Telmisartan Attenuates the Growth of Epithelium-like Cells and Glomerular Injury in Spontaneously Hypertensive Rats

The abnormal growth of epithelium-like cells has been noticed in spontaneously hypertensive rats(SHRs)with hypertensive nephropathy.However,the characteristics of abnormal epithelium-like cells and their pathogenesis in hypertensive nephropathy are not fully understood.In the present study,we investigated the correlation of epithelium-like cells with glomerular injury,and the effects of early drug intervention with telmisartan,an anti-hypertensive drug,on the growth of epithelium-like cells.The results showed that the epithelium-like cells were obviously observed lining along the luminal surface of Bowman’s capsule in glomeruli,significantly resulting in the atrophy of the glomerular tuft.Some of the epithelium-like cells strongly expressed proliferating cell nuclear antigen(PCNA)and vimentin,indicating active cellular proliferation.The incidence of epithelium-like cells varied from 13.6%to 54.4%of glomeruli in 48-week-old SHRs,and from 5.1%to 18.0%of glomeruli in age-matched Wistar-Kyoto(WKY)rats(P<0.01).The linear regression analysis further confirmed an obvious correlation between the incidence of epithelium-like cells and the glomerular injury.Moreover,early intervention with telmisartan could dramatically attenuate the progression of epithelium-like cells growth.However,no significant effect of telmisartan on the established epithelium-like cells was observed.Taken together,we demonstrated the involvement of abnormal epithelium-like cells growth in glomerular injury during hypertensive nephropathy in SHRs,and firstly showed the positive effects of the anti-hypertensive drug on the progression of epithelium-like cells growth.

Endothelin-1, an important mitogen of smooth muscle cells of spontaneously hypertensive rats

OBJECTIVE: To study the features of vascular smooth muscle cell (VSMC) proliferation induced by endothelin-1 (ET-1). METHODS: VSMCs of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats were cultured and treated with ET-1. Basic fibroblast growth factor (bFGF) gene expression was measured using both Northern blot and an enzyme-linked immunoassay. RESULTS: ET-1 resulted in an increase in bFGF transcripts at 8 - 24 h; bFGF levels were significantly higher in VSMCs treated with ET-1 than in those not treated. However, VSMCs growth responses in SHR and WKY were different. Smooth muscle cells of SHR were hyper-responsive to ET-1. Maximal bFGF mRNA levels were elevated 3.5-fold at 4 h of stimulation in WKY and 8-fold at 8h in SHR4. Moreover, the proliferation of VSMCs induced by ET-1 was inhibited by antisense phosphorothioate oligodeoxynucleotides (10 micromol/L AS-bFGF) but not sense bFGF oligomers at the same concentrations, being reduced by 80% in SHR and 40% in WKY vs control, respectively. Furthermore, the effect of AS-bFGF oligomers on SHR SMC proliferation is significantly greater than on WKY SMC proliferation. CONCLUSION: ET-1 may be required for exaggerated vascular growth responses in SHR and bFGF may be involved.

Influence of Valsartan on myocardial apoptosis in spontaneously hypertensive rats

OBJECTIVE: To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. METHODS: Thirty spontaneously hypertensive rats (SHRs) were divided into two groups: 15 treated with Valsartan (20 mg x kg(-1) x d(-1)) (SHR + Valsartan group), the others with placebo (SHR + placebo group), with 15 normal Wistar rats as control. Systolic blood pressure was measured by the tail-cuff method. The observation period was from 8 to 16 weeks of age. Cardiac apoptosis was evaluated by a Terminal Deoxynucleotidyl Transferase-Mediated dUTP-biotin Nick End Labeling (TUNEL) assay. RESULTS: Mean blood pressure values were 127 +/- 2 mm Hg in controls, 163 +/- 6 mm Hg in the SHR + Valsartan group and 193 +/- 7 mm Hg in the SHR + placebo group at 16 weeks of age, whereas the blood pressure in 8-week-old SHR and Wistar rats were 175 +/- 3 mm Hg and 125 +/- 5 mm Hg, respectively. The ratio of the heart weight over body weight declined in Wistar (3.07 +/- 0.03 mg/g) and SHR + Valsartan groups (3.22 +/- 0.19 mg/g) compared with the SHR + placebo group (4.02 +/- 0.31 mg/g) (P

