心脏肥大细胞密度在自发性高血压大鼠心肌重构中的作用

目的探讨心脏肥大细胞在自发性高血压大鼠(SHR)心肌重构中的作用.方法应用病理检查、计算机分析结合逆转录-聚合酶链式反应等方法,观察SHR及对照Wistar Kyoto大鼠(WKY)的收缩压(SBP)、左心室重量指数(LVI)、心肌细胞直径、肥大细胞密度、心肌胶原容积分数(CVF)、心肌血管周围胶原面积比(PVCA)和心肌Ⅰ、Ⅲ型胶原mRNA表达的变化.肥大细胞密度与LVI、CVF及PVCA之间的关系采用相关分析.结果与WKY组比较,SHR组SBP、LVI、心肌细胞直径、心肌细胞短径、肥大细胞密度、CVF、PVCA、心肌Ⅰ、Ⅲ型胶原含量均明显增加(P＜0.01).心脏肥大细胞密度与LVI、CVF及PVCA存在明显的正相关(相关系数分别为0.67、0.87和0.95,P＜0.01).结论心脏肥大细胞密度增加可能是促进SHR心肌重构的重要原因.     

高血压大鼠肾内一氧化氮合酶活性

目的　观察自发性高血压大鼠肾脏内一氧化氮合酶(NOS)活性变化 ,以探讨高血压病的发病机制 .方法　采用 3H-精氨酸转变成 3H-胍氨酸方法测定 NOS活性 .结果　自发性高血压大鼠 (SHR)肾蛋白内神经型 NOS(n NOS)活性(2 1.9± 7.4) k Bq· g- 1明显低于 Wistar Kyoto(WKY)大鼠(4 .32± 9.3) k Bq·g- 1 ,P<0 .0 5 .在乙酰胆碱 (Ach)刺激后 ,SHR肾内内皮型 NOS(e NOS)活性为 (6 7.3± 14.6 ) k Bq·g- 1 ,而 WKY肾内 e NOS则为 (85 .7± 2 3.8) k Bq· g- 1 ,SHR也显著低于 WKY(P<0 .0 5 ) .结论　n NOS和 e NOS活性不足在高血压病的发生和发展过程中可能起一定作用     

Superoxide dismutase gene expression and activity in the brain of spontaneously hypertensive rats and normotensive rats

Ｍｅｍｂｒａｎｅａｂｎｏｒｍａｌｉｔｉｅｓｉｎｈｕｍａｎｅｓｓｅｎｔｉａｌｈｙｐｅｒｔｅｎｓｉｏｎｓａｒｅｗｅｌｌｅｓｔａｂｌｉｓｈｅｄ1　Ｔｏｘｉｃｏｘｙｇｅｎｍｅｔａｂｏｌｉｔｅｓｓｕｃｈａｓｓｕｐｅｒｏｘｉｄｅａｎｉｏｎｓｈａｖｅｂｅｅｎｉｍｐｌｉｃａｔｅｄｉｎｔｉｓｓｕｅｉｎｊｕｒｙｔｏｔｈｅｂｒａｉｎａｎｄｏｔｈｅｒｏｒｇａｎｓ2　Ｔｏｐｉｃａｌａｐｐｌｉｃａｔｉｏｎｏｆｆｒｅｅｒａｄｉｃａｌｓｃａｖｅｎｇｅｒｓｔｏｔｈｅｂｒａｉｎｉｎｈｉｂｉｔｓｔｈｅｄｅｖｅｌｏｐｍｅｎｔｏｆｐｉａｌ…     

Stroke-prone renovascular hypertensive rats

ＰｕｒｐｏｓｅＴｏｓｕｍｍａｒｉｚｅｄｔｈｅｍｅｔｈｏｄｓｆｏｒｅｓｔａｂｌｉｓｈｍｅｎｔ,ｃｈａｒａｃｔｅｒｉｓｔｉｃｓｏｆｖａｓｃｕｌａｒｌｅｓｉｏｎｓｉｎｂｒａｉｎａｎｄｈｅａｒｔａｎｄｔｈｅａｐｐｌｉｃａｔｉｏｎｏｆｓｔｒｏｋｅｐｒｏｎｅ...     

