肾性和自发性高血压大鼠心肌肥大前后心肌Gαq/11含量的变化

目的 :探讨Gαq/11在不同原因所致心肌肥大中的变化。方法 :两肾一夹肾性高血压大鼠 (RHR)和自发性高血压大鼠(SHR)模型 ,测定动脉血压和心肌肥大指数 ,放免法测定心肌血管紧张素II(AngII)含量 ,免疫印迹法测定心肌Gαq/11含量。 结果 :RHR术后 1周动脉血压、心肌肥大指数及Gαq/11含量与假手术组无差异 ,心肌AngII含量显著升高 (P <0 .0 1) ;术后 8周上述各指标均较假手术组升高。 12周龄SHR动脉血压、心肌肥大指数和AngⅡ含量均较同龄WKY升高 (P均 <0 .0 1) ,但心肌Gαq/11含量却无明显变化 ;4周龄时上述各指标与同龄对照相比均无明显差异。 结论 :Gαq/11在肾性和自发性高血压心肌肥大中有不同变化。     

钙调神经磷酸酶在肾血管性高血压大鼠心肌肥厚发展中的作用

本文观察了钙调神经磷酸酶(calcineurin,CaN)在肾血管性高血压大鼠肥厚心肌中的表达和活性以及CaN抑制剂——环孢菌素A(cyclosporine A,CsA)对逆转心肌肥厚的影响。利用两肾一夹肾血管性高血压大鼠心肌肥厚模型,观察大鼠心肌肥厚程度、CaN mRNA和蛋白质表达及CaN活性的改变。结果显示:大鼠左室重与胫骨长度的比值和光镜下心肌细胞横截面积在两肾一夹2月和3月组都较相应假手术组增高(P<0.05),CsA组大鼠左室重与胫骨长度比值、心肌细胞横截面积较两肾一夹2月和3月组均显著下降(P<0.05),与假手术组无显著性差异。大鼠心肌CaN mRNA和蛋白质表达及CaN活性在两肾一夹2月和3月组均高于相应假手术组(P<0.05),在CsA组低于两肾一夹2月和3月组(P<0.05)。这些结果提示,CaN参与肾血管性高血压大鼠心肌肥厚发展,抑制CaN活性可逆转心肌肥厚。     

两种高血压大鼠模型证候特征差异性的研究

目的探讨两种经典高血压实验动物模型的证候特征,以便更好地考察降压中药疗效及作用机理。方法选择自发性高血压大鼠和肾性高血压大鼠两种经典常用动物模型,从宏观表征和行为学的角度,对二者的证候特征及其差异性进行辨析比较。结果自发性高血压大鼠在14～18周龄,基本符合高血压中医辨证分型中肝火上炎证型的表现;两肾一夹型肾性高血压大鼠在术后4～8周,基本符合高血压中医辨证分型中阴虚阳亢证型的表现。结论两种高血压动物模型的中医证候特征不同,在进行降压中药的疗效评价和作用机理实验研究时,可以考虑有针对性地选用。     

氯沙坦对原发性高血压患者左心室肥厚及血清MMP-9的影响

目的:探讨氯沙坦对原发性高血压伴左心室肥厚患者左心室结构及血清MMP-9的影响.方法:86例原发性高血压伴左心室肥厚患者分为氯沙坦治疗组(n=46)和对照组(n=40).在治疗前及治疗后8w,测定收缩压和舒张压,用彩色多普勒超声诊断仪测量舒张期左心室后壁厚度(PWT),舒张期室间隔厚度(IVST),左心室舒张末内径(LVID),并计算左室重量指数(LVMI)以判定左心室肥厚程度,另外,采用酶联免疫吸附法(ELISA)检测血清MMP-9.结果:治疗8w后,两组患者的收缩压、舒张压、LVMI值、血清MMP-9均较治疗前低(P<0.01或P<0.05),且氯沙坦治疗组患者的收缩压、舒张压、LVMI值、血清MMP-9较对照组低(P<0.01或P<0.05).结论:氯沙坦能降低原发性高血压血压、逆转左心室肥厚,并且能降低血清MMP-9表达.     

感觉神经损伤性盐敏感性高血压大鼠左心室肥厚与血压的关系

目的研究感觉神经损伤性盐敏感性高血压大鼠左心室肥厚与血压的关系。方法建立感觉神经损伤性盐敏感性高血压大鼠模型,计算左心室相对重量,观察左心室组织病理学形态特点。结果感觉神经损伤性盐敏感性高血压大鼠CAP-HS组收缩压明显升高,左心室明显增重,心肌细胞肥大,肌纤维排列紊乱,心肌间质纤维化,其左心室重量指数明显升高（P〈0.01）;CON-HS组大鼠左心室重量指数也有升高（P〈0.05）。结论感觉神经损伤性盐敏感性高血压大鼠左心室增重,心肌组织病理学改变与血压升高和摄入高盐有关。     