Endothelin receptor antagonist combined with a calcium channel blocker attenuates renal injury in spontaneous hypertensive rats with diabetes

OBJECTIVE: To investigate the effects of the mixed endothelin receptor antagonist, bosentan, combined with the long-acting calcium channel blocker, amlodipine, compared to the angiotensin-converting enzyme inhibitor, cilazapril, on the progressive renal injury in spontaneous hypertensive rats (SHR) with diabetes. METHODS: Diabetic hypertensive rats (SHR-DM) were induced by streptozotozin injected in male SHR (7-week-old),and divided into an untreated and three treated groups: 1) cilazapril treated group; 2) bosentan+amlodipine treated group; and 3) amlodipine treated group. Wistar Kyoto rats (WKY) and SHR rats served as normotensive and hypertensive control, respectively. The mean arterial blood pressure, renal function, endothelin and angiotensin II levels as well as the protein expression of renal extracellular matrix components and transforming growth factor (TGF)-beta1 were determined at the end of the 4th week. RESULTS: Mean arterial blood pressure significantly increased in SHR and SHR-DM rats compared to WKY rats. All the therapies reduced the blood pressure to normal levels. However, the enhanced urinary protein excretion, the decreased creatinine clearance as well as the increased plasma and intrarenal endothelin and angiotens in II levels were found in the untreated SHR-DM and prevented by treatment with bosentan+amlodipine and cilazapril. Similarly, these two kinds of therapies in SHR-DM abolished the overexpression of renal TGF-beta1 by Western blot analysis and reduced the accumulation of collagen type IV, laminin and fibronectin proteins by an immunochemical approach. Amlodipine monotherapy had no detectable effects on the above parameters. CONCLUSION: Bosentan combined with amlodipine can offer similar renoprotective effects on that of cilazapril and may be a potent therapy to attenuate renal injury by reducing renal protein levels of TGF-beta1 in diabetes with a hypertensive state.

Ventricular remodeling by Scutellarein treatment in spontaneously hypertensive rats

OBJECTIVE: To observe reversal of ventricular remodeling by the protein kinase C inhibitor Scutellarein in spontaneously hypertensive rats (SHRs). METHODS: Twelve SHRs were randomly divided into two groups. Scutellarein and saline (10 mg x kg(-1) x d(-1)) were given by intraperitoneal injection to two groups of rats separately. Systolic blood pressure (SBP) and ventricular weight index (LVW/BW, RVW/BW) were measured. A polarization microscope and an image analyzer system (IAS) were used to observe changes in cardiovascular structure and to count the content of cardiac muscle interstitial collagen. RESULTS: The pathologic changes in the left ventricle in the Scutellarein group rats (SHR(D)) improved to varying degrees, including hypertrophy of the cardiac muscle and collagen volume fraction. CONCLUSION: Scutellarein can reverse ventricular remodeling, improve myocardial stiffness and protect heart cardiac muscle.

Proliferation of aortic smooth muscle cells and renin-angiotensin system in SHR rats

目的：探讨ＳＨＲ大鼠主动脉平滑肌细胞（ＡＳＭＣ）异常增殖和肾素血管紧张素系统（ＲＡＳ）的关系．方法：测定血管紧张素Ｉ（Ａｎｇ）、卡托普利（Ｃａｐ）、沙拉新（Ｓａｒ）对培养的ＳＨＲ、ＷＫＹＡＳＭＣ增殖和Ａｎｇ、血管紧张素转化酶（ＡＣＥ）的影响．结果：Ａｎｇ在２％血清培养基中可刺激ＳＨＲＡＳＭＣ增生．ＳＨＲＡＳＭＣ分裂增殖能力比ＷＫＹ强，ＳＨＲＡＳＭＣＲＡＳ处于高功能状态．Ｃａｐ长期（４周）干预显著抑制ＳＨＲＡＳＭＣ异常增殖和Ａｎｇ、ＡＣＥ活性，Ｓａｒ长期干预同样抑制ＳＨＲＡＳＭＣ的增殖和ＡＣＥ活性，但Ａｎｇ水平反而升高．Ｃａｐ短期（２４小时）干预不影响两种大鼠ＡＳＭＣＲＡＳ．结论：Ｃａｐ和Ｓａｒ长期干预通过减少ＳＨＲＡＳＭＣＡｎｇ生成或阻断Ａｎｇ和特异受体结合，抑制其异常增殖．