妊娠高血压妇女甲状腺功能和微量白蛋白尿的关系

[目的]分析妊娠高血压妇女甲状腺功能和微量白蛋白尿(MAU)的关系.[方法]选取2018年5月至2020年5月某院收治的168例妊娠高血压妇女的临床资料进行回顾性分析,依据是否出现MAU将其分为MAU组(n=31)和对照组(n=137).比较两组妇女甲状腺激素水平、单因素和Logistic多因素分析妊娠高血压妇女微量白...     

痛泻二草方对溃疡性结肠炎模型大鼠肠黏膜乳酸含量和髓过氧化物酶活性的影响

目的 通过痛泻二草方对溃疡性结肠炎（UC）模型大鼠肠粘膜乳酸（LA）含量和髓过氧化物酶（MPO）活性的影响,探讨痛泻二草方防治UC的作用机理。方法 采用抗原免疫法和局部刺激法建立UC动物模型。将50只大鼠随机分愈合的为空白组、模型组、痛泻二草方组、痛泻要方组和补脾益肠丸组,分别对各组大鼠肠粘膜LA含量、MPO活性进行检测。结果 与空白组比较,模型组大鼠肠粘膜LA含量,MPO活性显著升高（P〈0．01,P〈0．05）;经药物治疗后与模型组比较,痛泻二草方可显著降低UC模型大鼠肠粘膜LA含量和MPO活性（P〈0.05）。结论 痛泻二草方具有抑制MPO活性,减少中性粒细胞浸润和清除LA而减轻炎性反应、促进溃疡愈合的作用。     

血脂康联合依折麦布对原发性高血压合并血脂异常患者髓过氧化物酶和尿微量白蛋白的影响

目的 观察血脂康联合依折麦布对原发性高血压合并血脂异常患者的降脂效果及对髓过氧化物酶(MPO)及微量白蛋白尿(MAU)的影响,并探讨其降脂外心血管获益的机制.方法 入选血脂异常且未规律服用降脂药物的原发性高血压患者76例,随机分为3组.A组(n=24)血脂康治疗组:血脂康胶囊600 mg 2次/d;B组(n=20)依折麦布治疗组:依折麦布10 mg,1次/d;C组(n=32)血脂康联合依折麦布治疗组:血脂康600mg,2次/d+依折麦布10 mg 1次/d.常规检测血脂、肝生化、心肌酶谱、肾功、电解质、空腹血糖、同型半胱氨酸(Hcy),检测血MPO、尿微量白蛋白/肌酐(ACR).治疗2个月后再次复查上述指标,比较各组用药前后各项指标的差异.结果 A组治疗后三酰甘油、总胆固醇、低密度脂蛋白胆固醇(low density lipoprotein-cholesterol,LDL-C)显著下降,差异有统计学意义(P＜0.05),MPO水平较治疗前下降,差异有统计学意义(P＜0.05),而ACR水平无明显改变;B组治疗后三酰甘油、总胆固醇、LDL-C有下降,差异有统计学意义(P＜0.05),MPO及ACR水平无明显改变;C组治疗后三酰甘油、总胆固醇、LDL-C显著下降,差异有统计学意义(P＜0.05).MPO水平及ACR水平较治疗前明显下降,差异均有统计学意义(P＜0.05);3组治疗前后肝、肾功能及肌酸激酶无明显差异.3组中均未出现严重不良反应.结论 血脂康联合依折麦布的降低LDL-C的作用明显优于单用血脂康或依折麦布,显著降低MPO及ACR,改善氧化应激状态和血管内皮功能,对预防高血压合并血脂异常的患者发生心血管事件可能有着良好的干预作用.     

