结缔组织生长因子与高血压大鼠心肌纤维化相关性及伊贝沙坦的干预研究

目的探讨结缔组织生长因子(CTGF)在高血压大鼠心肌纤维化发生发展中的作用,以及伊贝沙坦改善高血压所致心室重构和心肌纤维化可能的作用机制。方法20只12周龄雄性自发性高血压大鼠(SHR)随机分为SHR组和伊贝沙坦(IRB)组各10只,IRB组每只大鼠予以伊贝沙坦50 mg.kg-1.d-1灌胃,给药时间12周,同时取10只12周龄雄性Wistar大鼠作为对照组(WKY组),用免疫组织化学的方法对转化生长因子β1(TGF-β1)、CTGF在3组大鼠的左室心肌的分布及表达进行半定量分析;用逆转录-聚合酶链反应检测TGF-β1、CTGF mRNA在心肌表达水平;用MOSSON染色法观察左室心肌胶原形态,图像分析测量胶原容积分数(CVF)和血管周围胶原面积(PVCA)。结果(1)左室重量指数(LVI)、CVF、PVCA在SHR大鼠组明显高于WKY大鼠组(P<0.01);与SHR组比较,伊贝沙坦组则显著降低(P<0.05)。(2)CTGF主要在血管平滑肌和心肌间质中表达,相关分析表明:CTGF与TGF-β1(r=0.562,P<0.05)、CVF(r=0.715,P<0.01)、PVCA(r=0.786,P<0.01)呈正相关;(3)CTGF及其mRNA在SHR组左室心肌中的表达较WKY组明显增强(P<0.05),与SHR组比较,IRB组则明显减少。结论高血压大鼠心室肌CTGF表达增加,伊贝沙坦能抑制高血压大鼠心室肌CGTF表达,且明显改善了高血压心室重构和心肌纤维化。     

卡托普利对高血压左心室肥大心肌细胞中GRK_2表达和亚细胞分布的影响

目的:研究G蛋白偶联受体激酶2(GRK2)在高血压心肌肥大发生发展机制中的作用和卡托普利对心肌中GRK2表达水平、活性及亚细胞分布的影响,探讨卡托普利抑制心肌肥大的机制.方法:通过免疫荧光标记、共聚焦显微镜及Western blot等方法,检测6月龄的WKY(WKY组)、自发性高血压(SHR,SHRA组)大鼠,8月龄SHR(SHRB组)和卡托普利干预SHR(SHRC组)大鼠左心室心肌细胞中GRK2的表达及其分布.结果:各组大鼠左室心肌组织总蛋白中GRK2表达无明显变化(P>0.05).细胞质中GRK2表达SHRA组比WKY组表达减少(P<0.01);SHRB组比SHRC组GRK2表达进一步减少(P<0.01);而SHRC组比SHRB组GRK2表达增加( P<0.05).细胞膜蛋白中GRK2在SHRA组比WKY组表达增加(P<0.01);SHRB组比SHRA组GRK2表达进一步增加(P<0.05);而SHRC组比SHRB组GRK2表达减少(P<0.01).细胞核蛋白中无GRK2表达.共聚焦显微镜观察发现GRK2在SHR大鼠细胞膜特别是心肌细胞两端的闰盘聚集明显,卡托普利能减少GRK2在细胞膜分布.结论:GRK2与心肌细胞肥大发生发展关系密切,参与心肌肥大细胞信号转导的调控,卡托普利能通过调节GRK2亚细胞分布而发挥抑制心肌肥大作用.     

贝那普利阻断RAS系统对自发性高血压大鼠心肌JAK-STAT信号通路的影响

目的探讨贝那普利对自发性高血压大鼠(SHR)心肌组织JAK-STAT信号转导通路及细胞凋亡的影响。方法30周龄WKY大鼠12只,同龄SHR24只,随机分为SHR组,贝那普利组10mg/(kg·d)。RT-PCR法检测AT1mRNA、AT2mRNA表达,免疫组化法检测心肌组织STAT1、STAT3表达及TUNEL末端标记法进行细胞凋亡检测。结果与SHR组比较,贝那普利组AT1mRNA表达水平显著降低(P<0.01),AT2mRNA表达水平显著增高(P<0.01)。与SHR组比较,贝那普利能降低STAT1表达(P<0.01),升高STAT3表达(P<0.01)。贝那普利组心肌细胞凋亡显著低于SHR组(P<0.01)。结论贝那普利能调节心肌组织JAK-STAT信号转导通路,抑制细胞凋亡,从而发挥其心脏保护作用。     