Inhibitory effect of antisense basic fibroblast growth factor oligonucleotides on proliferation of cultured aortic smooth muscle cells induced by angiotensin Ⅱ in SHR rats

目的：研究转染反义碱性成纤维细胞生长因子（ｂＦＧＦ）寡核苷酸（ＯＤＮ）对培养的自发性高血压大鼠（ＳＨＲ）主动脉平滑肌细胞（ＳＭＣ）生长的影响．方法：用脂质体介导法将反义ｂＦＧＦＯＤＮ转入ＳＭＣ内，用Ｎｏｒｔｈｅｒｎ杂交检测ｂＦＧＦ基因表达，并测定［３Ｈ］ｔｈｙｍｉｄｉｎｅ掺入和细胞计数．结果：转染反义ｂＦＧＦＯＤＮ（５μｍｏｌ·Ｌ－１）几乎完全抑制血管紧张素Ⅱ（ＡｎｇⅡ，１μｍｏｌ·Ｌ－１）诱导增高的ｂＦＧＦｍＲＮＡ表达和明显抑制ＳＭＣ增殖，在基础状态和ＡｎｇⅡ刺激条件下，［３Ｈ］ｔｈｙｍｉｄｉｎｅ掺入分别被抑制２６５％（Ｐ＜００１）和４２０％（Ｐ＜００１），细胞数分别被抑制１７３％（Ｐ＜００１）和２２２％（Ｐ＜００１）．结论：反义ｂＦＧＦＯＤＮ能有效抑制ＡｎｇⅡ诱导的ｂＦＧＦ基因表达和ＳＭＣ增殖．

Mechanism and effect of Shijueming (Concha Haliotidis) on serum calcium in spontaneously hypertensive rats

OBJECTIVE： To observe the impact of Shijueming （Concha Haliotidis） on spontaneously hypertensive rats via blood pressure, serum calcium, vascular smooth muscle membrane L-type calcium channel α1 C subunit （CaL-α1C）, plasma membrane calci- um-ATPase （PMCA） mRNA expression, and the L-type calcium channel in vascular smooth muscle cells. METHODS： Twelve-week-old male rats with sponta- neous hypertension were divided into three groups： a Shijueming （Concha Haliotidis） group （group 1）, a nifedipine group （group 2）, and a dis- tilled water group （group 3）. All were given a four-week treatment. Blood pressure and dissocia- tive serum calcium were examined before treat- ment. Blood pressure was taken every week during treatment. Atomic absorption spectrometry was used to examine dissociative serum calcium. Re-verse transcription-polymerase chain reaction was used to examine the expression of CaL-α1C and PM- CA1 mRNA. The patch clamp technique was used to examine the electrophysiological characteristics of the vascular smooth muscle cell calcium chan- nels. RESULTS： After treatment, blood pressure of the Shijueming （Concha Halioticlis） group lowered but not significantly （P〉0.05）. Blood pressure of the nifedipine group lowered significantly （P〈0.05）. Blood pressure of the distilled water group re- mained high. The concentration of serum calcium in the Shijueming （Concha Haliotidis） and the dis- tilled water groups lowered （P〈0.05）. Expression of CaL-α1C mRNA in the nifedipine group decreased compared with the distilled water group （P〈0.01）. There was the decreasing trend in the Shijueming （Concha Haliotidis） group, but it was not statistically significant. Shijueming （Concha Haliotidis） also had effects on the expression of PMCA1 mRNA but with- out statistical significance. However, there was a significant decreasing effect on vascular smooth muscle cell Ica-L flow. CONCLUSION： This study indicated that Shijuem- ing （Concha Haliotidis） could increase serum calci- um and decrease blood pressure. It may work by in- fluencing calcium channels, expression of PMCA1 mRNA, and regulating ion calcium channels and calcium-ATPase.

