梗死患者NO含量明显低于正常对照组（P〈0．01），血浆ET和D-二聚体含量显著高于对照组（P〈001和P〈0．05）。溶栓后有效组24h后NO明显升高，与溶栓前差异有统计学意义，而无效组无显著变化。有效组4h后ET明显下降，以后降幅较小，但明显低于无效组。结论 血浆NO、ET和D-二聚体含量可以作为急性脑梗死的诊断指标，溶栓治疗后NO、ET与D-二聚体水平变化对判断疗效有一定指导意义。     

丹红注射液对急性冠脉综合征患者血管内皮功能的影响

目的：探讨丹红对急性冠脉综合征（ACS）患者血管内皮功能的影响。方法：62例急性冠脉综合征患者分成丹红组32例，常规组30例。丹红组在常规治疗基础上每天加用丹红注射液20ml共3周，常规组仅予普通治疗。另选同期健康体检者30名作为正常组。使用高分辨B超检测3组肱动脉内皮依赖性舒张功能，比较各组一氧化氮（NO）和血浆内皮素-1（ET-1）的水平及丹红组与常规组治疗结束前1周心绞痛发作的频率。结果：ACS患者肱动脉血流介导性舒张（FMD）功能较正常人明显减弱，ET-1水平明显高于正常人，NO低于正常人（P〈0．05）；治疗后2组FMD功能明显增强，NO增加，ET-1含量显著减少（P〈0．05），丹红组以上改善优于常规组，2组比较差异有统计学意义（P〈0．05）；丹红组疗程结束前1周平均心绞痛发作次数较常规组低（P〈0．01），次数减少与FMD功能增强、NO增加及ET-1含量减少有明显相关性（P〈0．05）。结论：丹红能够改善急性冠脉综合征患者的血管内皮功能。     

高糖、高胰岛素与糖尿病血管并发症的关系

目的 探讨高糖血症、高胰岛素血症对ET－1缩血管作用的影响及机制。方法 复制大鼠高糖血症模型,观察高糖组和对照组大鼠的主动脉血管环在40mIU／L胰岛素中对10^-9mol/L ET－1的反应;测定血浆NO2^-含量和血管壁一氧化氮合酶（NOS）的活性。结果 高糖大鼠对ET－1的缩血管反应明显强于对照组（P＜0．05）;高糖组NO2^-含量和tNOS活性明显低于对照组,其中以cNOS降低为主（P＜0．01）。结论 长期高糖血症通过损伤血管内皮功能使NO合成减少,血管对活性物质ET－1的反应性增强、血管张力增加,此机制可能参与了动脉粥样硬化等血管并发症的发病。     

2型糖尿病患者血清肝细胞生长因子变化与血管内皮功能的关系

目的探讨血清肝细胞生长因子（HGF）与血管内皮功能在2型糖尿病（DM）患者体内的关系。方法将48例2型DM患者分为单纯DM组和伴血管病变的DM组各24例，同时用20名体检健康者作为对照，检测其血糖、血清HGF、NO及血浆内皮素（ET）水平。结果与对照组比较，单纯DM组和伴血管病变的DM组血清HGF、血浆内皮素（ET）含量显著升高，血清NO水平显著下降（P〈0．05）。与单纯DM组比较，伴血管病变的DM组血清HGF、NO和血浆ET改变显著，差异有统计学意义（P〈0．05）。相关分析显示，血清HGF水平与患者的ET水平呈正相关，与NO水平呈负相关（spearman相关系数分别为0．728和-0．675，P均〈0．01）。结论血清HGF水平反映了2型DM患者的血管内皮受损程度，可用于临床上监测DM患者的血管病变情况。     

冠心病患者外周血肿瘤坏死因子、一氧化氮与血浆内皮素的关系及临床意义

目的探讨冠心病患者外周血肿瘤坏死因子-α（TNF-α）、一氧化氮（NO）和血浆内皮素（ET）的关系与临床意义。方法检测82例冠心病患者（急性心肌梗死32例，不稳定型心绞痛36例，稳定性心绞痛16例）与30例健康体检者TNF-α、NO和ET的含量，并进行分析比较。结果与正常对照组比，较冠心病患者TNF-α和ET均显著升高（P〈0．05或P〈0．01），而NO均显著降低（P〈0．05或P〈0．01）。结论TNF-α、NO和ET均参与冠心病的病理过程及发生发展，ET与其他两个指标存在相互联系、相互影响，三个指标水平的高低变化与病情轻重均呈现出一定的关系。     