大鼠肾性高血压发生过程中α和β肌球蛋白重链基因表达的变化

实验用二肾一夹肾性高血压大鼠模型,探讨心肌肥厚发生和逆转以及肌球蛋白重链（ｍｙｏｓｉｎ ｈｅａｖｙ ｃｈａｉｎ,ＭＨＣ）基因表达的改变。结果表明;（１）２Ｋ１Ｃ肾性高血压大鼠术后第２￣１２周,动脉血压持续升高;左室重量／体重（ＬＶＷ／ＢＷ）比值明显升高;左心室α－ＭＨＣ基因表达明显减弱;β－ＭＨＣ基因表达明显增强。（２）术后第４周给予血管紧张素转换酶抑制剂、巯甲丙腈酸和术后第８周切除肾动脉狭窄侧肾     

高血压左心室肥厚机制的研究进展

高血压左心室肥厚（LVH）是指由于高血压导致左室重量增加,病理表现为心室壁的增厚及心肌重量的增加和以心肌细胞肥大、心肌纤维化为主的心肌重构。LVH一方面是心脏的适应性肥厚,是一种代偿机制;另一方面它又是心血管事件一个独立的危险因素。随着高血压LVH进展,冠状动脉储备功能减低,心肌缺血、心力衰竭、心律失常、猝死等事件明显上升。因此,逆转左心室肥厚的治疗能改善高血压病人的预后,并减少心血管疾病的发病率和死亡率。本文就近年来高血压LVH的机制研究进展作一综述。     

氨氯地平联合依那普利治疗原发性高血压的临床疗效及对患者左心室肥厚的影响

摘要目的：探讨氨氯地平联合依那普利治疗原发性高血压的临床效果,观察联合用药对左心室肥厚的影响。方法：选择本院收治的原发性高血压患者92例,随机分为观察组和对照组,各46例,对照组给予苯磺酸左旋氨氯地平5mg,1次／d,口服;观察组在对照组基础上加用马来酸依那普利10mg,2次／d,口服,疗程均为24周。观察两组治疗前后血压变化,应用超声心动图测量两组左心室厚度变化。结果：治疗后,观察组总有效率为91_3％;对照组总有效率为73．9％,观察组总有效率高于对照组（P〈0．05）。治疗前两组心率、血压比较无统计学差异（P〉0．05）,治疗后两组血压均明显降低,观察组收缩压、舒张压明显低于对照组（P〈O．05）;观察组心率明显低于对照组（P〈0．01）。治疗前两组左心室舒张末期室间隔厚度（Leaventricularend—diastolicventricularseptalthickness,IVST）、左心室后壁厚度（1eftventricularposteriorwallthickness,U,PwT）和左室射血分数（Leftventricularejectionfxaction,LVEF）比较无统计学差异（P〉0．05）;治疗后观察组IVST、L、,PwT明显低于对照组,LVEF明显高于对照组（P〈0．05）。结论：氨氯地平联合依那普利治疗原发性高血压能有效扭转左心室肥厚,降压效果较单独应用氨氯地平更佳。     

缬沙坦联合氨氯地平治疗高血压伴左心肥厚的疗效及对心功能的影响

目的:通过探讨缬沙坦联合氨氯地平治疗高血压伴左心肥厚患者的疗效及对心功能的影响,为临床治疗提供依据。方法:选择2010年1月~2014年12月我院收治的高血压伴左心室肥厚患者共120例,按照随机数字表法随机分为观察组和对照组。对照组患者给予氨氯地平,观察组患者缬沙坦联合氨氯地平治疗,治疗6个月后,观察两组患者舒张压(DBP)、收缩压(SBP)、心率(HR)、室间隔厚度(IVST),左室后壁厚度(LVPWT)、左室舒张末期内径(LVDd)和左室重量指数(LVMI)。结果:治疗后,两组患者SBP、DBP和HR均较治疗前显著降低,差异有统计学意义(P0.05);观察组患者SBP、DBP和HR均低于对照组,差异有统计学意义(P0.05)。治疗后,两组患者IVST、IVPWT、LVDd和LVMI均较治疗前显著降低,差异有统计学意义(P0.05);观察组患者IVST、IVPWT、LVDd和LVMI均低于对照组,差异有统计学意义(P0.05)。结论:缬沙坦联合氨氯地平治疗高血压伴左心肥厚患者,能够降低患者血压、逆转左心室肥厚,改善患者心功能,疗效优于氨氯地平单独治疗,值得临床推广应用。     

肾性高血压大鼠延髓尾端神经元型一氧化氮合酶表达的改变

实验采用免疫组织化学方法观察两肾一夹肾性高血压大鼠延髓尾端两个区域（延髓腹面降压区和尾端加压区）内神经元型一氧化氮合酶（neuronal oxide synthase,nNOS）表达的变化。肾性高血压大鼠延髓尾端这两个区域的nNOS的表达均增加,说明高血压对L-Arg-NO通路活性增强。NO的前体L-Arg能增强nNOS的表达,nNOS抑制剂L-NAME则降低nNOS的表达。以上两个区域nNOS表达变化的特点在肾性高血压4周和7周的动物相同,肾性高血压7周的nNOS表达和4周比较,未见明显差异。     

A hypertensive substance found in the blood of spontaneously hypertensive rats

A substance has been obtained from the blood of spontaneously hypertensive rats which produces a hypertensive elevation of the blood pressure in normotensive rats. The substance is dialyzable and is associated with the erythrocyte membrane. It appears to be relatively long-lived in its effect on arterial pressure. The erythrocyte fractions that exhibit pressor activity also stimulate the in vitro uptake of calcium by aortas obtained from normotensive animals. This suggests that the hypertensive factor or related substances may influence the calcium metabolism of vascular tissue.     