Five novel monoclonal antibodies to thymic epithelial cell surface antigens in rats

OBJECTIVE: To establish monoclonal antibodies (mAbs) against thymic epithelial cells and study the function of epithelial cells during T-cell differentiation in the thymus. METHODS: Hybridomas secreting mAbs against thymic epithelial cells were derived by immunization of Balb/c mice with two thymic epithelial cell lines, TaD3 and FTE. The distribution of antigens recognized by these mAbs was detected by immunochemical staining and cytofluorographic analysis, and the molecular weight of the antigens by immunoblotting. RESULTS: Five specific monoclonal antibodies (mAb) were obtained. On the basis of their distribution in the thymus determined by immunochemical staining, mAb RE-4D8 was regarded as clusters of thymic epithelium staining (CTES) type IIA: mAb RE-12B2, which showed a unique distribution pattern only in the medulla, was CTES type V: mAb RE-5C6 was CTES type IV: mAb RE-6D6 might be CTES type IIB: and mAb RE-1D4 was classified as type V. The molecular weight (MW) of antigen RE-4D8, RE-6D6 and RE-12B2 were 120 kDa, 220 kDa and 35 kDa, respectively. Antigen RE-1D4 is a novel marker of cortical epithelium, several established thymic epithelial cell lines were classified and their original intrathymic locations were determined by these mAbs. Thymic cell lines, TuD3 and FTE were cortical phenotypes whereas TaD3 had a medullar phenotype. CONCLUSIONS: These mAbs clearly demonstrate the heterogeneity of the thymic epithelium; they could detect antigens not only in the cytoplasm but also on the surface of thymic epithelial cells. Our data suggest that these newly established mAbs may help elucidate the interaction between thymocytes and epithelial cells during T cell maturation.

运动训练对SHR/SP大鼠VD模型认知功能及海马ChAT、AchE活性的影响

目的观察运动训练对自发性高血压脑卒中倾向大鼠(SHR/SP)血管性痴呆(VD)模型认知能力及ChAT、AchE活性的影响。方法将雄性SHR/SP大鼠30只,分为假手术组、模型组、运动组,每组各10只,采用分次结扎2-VO法制作VD模型,假手术组、模型组术后正常饲养不做干预;运动组术后采用跑台训练(DSPT-1)8周,训练完成后采用Morris水迷宫检测各组大鼠认知功能,最后处死大鼠取材检测海马胆碱乙酰转移酶(ChAT)及乙酰胆碱酯酶(AchE)活性。结果在定位航行训练中,假手术组大鼠潜伏期明显少于运动组和模型组大鼠,但运动组大鼠潜伏期明显短于模型组大鼠(P<0.05);在空间探索实验中,假手术组大鼠跨越原平台次数明显多于其他两组大鼠,运动组大鼠跨越原平台次数明显多于模型组(P<0.05);运动训练可增加海马ChAT活性及降低AchE活性。结论运动训练可改善SHR/SP大鼠VD模型海马胆碱能系统的功能,进而提高认知能力。

提取紫薯淀粉的副产物对SHR血压的影响

以紫薯为原料,12周龄雄性原发性高血压大鼠(SHR)和Wistar大鼠为受试动物,研究紫薯全粉、滤渣、淀粉、水溶性提取物的降血压作用。上述分别以低、中、高3个剂量(0.1、1、5g/kgbw)灌胃SHR大鼠和Wistar大鼠,观察对大鼠血压的影响。结果表明:在所选定的灌胃剂量范围内紫薯各成分对正常大鼠(Wistar大鼠)血压无影响。除淀粉外,其他各成分对SHR大鼠的血压均具有显著降低的作用,其中以水溶性提取物作用最为明显,灌胃后,低剂量组在1h时达到最低值,下降了20.83mmHg,中剂量组在2h时达到最低值,下降了23.50mmHg,高剂量组在4h时达到最低值,下降了24.48mmHg,然后血压开始慢慢回升,在8h时基本恢复到灌胃前的水平。提取紫薯淀粉后的副产物均有明显降血压作用。