裙带菜膳食纤维对高血脂大鼠血管内皮功能的影响

目的研究裙带菜可溶性膳食纤维对高脂血症大鼠内皮功能的影响。方法40只大鼠分为4组(n=10):正常对照组,高脂模型组,膳食纤维低剂量组(5%),膳食纤维高剂量组(10%);经裙带菜可溶性膳食纤维处理8w后,检测离体血管的内皮依赖性舒张效应,血浆丙二醛(MDA),一氧化氮(NO),内皮素-1(ET-1)水平,并用Western blotting检测内皮型一氧化氮合酶(eNOS)蛋白表达水平。结果裙带菜可溶性膳食纤维显著降低MDA,ET-1水平,显著改善内皮功能及血浆NO的水平并伴随着eNOS蛋白表达水平的上调。结论裙带菜可溶性膳食纤维能改善高脂血症大鼠的血管内皮功能,这可能与其降低ET-1水平,增加NO的产生有关。     

高胆固醇膳食对兔动脉壁一氧化氮合成的影响

动脉内皮及其一氧化氮（NO）代谢正常与否，对维持正常的血管功能至关重要。高脂高胆固醇膳食对动脉壁内皮一氧化氮（NO）合成的影响尚无定论。本研究在雄性纯种新西兰兔中，观察高脂高胆固醇膳食对动脉内皮壁一氧化氮合成影响。结果表明：高脂高胆固醇膳食8周后，内皮型一氧化氮合酶（eNOS）mRNA表达下降、总NOS活力减弱、血浆一氧化氮代谢产物（NOP）水平降低（P＜0．05）；血浆超氧歧化酶（SOD）减低，内皮素（ET）水平上升。结果提示：高脂高胆固醇膳食引起高脂血症，可损害动脉内皮，降低NO合成酶的基因表达，抑制NO的合成。     

beta-carotene attenuates the paradoxical effect of tobacco smoke on the mortality of rats after experimental myocardial infarction

The objective of this study was to investigate the effects of exposure to tobacco smoke (ETS) in rats that were or were not supplemented with dietary beta-carotene (BC), on ventricular remodeling and survival after myocardial infarction (MI). Rats (n = 189) were allocated to 4 groups: the control group, n = 45; group BC administered 500 mg/kg diet, n = 49, BC supplemented rats; group ETS, n = 55, rats exposed to tobacco smoke; and group BC+ETS, n = 40. Wistar rats weighing 100 g were administered one of the treatments until they weighed 200 to 250 g (approximately 5 wk). The ETS rats were exposed to cigarette smoke for 30 min 4 times/d, in a chamber connected to a smoking device. After reaching a weight of 200-250 g, rats were subjected to experimental MI (coronary artery occlusion) and mortality rates were determined over the next 105 d. In addition, echocardiographic, isolated heart, morphometrical, and biochemical studies were performed. Mortality data were tested using Kaplan-Meyer curves and other data by 2-way ANOVA. Survival rates were greater in the ETS group (58.2%) than in the control (33.3%) (P = 0.001) and BC+ETS rats (30.0%) (P = 0.007). The groups did not differ in the other comparisons. Left ventricular end-diastolic diameter normalized to body weight was greater and maximal systolic pressures were lower in the ETS groups than in non-ETS groups. Previous exposure to tobacco smoke induced a process of cardiac remodeling after MI. There is a paradoxical protector effect with tobacco smoke exposure, characterized by lower mortality, which is offset by BC supplementation.     

Food restriction does not impair myocardial mechanics during the healing period of myocardial infarction in the rat

Papillary muscle mechanics were studied in 4 groups of rats: control (C) noninfarcted (n = 9), C infarcted (n = 9), food-restricted (FR) noninfarcted (n = 8) and FR infarcted (n = 9). Food-restricted animals were fed with 50% of chow consumed by the C rats. Myocardial infarction (MI) was promoted 6 weeks after food restriction, and myocardial contraction and relaxation were studied 3 weeks thereafter. Interestingly, MI size was larger (P < .04) in C (50% ± 8%) than in FR (40% ± 10%) rats. Maximal developed tension, rate of tension rise and decay, resting tension, and time to 50% relaxation studied at calcium concentrations of 0.5, 1.0, 1.5, 2.0, and 2.5 mmol/L were essentially similar in the 4 groups. Infarcted and noninfarcted FR rats presented longer time to peak tension. These unprecedented data indicated that food restriction (1) seems to engender myocardial protection against ischemia/reperfusion injury and (2) does not affect myocardial mechanical function at the end of the healing period of MI.     