脑内活性氧抑制对醋酸去氧皮质酮-盐型高血压大鼠交感神经活动的影响

目的探讨脑内活性氧是否介导醋酸去氧皮质酮（DOCA）-盐型高血压大鼠的交感神经活动增强效应。方法雄性SD大
鼠,行左肾切除术后皮下注射DOCA,并饮用1%氯化钠溶液4周,建立DOCA-盐型高血压模型。轻度麻醉状态下,记录大鼠平
均动脉压（MAP）、心率（HR）和肾交感神经活动（RSNA）;记录基础值后,静脉注射六烃季胺,观察MAP的变化;侧脑室注射
tempol（20 μmol/L,10 μl）或对照液,观察MAP、HR和RSNA的变化。酶联免疫法（ELISA）分析血浆去甲肾上腺素（NE）水平;化
学发光法检测下丘脑超氧阴离子水平和NAD(P)H氧化酶活性。结果DOCA-盐型大鼠的MAP和血浆NE水平较对照组均显
著增加（P<0.01）;静脉注射神经节阻滞剂六烃季胺,在DOCA-盐型大鼠引起的血压降低是对照大鼠的240%;DOCA-盐型大鼠
的下丘脑超氧阴离子水平和NAD(P)H氧化酶活性显著增加（P<0.01）;侧脑室微注射tempol在DOCA-盐型大鼠的MAP、HR和
RSNA降低与对照组存在显著差异（P<0.01）。结论DOCA-盐型高血压大鼠可能通过增加下丘脑内NAD(P)H氧化酶来源的
活性氧水平,提高交感神经活性,参与高血压的形成和进展。
     

The relationship between LDL oxidation and macrophage myeloperoxidase activity

Objective To explore low density lipoprotein (LDL) oxidation by macrophage myeloperoxidase(MPO) at molecular level.Methods Using a mouse macrophage model, we examined the relationship between LDL oxidation and macrophage MPO by measuring macrophage MPO activity, LDL oxidation products, MPO gene expression and cellular orientation of LDL oxidation.Results MPO gene expression increased to its maximum gradually when the concentration of LDL was increased, and then maintained at that level. NaN3 inhibied the elevation of MPO activity and LDL oxidation, which was LDL concentration-dependent. After the composition of macrophage membrane was roughly analyzed, it was determined that the contents of MPO and LDL in 5% sucrose were 7. 667 and 21 times higher than those in 10% sucrose, respectively.Conclusion LDL is attached to the “microdomain” of the macrophage membrane in which LDL is oxidized by MPO.     

醛固酮介导的肾性高血压相关靶器官组织钙调神经磷酸酶活性的变化

目的研究醛固酮介导一肾一夹肾性高血压大鼠脑、肾、脾、肺、主动脉和肝脏组织钙调神经磷酸酶(CaN)活性的变化.方法取20只Wistar大鼠随机分为3组:假手术组(sham op,n=6),一肾一夹手术组(op,n=7)和螺内酯干预组(spiro,n=7).以PNPP为底物测定术后4周大鼠各组织器官CaN活性.结果肾性高血压大鼠脾、肾脏、肺、脑CaN活性较假手术组分别上升90%,84%,57%和43%(均P＜0.05),螺内酯干预组上述组织器官CaN活性较手术组明显下降(P＜0.05).肾性高血压大鼠组肝脏CaN活性较假手术组下降27%(P＜0.05),螺内酯干预组肝细胞CaN活性较手术组有下降趋势,但差异无显著意义.各组大鼠主动脉中CaN活性无明显变化.结论醛固酮对肾性高血压相关靶器官-脑、肾、脾、肺组织细胞内信号分子CaN的激活具有重要作用.     

活血潜阳颗粒对自发性高血压大鼠血液流变学及纤溶系统活性的影响

目的探讨活血潜阳颗粒对自发性高血压大鼠(SHR)血液流变学、纤溶系统活性的影响。方法SHR 72只,随机分为活血潜阳颗粒大、中、小剂量组及卡托普利组、松龄血脉康组、双蒸水组,并以正常血压Wistar(WKY)大鼠为对照组,给药10周后检测各组大鼠血液流变学指标、血浆组织型纤溶酶原激活物(t-PA)及其抑制物(PAI)。结果与正常WKY大鼠比较,SHR全血黏度、血浆黏度、红细胞聚集指数均明显升高,而经活血潜阳颗粒治疗后上述各项指标较SHR组有不同程度改善(P<0.05或P<0.01)。SHR PAI升高、t-PA降低,经活血潜阳颗粒灌服后PAI降低、t-PA升高(P<0.05或P<0.01)。结论活血潜阳颗粒对自发性高血压大鼠血液流变学、纤溶系统活性具有调节作用。     