肝细胞生长因子与自发性高血压大鼠心肌纤维化的相关研究

目的 探讨高血压进展过程中肝细胞生长因子(hepatocyte growth facor,HGF)表达与心肌纤维化的关系及血管紧张素Ⅱ受体1(ATl)拮抗剂洛沙坦的干预作用. 方法 以不同周龄自发性高血压大鼠(SHR)为心肌纤维化模型,WKY(Wistar-Kyoto)大鼠为对照组.用洛沙坦对SHR大鼠进行治疗.各周龄组WKY、SHR大鼠及干预后的SHR大鼠处死后取心脏制成石蜡切片,利用麦松三色法检测心肌胶原,免疫组织化学方法检测心肌组织HGF,Leica Qwin彩色图像分析系统分析图片. 结果 SHR大鼠心肌胶原容积(collagen volume fraction,CVF)随周龄增长而增加,8、12、16、24和32周分别为(1.8±0.1)%、(1.8±0.1)0A、(3.8±0.4)%、(7.3±0.4)%和(13.4±1.8)%,与心肌组织HGF含量呈负相关(r=-0.8820,P<0.05).洛沙坦十预可增加HGF表达,降低CVF.结论 高血压心肌纤维化可能与心肌组织HGF抗纤维化作用降低有关,AT<,1>拮抗剂治疗可以增加心肌组织HGF表达从而改善心肌纤维化.     

葛根素对异丙肾上腺素诱导的心肌纤维化和心肌结缔组织生长因子表达的影响

目的:研究葛根素对异丙肾上腺素(isoprenaline,ISO)诱导的大鼠心肌纤维化和心肌结缔组织生长因子(connective tissue growth factor,CTGF)的影响。方法:雄性SD大鼠随机分成4组:①造模组(M组)16只,采用0.05%ISO(5mg·kg-1.d-1×10d)皮下注射制作大鼠心肌纤维化模型;②早期干预组(Pa组)12只,造模同时给予葛根素(100mg·kg-1.d-1)腹腔注射56d;③后期治疗组(Pp组)12只,造模10d后给予葛根素腹腔注射46d;④对照组(C组)8只。对各组计算左心室质量指数,检测左室心肌组织中羟脯氨酸浓度,进行VG染色、免疫组化染色,测算胶原容积积分(collagen volume fraction,CVF)和CTGF蛋白含量,RT-PCR检测CTGF mRNA水平。结果:Pa组、Pp组和M组的左心室质量指数、CVF、心肌组织羟脯氨酸浓度和CTGF均较C组明显增加(P<0.01);Pa组和Pp组的左心重量指数、CVF、心肌组织羟脯氨酸浓度和CTGF均较M组明显减少(P<0.01),Pa组减少更明显。结论:葛根素减少胶原沉积,从而减轻和延缓ISO诱导的心肌纤维化,早期干预效果更明显,这种作用机制可能是通过抑制CTGF的过度表达来实现。     