超短肠大鼠结肠代偿的细胞超微结构变化

目的 观察超短肠大鼠结肠黏膜细胞超微结构和吸收功能的变化.方法 将30只雄性SD大鼠随机分为超短肠组（手术切除大鼠90%～95%的小肠）、假手术组和正常对照组,每组10只.给予肠内营养支持21 d后,采用扫描电镜观察结肠黏膜表画形态,透射电镜观察结肠黏膜上皮细胞超微结构变化.用D-木糖溶液和15N-甘氨酸对结肠进行封闭式连续循环灌注3 h,测定结肠对水、碳水化合物、氨基酸的吸收情况.结果 透视电镜观察结果显示,超短肠组大鼠较正常大鼠的结肠黏膜杯状细胞减少,吸收上皮细胞增多,微绒毛变长变密,细胞膜表面积增加,细胞间连接明显增多,桥粒、紧密连接和缝隙连接较多,内质网和高尔基体发达,线粒体数量明显增多.扫描电镜观察结果显示,超短肠组大鼠较正常大鼠的结肠皱襞深度增加,黏膜增厚,隐凹开口明显增多;隐凹内微绒毛样结构数目明显增多,长度增长且密度增加.超短肠组大鼠结肠对水的吸收能力明显高于假手术组和正常对照组（P均=0.000）;1、2、3 h内木糖吸收率和15N-甘氨酸吸收率均明显高于假手术组和正常对照组（P均＜0.01）.结论 超短肠大鼠结肠吸收能力可代偿增强.结肠黏膜细胞凋亡减少、吸收细胞增多、微绒毛增生、细胞膜表面积增加和线粒体增多可能是其物质和能量基础.     

Vascular changes in the human endometrium following the administration of the progesterone antagonist RU 486

Eleven healthy women were assigned to one of two groups. They received 50 mg RU 486 orally per day either on cycle days 7 to 10 (preovulatory group n = 5) or on cycle days 20 to 23 (postovulatory group, n = 6). An endometrial biopsy was taken on the fourth day of the RU-treatment in the preovulatory group and on the second (n = 2) or fourth (n = 4) treatment day in the postovulatory group. Biopsies from 34 untreated women representing matched samples from early and mid preovulatory phase (n = 10) and mid and late postovulatory phase (n = 24) were used as control. The ultrastructure of the endometrial capillaries was investigated by morphometric methods. The administration of RU 486 during the preovulatory phase did not modify the vascular structure. However, when given in the postovulatory phase, necrosis occurred in the capillary endothelial cells with and without regressive changes of the adjacent stroma. The area and diameter of the capillary lumen and the area of the adventitia was smaller than in the control material (p less than 0.01). The result of the study suggests that RU 486, when administered in the postovulatory phase, directly affects the capillary vessels of the endometrium.     

Retinoic acid supplementation attenuates ventricular remodeling after myocardial infarction in rats

The objective of this study was to evaluate the role of retinoic acid in experimental postinfarction myocardial remodeling. Wistar rats were subjected to myocardial infarction (MI) and treated with retinoic acid (RA), 0.3 mg/(kg x d) (MI-RA, n = 29), or fed a control diet (MI, n = 34). After 6 mo, the surviving rats (MI-RA = 18 and MI = 22) underwent echocardiograms, and isolated hearts were tested for function in vitro. The cross-sectional area of the myocyte (CSA) and interstitial collagen fraction (IC) were measured in a cross section of the heart stained by hematoxylin-eosin and picrosirius red, respectively. The CSA was smaller in the MI-RA group [229 (220,234) microm2] [medians (lower quartile, upper quartile)] than in the MI group [238 (232,241) microm2] (P = 0.01) and IC was smaller in the MI-RA group [2.4 (1.7, 3.1)%] than in the MI group [3.5 (2.6, 3.9)%] (P = 0.05). The infarct size did not differ between the groups [MI = 44.6 (40.8, 48.4)%, MI-RA = 45 (38.6, 47.2)%]. Maximum rate of rise of left ventricular pressure (+dp/dt) was greater in the MI-RA group (2645 +/- 886 mm Hg/s) than in the MI group (2081 +/- 617 mm Hg/s) (P = 0.05). The other variables tested did not differ between groups. Retinoic acid supplementation of rats for 6 mo attenuates the ventricular remodeling process after MI.     

精氨酸增强全肠外营养对急性胰腺炎大鼠肠粘膜屏障的影响

目的：探讨精氨酸增强精氨酸增强ＴＰＮ对急性胰腺炎（ＡＰ）大鼠肠粘膜屏障的影响。方法：雄性ＳＤ大鼠６４只，随机分成：①对照组（ｎ＝１６）；②ＡＰ组（ｎ＝１６）；③ＡＰ＋ＴＰＮ组（ＴＰＮｓ组ｎ＝１６）；④ＡＰ＋ＴＰＮ＋精氨酸组（ＴＰＮａ组ｎ＝１６）。分别于建立急性胰腺炎模型后第１及第５天剖杀每组８只大鼠取材，检测肠粘膜一氧化氮（ＮＯ）、丙二醛、蛋白质含量、肠系膜淋巴结及门静脉血细菌移位率。结果：与对照组比较，术后１天及５天时，ＡＰ组肠粘膜丙二醛焦点量及肠系膜淋巴结细菌移位率显著升高；５天时蛋白质含量显著降低，而门静脉血细菌移位率明显升高。与ＴＰＮｓ组比较，ＴＰＮａ组１天时肠粘膜ＮＯ含量即明显升高；肠系膜淋巴结细胞移位率显著降低；５天时肠粘膜ＮＯ与蛋白质含量均显著升高；丙二醛含量显著降低。结论：急性胰腺炎可引起肠粘膜