Effects of electroacupuncture at Taichong(LR 3) and Baihui(DU 20)on cardiac hypertrophy in rats with spontaneous hypertension

OBJECTIVE: To investigate the effects of electroacupuncture(EA) at Taichong(LR 3) and Baihui(DU 20)on myocardial hypertrophy in spontaneously hypertensive rats(SHRs).METHODS: Thirty-six SHRs were randomly assigned to model, EA, and Losartan groups, with twelve rats per group. Twelve Wistar Kyoto rats were selected as the normal control group. Systolic blood pressure(SBP) and cardiac function were measured in all rats.Expression levels of factors associated with the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR) pathway were evaluated by Western blotting and real-time PCR.Pathological changes of the heart tissue were observed by hematoxylin-eosin staining.RESULTS: After treatment, enhanced SBP was significantly decreased in the EA and Losartan groups compared with the model group(P < 0.01). Echocardiographic and morphological analyses revealed that enhanced end-diastolic interventricular septal thickness and left ventricular posterior wall thickness, as well as ratio of left ventricular weight to body weight were markedly diminished in the EA and Losartan groups(P < 0.01 or P < 0.05), while reduced left ventricular end-diastolic dimension and left ventricular ejection fraction were significantly ameliorated(P < 0.01). Real-time PCR and western blotting analyses showed that the expression levels of PI3K,Akt, and mT OR in SHRs were significantly up-regulated by EA and Losartan(P < 0.01), while the expression levels of PTEN and ANP were down-regulated(P < 0.01).CONCLUSION: EA at Taichong(LR 3) and Baihui(DU20) inhibited the development of cardiac hypertrophy and improved the cardiac function in SHRs, possibly through regulation of the PI3K/Akt/mTOR signalling pathway.

SHR高血压进程中不同类型血管内皮功能损伤及药物修复研究

目的探讨SHR大鼠在高血压发展进程中,不同血管内皮功能损伤程度及抗高血压药物对其的修复。方法以SHR为模型,7～24wk(wk:周龄)给予卡托普利(3.375g.kg-1.d-1),停药观察至32wk。6、18、24和32wk时分别进行病理学切片检查胸主动脉、肠系膜上动脉和心尖小动脉形态结构,及胸主动脉和肠系膜上动脉乙酰胆碱(ACh)浓度依赖性血管舒张功能检测(n=6)。结果SHR在18wk时胸主动脉、肠系膜上动脉和小动脉均出现结构病变,并随时间逐渐加重,三级动脉中胸主动脉病变较之严重,表现为内皮细胞脱落和中膜增厚;随年龄增大SHR胸主动脉和肠系膜上动脉ACh依赖性舒张度均下降,但胸主动脉舒张度降低幅度大于肠系膜上动脉(P=0.10,18wk;P<0.01,24、32wk);卡托普利能抑制18wkSHR胸主动脉舒张度的降低(P<0.05vsSHR),但对肠系膜上动脉没有该作用。结论伴随SHR高血压的发病进程,体内各级动脉内皮细胞均发生损伤,内皮依赖性舒张功能降低,大动脉内皮功能损伤出现早,程度也往往高于中、小动脉,抗高血压药物可抑制大动脉内皮功能障碍,但对中、小动脉内皮功能损伤无作用。

不同剂量缬沙坦单用或与苯那普利钠联合应用对SHR血压和左室心肌肥厚的影响(英文)