自发性高血压大鼠肥厚左室心肌组织微小RNA-1与内向整流钾通道2.1表达的改变及其意义

目的观察自发性高血压大鼠(SHR)肥厚的左室心肌组织微小RNA-1、内向整流钾通道2.1(Kir2.1)表达的变化及其关系,以探讨高血压左心室肥厚(LVH)发生室性心律失常的分子机制。方法取10只17周龄雄性SHR为LVH组,10只8周龄雄性SHR为阳性对照组,10只17周龄雄性WKY大鼠作为空白对照组,通过HE染色、心肌细胞横径测量、实时荧光定量聚合酶链反应(qRT-PCR)、免疫组织化学法及Western blot检测等方法,检测大鼠左室心肌组织病理学改变、微小RNA-1表达、Kir2.1蛋白表达水平的改变。结果①与空白对照组比较,LVH组和阳性对照组的收缩压、舒张压明显升高(分别P<0.01,P<0.05);②与两对照组相比,LVH组的左室质量指数及心肌细胞横径均明显增大(均P<0.05),左室心肌细胞明显肥大,心肌间质增多,伴随着微小RNA-1表达水平明显升高,Kir2.1蛋白表达水平显著降低(P<0.05);③LVH组大鼠左室心肌组织微小RNA-1与Kir2.1蛋白的表达水平呈负相关(r=-0.720,P<0.05)。结论SHR肥厚左室心肌组织微小RNA-1表达上调,并伴随Kir2.1表达下调。     

葛根素对心肌纤维化模型大鼠左室心肌组织中转化生长因子β_1和结缔组织生长因子表达的影响

目的:研究葛根素对心肌纤维化模型大鼠左室心肌组织中转化生长因子β1(TGF-β1)和结缔组织生长因子(CTGF)表达的影响。方法:采用异丙肾上腺素(5mg·kg-1.d-1×10d)皮下注射诱导大鼠心肌纤维化,给予葛根素(100mg·kg-1.d-1)干预,实验共8周。32只雄性SD大鼠随机分成4组:模型组,空白对照组,葛根素早期干预组,葛根素后期干预组;每组于实验末,计算左室质量指数,取左室心肌组织进行VG染色、免疫组化染色,分别测算胶原容积积分(CVF)、CTGF蛋白和TGF-β1蛋白含量,取左室游离壁心肌组织检测羟脯氨酸浓度和运用RT-PCR半定量分析CTGFmRNA和TGF-β1mRNA水平。结果:葛根素减少模型组大鼠左室质量指数、左室心肌组织CVF及羟脯氨酸浓度(P0.01),模型组大鼠左室心肌组织CTGF和TGF-β1的过度表达(P0.05)。相关分析显示4组大鼠的左室心肌组织CTGF蛋白含量与左室心肌组织CVF和羟脯氨酸浓度呈正相关(P0.05)。结论:葛根素减少心肌纤维化大鼠的左室心肌间质胶原沉积,减轻和延缓大鼠心肌纤维化,这种作用机制可能是通过抑制左室心肌组织中CTGF、TGF-β1的过度表达来实现。     

阿托伐他汀对肾血管性高血压大鼠心肌纤维化及CTGF表达的影响

目的探讨阿托伐他汀对肾性高血压大鼠心肌纤维化以及结缔组织生长因子(CTGF)表达的影响。方法建立肾性高血压大鼠模型,将实验大鼠24只随机分为3组,每组8只,对照组、高血压组、阿托伐他汀组。术后4周末开始用阿托伐他汀50mg/(kg.d)连续灌胃8周。测量大鼠尾动脉收缩压,检测心肌胶原浓度、心肌总胶原容积分数(t-CVF)以及免疫组化检测心肌CTGF的表达。结果高血压组尾动脉收缩压、心肌羟脯氨酸含量、t-CVF以及CTGF的表达显著高于对照组(P<0.01);阿托伐他汀组大鼠的心肌羟脯氨酸含量、t-CVF和CTGF的表达低于高血压组(P<0.01)。结论阿托伐他汀具有抑制心肌纤维化的作用,其机制可能与下调CTGF的表达有关。     