妊娠肝内胆汁淤积症胎兔心肌细胞损伤的研究

目的 观察妊娠肝内胆汁淤积症(intrahepatic cholestasis of pregnancy,ICP)胎兔心肌细胞超微结构及细胞凋亡率,检测心肌腺苷三磷酸(ATP)、超氧化物歧化酶(SOD)、丙二醛(MDA)含量.方法 16只孕兔,分为ICP组和对照组.ICP组自妊娠第22天,颈后皮下注射苯甲酸雌二醇0.1 mg·kg-1·d-1,对照组颈后皮下注射0.9%生理盐水,直至分娩.观察ICP组和对照组胎兔心肌细胞超微结构,检测心肌细胞ATP、SOD、MDA含量及细胞凋亡指数.结果 电镜观察见ICP胎兔心肌细胞线粒体轻度肿胀、髓鞘样结构形成,细胞质内糖原颗粒分布减少,对照组超微结构无明显改变.ICP组胎心组织ATP、SOD含量减少,MDA含昔和细胞凋亡数明显增多,与对照组相比差异均有统计学意义(P<0.05).结论 ICP胎兔存在心肌细胞损伤.     

Endothelium-dependent inhibition of the contractile response is decreased in aorta from aged and spontaneously hypertensive rats

BACKGROUND: Stimulation of vascular 5-hydroxytryptamine-2C (5-HT(2c)) receptors produces contraction in rat aorta. We investigated the effect of aging on endothelium-dependent inhibition of contractile responses in thoracic aorta from normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR). METHODS: Endothelium-intact and denuded aortic rings were prepared from young (7-9 weeks old) and senescent (65-70 weeks old) WKY and SHR rats. Changes in isometric tension elicited by 5-HT, in the absence or in the presence of N(G)-nitro-L-arginine methyl ester (L-NAME) or indomethacin were recorded. RESULTS: In aorta from WKY and SHR, 5-HT elicited concentration-dependent contractions, which were increased by endothelium removal. The ability of endothelium to depress contractile response to 5-HT was found to be reduced in vessels from senescent animals, mainly in SHR. L-NAME increased the sensitivity and maximal effect to 5-HT in endothelium-intact but not in denuded aortic rings from young WKY rats. The effect of L-NAME was lower in young SHR compared with age-matched WKY rats, but it did not modify the response to 5-HT in senescent rats. Indomethacin did not affect contraction in arteries from young WKY or in denuded aortic rings from young SHR and aged WKY. In contrast, the inhibitor attenuated the response in endothelium-intact vessels from young SHR and aged WKY, and this effect was more marked in arteries with and without endothelium from senescent SHR. Thus, inhibition of cyclooxygenases by indomethacin revealed an enhanced endothelium-dependent modulation of contraction in senescent and hypertensive rats. CONCLUSIONS: Results indicate that hypertension and aging decrease the negative modulator role of endothelium, in 5-HT-induced vasoconstriction in aorta from WKY and SHR. Data also point out that endothelial dysfunction involves an increased formation of vasoconstrictor prostanoids, which counteract nitric oxide effects. In addition, SHR endothelium releases contractile prostanoids at an early stage of hypertension, whereas in old SHR vascular smooth muscle also releases prostanoids, which contribute to 5-HT-induced contraction.     