目的 :评价不同剂量AT1受体拮抗剂valsartan单用和与benazepril联合应用对SHR的降压疗效、逆转心肌肥厚作用和对RAAS、内洋地黄素水平的影响。方法 :30只 14周龄雄性SHR随机分成空白对照组、benazepril组、小剂量valsartan组、大剂量valsartan组和小剂量valsartan与benazepril联用组 ,另设WKY正常对照组 ,分别给予生理盐水、benazepril1mg·kg-1、valsartan 8mg·kg-1、valsartan 2 4mg·kg-1、valsartan 8mg·kg-1+benazepril1mg·kg-1,每日 1次灌胃给药 ,持续 8周。结果 :药物干预各组SHR动脉收缩压 (SBP)水平明显下降 ,尤以大剂量valsartan组和联合用药组SBP下降最显著 ;药物干预各组血浆和心肌组织肾素活性均明显升高 ;benazepril组和小剂量valsartan与benazepril组血浆和心肌组织AngⅡ水平降低 ;大、小剂量valsartan组血浆和心肌组织AngⅡ水平均明显升高 ,valsartan剂量越大 ,血浆和心肌组织AngⅡ水平升高越明显 ;随SBP水平的降低 ,心肌组织Na+ -K+ -ATP酶活性明显升高 ,而内洋地黄素水平则明显下降 ;药物干预各组LVM/BW、TDM均明显减低 ,尤以联合用药组改变最为显著。结论 :不同剂量AT1拮抗剂valsartan和benazepril单用或联用均有明显的降低SHR的SBP作用 ,能明显抑制左室肥厚进展 ;

口服螺内酯对SHR心肌组织TNF-α表达的影响

目的:观察口服小剂量螺内酯对自发性高血压大鼠(SHR)心肌组织TNF-α表达水平的影响。方法:20只8周龄雄性SHR随机分为螺内酯组和安慰剂组,每组10只,另设对照组(Wistar-kyoto,n=7)。螺内酯组螺内酯双蒸水溶解,20mg/(kg.d)灌胃,安慰剂组和对照组等容积双蒸水灌胃,持续16周,24周龄大鼠称取体质量,颈动脉插管检测动脉血压。摘取心脏,心尖部横断为两片,分别投入液氮罐中和10%中性甲醛固定液中,用ELASA方法检测心肌组织匀浆上清液TNF-α水平,免疫组化观察TNF-α表达。结果:螺内酯组与安慰剂组比较,收缩压、舒张压、平均动脉压水平无明显变化(P>0.05),但两组的收缩压、舒张压、平均动脉压均明显高于对照组,差异有统计学意义(P<0.05)。安慰剂组与对照组比较,心肌组织TNF-α水平明显升高,螺内酯组与安慰剂组比较心肌组织TNF-α水平降低,差异有统计学意义(P<0.01),但未达对照组水平(P>0.05)。结论:SHR大鼠心肌组织TNF-α高表达,口服小剂量螺内酯可降低SHR大鼠心肌组织TNF-α水平。

基于高盐诱导的SHR大鼠肾损伤探讨中医理论“盐胜血”的机理研究

目的研究关于高盐诱导的SHR大鼠肾损伤的相关基础,并探讨中医理论"盐胜血"的内涵。方法 WKY大鼠为正常组,SHR大鼠随机等分为2组,分为普通饲料组(SHR)与高盐饲料组(SHR+HS),SHR+HS组大鼠从10周龄开始给予4%高盐饮食。每2周检测尿m-ALB与NAG。20周龄大鼠麻醉后腹主动脉取血,检测血液流变学指标与凝血4项;处死大鼠,取肾脏,分为2部分,一部分中性福尔马林固定,HE病理检测;一部分采用Western blot法检测细胞间粘附因子1(ICAM-1)、血管细胞粘附因子1(VCAM-1)、白介素6(IL-6)的表达情况。结果喂养高盐饲料6周后,尿m-ALB与NAG显著增高(P<0.05)。20周龄时SHR+HS组的全血黏度值与血浆黏度值显著大于SHR组(P<0.05);APTT、PT显著缩短(P<0.05)及FIB显著增加(P<0.05);肾脏病理检测可见SHR+HS组的病变积分值更高,且肾脏炎症因子ICAM-1、VCAM-1、IL-6表达增加(P<0.05)。结论高盐可以增加SHR组大鼠的全血黏度、缩短APTT、PT与增加FIB,增加肾脏炎症因子ICAM-1、VCAM-1、IL-6表达,加重SHR组大鼠的肾损伤,这可能是"盐胜血"与"咸走肾"的部分科学内涵。