Alterations in hypertensive arteries

Mentoring in academia is often carried out in an informal way depending on individuals and circumstances. I was quite fortunate to make the acquaintance of Professor E.E. Daniel when I was making a transition from my research in entomology to biomedical sciences. Here I recount some of that experience, and describe some of the lessons I have learned from this experience, as my tribute to Dr. Daniel on the occasion of his 80th birthday.     

Plasma concentrations of endothelin-1 in spontaneously hypertensive rats and DOCA-salt hypertensive rats

To investigate the possible involvement of endothelin-1 (ET-1), an endothelium-derived potent vasoconstrictor peptide, in the pathophysiology of hypertension, plasma ET-1 levels in 15-week-old spontaneously hypertensive rats (SHR) and DOCA-salt hypertensive rats were measured with a sandwich-type enzyme immunoassay. The vasocontractile effect of ET-1 in aortic helical preparations was significantly more sensitive in DOCA-salt hypertensive rats than in control sham-operated rats, but plasma levels of ET-1 did not differ between them. Plasma ET-1 levels in genetically hypertensive rats (SHR and stroke-prone SHR) were significantly lower than those in age-matched normotensive Wistar-Kyoto (WKY) rats. The plasma concentrations of big ET-1, a precursor of ET-1, in both SHR and SHR-SP were significantly lower than those of WKY, suggesting that the production of ET-1 is decreased in rats of genetic hypertension. Although the vascular reactivity to ET-1 increased in both DOCA-salt hypertensive and genetically hypertensive rats, present findings of the plasma ET-1 levels suggest that the role of ET-1 in the vascular control system may be different in DOCA-salt hypertensive rats and genetically hypertensive rats.     

Cerebral artery responses to pressure and flow in uremic hypertensive and spontaneously hypertensive rats

Impaired cerebral blood flow autoregulation is seen in uremic hypertension, whereas in nonuremic hypertension autoregulation is shifted toward higher perfusion pressure. The cerebral artery constricts in response to a rise in either lumen pressure or flow; we examined these responses in isolated middle cerebral artery segments from uremic Wistar-Kyoto rats (WKYU), normotensive control rats (WKYC), and spontaneously hypertensive rats (SHR). Pressure-induced (myogenic) constriction developed at 100 mmHg; lumen flow was then increased in steps from 0 to 98 microl/min. Some vessels were studied after endothelium ablation. Myogenic constriction was significantly lower in WKYU (28 +/- 2.9%) compared with both WKYC (39 +/- 2.5%, P = 0.035) and SHR (40 +/- 3.1%, P = 0.018). Flow caused constriction of arteries from all groups in an endothelium-independent manner. The response to flow was similar in WKYU and WKYC, whereas SHR displayed increased constriction compared with WKYU (P < 0.001) and WKYC (P < 0.001). We conclude that cerebral myogenic constriction is decreased in WKYU, whereas flow-induced constriction is enhanced in SHR.     

Photon radiation-induced structural and functional changes in the myocardium of hypertensive spontaneously hypertensive rats

Hypertensive SHR rates were irradiated with orange-red light using a Korobkov photon light-emitting diode matrix with a maximum radiation at 612 nm; irradiation was performed daily for 1 h for 13 days. After the course of irradiation, the rhythmoinothropic characteristics of the cardiac papillary muscle significantly improved. Morphological analysis revealed active rearrangement in myocytes, which were observed primarily in the structure of the sarcoplasmic reticulum (SR), whose relative area increased more than twice compared to the control. Apparently, photon therapy of hypertensive rats normalizes calcium homeostasis in myocytes and improves the calcium-transport function of SR. The normalization of structural and functional characteristics of the myocardium with hypertensive rates may result from an increase in the SR buffer capacity and activation of SR Ca²⁺-ATPase. Furthermore, qualitative and quantitative changes in the proportion of capillaries, myofibrils, and mitochondria in myocytes indicate the development of adaptive-compensatory processes leading to the activation of biosynthetic processes and an increase in the energy potential of the myocardium.     

Proteomic analysis of hypertrophied myocardial protein patterns in renovascularly hypertensive and spontaneously hypertensive rats

The cardiac protein profiles of spontaneously hypertensive and renovascularly hypertensive hypertrophy showed a significant alteration compared with normal hearts. Most proteins with significant modulations in their expressions belong to the category of metabolic and stress-related proteins. Among these proteins, glutathione-S-transferase mu2 and short-chain acyl-CoA dehydrogenase may be two candidate proteins associated with left ventricular hypertrophy in spontaneously hypertensive rats.