卡托普利在L-NAME高血压大鼠中的作用

目的探讨卡托普利在Ｎω－硝基－Ｌ－精氨酸甲酯（Ｌ－ＮＡＭＥ）高血压大鼠中的作用。方法雄性ＳＤ大鼠口服Ｌ－ＮＡＭＥ四周后,测量动脉血压,并取其主动脉进行离体血管环实验。结果用ＮＯＳ抑制剂长期抑制大鼠体内ＮＯ的产生,可引起血压升高,心肌肥厚,主动脉依赖内皮的血管舒张作用减小。如同时服用卡托普利作抗高血压治疗,可防止心肌肥厚,减弱血压的升高,使由Ｌ－ＮＡＭＥ引起的血管内皮机能失调得到改善。结论卡托普利可通过不依赖一氧化氮的机制,改善Ｌ－ＮＡＭＥ高血压大鼠的心血管机能。     

Depressed erythropoietic activity in Nigerian pregnant women

Reticulocytes production index was determined in 63 pregnant women and in 96 patients. The results show that 86% of the pregnant women, who were registering their pregnancy for the first time, were anaemic. There was significant reticulocytopenia in all the anaemic pregnant women and in the patients. Erythropoiesis was found to be depressed in all subjects and patients by two to seven times those expected in normal responsive bone marrows. There was no correlation of the bone marrow impairment with parity of the pregnancy. The bone marrow impairment was more pronounced during the 16th week of gestation and less so in older pregnancies. Malnutrition and infection (especially malaria) are suggested as the aetiological factors of the bone marrow depression of erythropoiesis.     

大鼠脑缺血后脑内MPO、NSE活性变化

目的 通过测定大鼠局灶性脑缺血-再灌流后不同时点脑组织中髓过氧化物酶(MPO)和神经元特异性烯醇化酶(NSE)活性的变化,探讨炎症反应与脑缺血损伤的关系.方法 用线栓法制备大鼠左侧大脑中动脉缺血-再灌流模型,检测缺血3h再灌流后6h、12h、24h、48h、72h和7d脑组织中MPO和NSE活性、脑梗死体积的变化.结果 缺血组脑组织中NSE和MPO活性升高,再灌流后48h的NSE为(5.44±0.95)ng/ml,MPO为4.49±0.22;72h分别为(5.36±0.65)ng/l和5.96±0.19,升高最为明显.脑梗死体积随再灌流时间延长而增加,第7d梗死体积百分比为(39.18±0.63)%.局灶性缺血脑组织中MPO活性与组织损伤(NSE活性)间具有高度正相关性.结论 炎症反应是加重脑缺血损伤的重要因素.     

雌激素对低氧性肺动脉高压大鼠NO、NOS的作用

目的探讨在雌激素干预下,低氧性肺动脉高压大鼠血浆及肺组织匀浆一氧化氮(NO)含量、一氧化氮合酶(NOS)活性和结构型NOS(cNOS)活性的变化。方法采用间断常压低氧法建立大鼠低氧性肺动脉高压模型。将18只雄性SD大鼠随机分成:正常对照组、雌激素组(每天低氧前腹腔注射17-β雌二醇30μg.kg-1,共3周)、低氧组(每天低氧前腹腔注射生理盐水2 ml,共3周)。以右心导管法测定平均肺动脉压(mPAP);测定右心室肥厚指数〔RV/(LV S)〕;肺组织切片采用HE染色,经图像分析技术测定大鼠肺小血管管壁厚度指标〔管壁厚度占外径的百分比(WT%)和管壁面积占总面积的百分比(WA%)〕。采用硝酸还原法检测各组大鼠血浆及肺组织匀浆NO含量;用化学比色法检测各组大鼠肺组织匀浆NOS和cNOS活性。结果低氧组的大鼠mPAP、RV/(LV S)、WT%和WA%均高于正常对照组(P<0.01);雌激素组的大鼠mPAP、RV/(LV S)、WT%和WA%均低于低氧组(P<0.01)。HE染色切片显示正常对照组大鼠肺小血管管壁菲薄,低氧3周后,低氧组大鼠肺小血管普遍增厚,管腔狭窄。雌激素组的肺小血管管壁及血管管腔狭窄程度较低氧组显著减轻。低氧组大鼠的血浆及肺组织匀浆NO含量、NOS活性和cNOS活性均较正常对照组明显降低(P<0.05)。雌激素组血浆及肺组织匀浆中NO含量、NOS活性和cNOS均较低氧组明显增加(P<0.05)。结论17-β雌二醇对低氧性肺动脉高压血管重建的预防作用可能部分是通过上调肺组织NO含量和NOS活性实现的。