高血压大鼠左心室肥大心肌细胞中Src激酶膜转位的研究

目的:探讨Src激酶在高血压所致左心室肥大发病机制中的作用。方法: 以自发性高血压大白鼠(SHR)为研究对象,通过免疫荧光标记、共聚焦显微镜观察及蛋白质印迹等方法,检测不同月龄的SHR左心室肥大心肌细胞中Src激酶的表达和定位的变化。结果: 蛋白质印迹检测显示,Src激酶在2、6、12和18月龄的SHR组左心室心肌组织抽提的总蛋白匀浆中的表达量与相同月龄的对照Wistar-kyoto(WKY)大鼠组相比较,无明显变化;而在其抽提的胞质蛋白匀浆中和膜蛋白匀浆中,2月龄的SHR组与对照WKY大鼠组相比较,Src激酶的表达无明显差别,但将6、12、18月龄的SHR组分别与相同月龄的WKY大鼠组比较,在胞质蛋白匀浆中Src激酶的表达显著减少(P<0.05),在膜蛋白匀浆中Src的表达则显著增加(P<0.05)。免疫荧光标记也显示,在6、12和18月龄的SHR心肌细胞中出现一些定位变化,主要表现为Src激酶在心肌细胞闰盘的聚集,在心肌细胞闰盘处可观察到较宽的明亮荧光带,这些变化正好与SHR左心室肥大心肌细胞失代偿性重构相吻合。结论:研究结果表明,在高血压所致失代偿性心肌肥大形成和发展的全过程中,存在Src激酶的膜转位,提示心肌细胞中Src激酶信号转导通路可能参与了高血压所致失代偿性左心室肥大的心肌重构过程。     

不同降压药物对自发性高血压大鼠模型左室心肌细胞中TRPC3及TRPC6表达的影响

目的:探讨缬沙坦、雷米普利及氨氯地平对自发性高血压大鼠（SHR）左室心肌中瞬时受体通道蛋白C亚族3及6(TRPC3及TRPC6)表达的影响。方法: 将24只12周龄SHR大鼠随机分为4组,即SHR组、缬沙坦组、雷米普利组及氨氯地平组,每组6只。另以6只同龄的Wistar Kyoto大鼠(WKY)为正常对照组。给药4周后,检测各组大鼠的血压、左室质量指数、左室心肌细胞横径;RT-PCR及Western Blot检测TRPC3及TRPC6 mRNA 及其蛋白的表达。结果: SHR组血压、左室质量指数及左室心肌细胞横径均明显高于对照组（P<0.05）,3个药物组上述指标均较SHR组降低（P<0.05）;5个组均有TRPC3及TRPC6的表达,SHR组TRPC3及TRPC6 mRNA及其蛋白的表达显著高于对照组（P<0.05）,3个药物组TRPC3 mRNA及TRPC6 mRNA及其蛋白的表达均显著低于SHR组（P<0.05）,缬沙坦组TRPC3 mRNA及其蛋白表达的减少最显著（P<0.05）;3个药物组TRPC6 mRNA及其蛋白的表达有所下降,但组间比较差异无显著性。结论: SHR组及对照组大鼠均有TRPC3及TRPC6的表达,TRPC3及TRPC6可能共同参与调节心肌肥厚的病理生理过程;缬沙坦可能通过抑制TRPC3蛋白的表达参与逆转左室肥厚的过程。     

Atorvastatin prevents left ventricular remodeling in spontaneously hypertensive rats

Statins improve left ventricular (LV) remodeling in spontaneously hypertensive rats (SHRs). This study was designed to investigate the effects of atorvastatin administered in the early stage on LV remodeling in SHRs, and to explore the underlying mechanisms.Sixteen male 8-week-old SHRs were randomized to receive distilled water (SHR-DW) or atorvastatin (SHR-ATV) for 12 weeks. Age-matched male Wistar-Kyoto (WKY) rats gavaged with distilled water served as controls. LV remodeling was evaluated, myocardial CTGF expression levels were detected using Western blotting, and cardiomyocyte apoptosis was detected with the TUNEL method.Compared with WKY and SHR-DW, atorvastatin treatment significantly decreased systolic blood pressure in SHRs; atorvastatin significantly inhibited LV remodeling, as indicated by the reduced LV weight/body weight ratio (SHR-ATV: 4.0 ± 0.4 versus SHR-DW: 4.7 ± 0.4 mg/g, P < 0.05), cardiomyocyte diameter (SHR-ATV: 16.2 ± 2.8 versus SHR-DW: 19.0 ± 1.0 μm, P < 0.05), and interstitial fibrosis (SHR-ATV: 3.3 ± 2.1 versus SHR-DW: 4.5 ± 1.8%, P < 0.05). Compared with WKY, myocardial CTGF expression was significantly increased and cardiomyocyte apoptosis decreased in SHRs. Compared with the SHR-DW group, atorvastatin treatment significantly inhibited myocardial CTGF expression (SHR-ATV: 0.69 ± 0.21 versus SHR-DW: 1.12 ± 0.27, P < 0.05) and induced cardiomyocyte apoptosis in SHRs (SHR-ATV: 5.2 ± 0.6 versus SHR-DW: 1.9 ± 0.3%, P < 0.05).The results indicate that early-stage administration of atorvastatin effectively prevented LV remodeling in SHRs, and that inhibition of myocardial CTGF expression and induction of cardiomyocyte apoptosis may be the underlying mechanisms.     