SHR、SHRsp、WKy三品系大鼠血液生化检查参数

目的 检查了解SHR、SHRsp、WKy三品系大鼠血液生化的参数。方法 每个品系分别取年轻大鼠(12周龄 )、年老大鼠 (2 2～ 2 8周龄 )各 14只 ,心脏取血 ,用自动生化分析仪检验血生化及电解质等指标。结果 年老SHR、SHRsp、WKy大鼠血肌酐平均水平较年轻大鼠分别高 8 5 %、9 2 %和 14 2 % (P =0 0 7;P =0 0 7;P =0 0 4 ) ,但血钙、血磷较低。同龄SHR、SHRsp血磷平均水平均较同龄WKy低 2 5 0 % (P =0 12～P <0 0 0 1)。同龄SHR、SHRsp的肌酸磷酸激酶同工酶 (CK MB)及乳酸脱氢酶同工酶 (LDH 1)较WKy升高 1～ 2倍 (P =0 15～P <0 0 0 1)。结论 SHR、SHRsp及Wky三种品系大鼠的血液生化参数多为相似 ,但也有一些差别。

清眩降压汤对自发性高血压大鼠(SHR)大脑保护作用的实验研究

目的:探讨清眩降压汤对自发性高血压大鼠(SHR)大脑保护作用的实验研究。方法:40只SHR随机平均分为中药高剂量组、中药低剂量组、西药组(替米沙坦)、模型组(矿泉水),另取10只wistar大鼠作为正常血压对照组(自由饮水),连续治疗8周,每周检测血压1次;8周结束后水合氯醛麻醉取血、处死,取大脑;生化检测循环NO、TNOS、iNOS、cNOS,HE染色检测大脑病理,免疫组化学检测大脑组织中淋巴管生成因子2和iNOS的表达。结果:清眩降压汤单次给药不能降低大鼠血压,连续治疗8周大鼠血压未见明显降低(P>0.05);西药组大鼠收缩压获得显著降低(P<0.01),舒张压未见显著降低(P>0.05)。模型组大鼠收缩压升高达25 mmHg(P<0.01),舒张压变化不明显(P>0.05)。所有治疗组大鼠循环NO水平均高于模型组大鼠(P>0.05),中药和西药均可升高大鼠cNOS水平,降低iNOS(P<0.05),各组间TNOS水平无显著差异(P>0.05)。结论:清眩降压汤可以控制SHR的收缩压进一步升高,减轻由于高血压导致的SHR脑部损害,其机制需要进一步探索。

复方七芍降压片对SHR血压、心脏的影响

目的探讨复方七芍降压片的降压效果及作用机制。方法以12只14周龄正常血压WKY大鼠为阴性对照,设为空白组;60只14周龄自发性高血压大鼠(spontaneously hypertensive rats,SHR)随机分为5组,设为复方七芍降压片高剂量组、中剂量组、低剂量组、卡托普利组、硫酸氢氯吡格雷片组;分别采用大鼠尾动脉法测血压,观察用药后各组大鼠心脏的形态、颜色、质地、病变特征,测左心室质量指数。结果给药4周后,各组治疗前后比较,复方七芍降压片高、中、低剂量组与卡托普利组均能够降低SHR血压,差异有统计学意义(P<0.01),其中复方七芍降压片高剂量组疗效显著;均可降低左心室质量指数,差异有统计学意义(P<0.05);硫酸氢氯吡格雷片组及空白组对SHR血压无明显影响(P>0.05)。结论复方七芍降压片能有效降低SHR血压、逆转左心室肥厚。

PVG大鼠生化标记基因的测定

目的 对PVG大鼠进行生化标记基因的测定。方法 依据国家标准GB/T 14927.1—2008《实验动物近交系小鼠、大鼠生化标记检测法》测定,随机抽取4只PVG大鼠,取(肺、肾、小肠、睾丸)组织器官进行样品制备,用醋酸纤维薄膜电泳法检测11个生化位点(Hbb、Cs1、Alp1、Akp1、Esl、Es3、Es4、Es6、Es8、Es9和Esl0)。结果 PVG大鼠11个位点的基因型分别是Hbb为b型,Cs1为b型,Alp1为b型,Akp1为a型,Esl为a型,Es3为d型,Es4为b型,Es6为b型,Es8为b型,Es9为a型和Esl0为a型,且均为纯合。结论 PVG大鼠遗传生化标记结果符合近交系特征。