Contribution of reactive oxygen species to the pathogenesis of left ventricular failure in Dahl salt-sensitive hypertensive rats: effects of angiotensin II blockade

OBJECTIVE: We investigated the contribution of reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase-dependent reactive oxygen species (ROS) generation to the pathogenesis of diastolic heart failure (DHF) in Dahl salt-sensitive (DS) hypertensive rats, with the aim of testing our hypothesis that the cardioprotective effects of angiotensin II (Ang II) blockade are provided by the suppression of this pathway. METHODS: DS rats were maintained on high (H: 8.0% NaCl) or low (L: 0.3% NaCl) salt diets from age 7 to 17 weeks. DS/H rats were also treated with candesartan cilexetil (10 mg/kg per day, orally) or a superoxide dismutase mimetic, tempol (3 mmol/l in drinking water) from age 7 to 17 weeks. RESULTS: DS/H rats represented hypertension, left ventricular (LV) relaxation abnormality and myocardial stiffening with preserved systolic heart function. As compared with DS/L rats, DS/H rats showed higher levels of transforming growth factor-beta (TGF-beta), connective tissue growth factor (CTGF), p22phox and gp91phox mRNA expression, NADPH oxidase activity and thiobarbituric acid-reactive substance (TBARS) contents in LV tissues. Gene expression of uncoupling protein-2 (UCP-2), an inner mitochondrial membrane proton transporter, was also 2.8 +/- 0.5-fold higher. In DS/H rats, treatment with candesartan did not alter blood pressure, but resulted in a marked improvement of the hemodynamic deterioration; these therapeutic effects were accompanied by decreases in myocardial NADPH oxidase activity, TBARS contents and the expression of TGF-beta, CTGF, p22phox, gp91phox and UCP-2. Similar therapeutic effects were provided by treatment with tempol in DS/H rats. CONCLUSIONS: Our data suggest that NADPH oxidase-mediated ROS production contributes to the pathogenesis of DHF in DS hypertensive rats, and that the cardioprotective effects of AngII blockade are, at least partially, mediated through the suppression of this pathway.     

Localization of prolyl hydroxylase by the immunoperoxidase method in cardiovascular tissues of hypertensive rats.

An immunohistochemical method and light microscopy were utilized to determine localization of prolyl hydroxylase in the cardiovascular tissues of hypertensive rats. The blood vessels and renal glomerulus from these animals demonstrated an enhanced immunoreaction for prolyl hydroxylase. As the most prominent staining was observed in medial smooth muscle cells of blood vessels, these are probably the major collagen-producing cells in arteriosclerotic lesions induced by hypertension. In the glomerulus, endothelial cells and probably mesangial cells are mainly responsible for the collagen formation. An intense immunoreaction was also found in the fibroblasts which proliferated in the area of myocardial fibrosis in hypertensive rats, while there was no specific staining in myocardial cells in either hypertensive or normotensive rats.     

Induction of pulmonary connective tissue growth factor in heart failure is associated with pulmonary parenchymal and vascular remodeling

OBJECTIVES: Pulmonary remodeling is a well recognized consequence of heart failure (HF). However, the cellular and molecular mechanisms orchestrating the structural alterations of the lungs in HF are poorly understood. We have previously reported induction of the profibrotic peptide connective tissue growth factor (CTGF) in myocardial tissue of rats with HF, suggesting a role of CTGF during myocardial remodeling. The aim of the present study was to explore the potential role of CTGF in pulmonary remodeling in HF. METHODS: Pulmonary tissue samples were obtained from rats with myocardial infarction (MI) subsequent to ligation of the left coronary artery. Real-time quantitative RT-PCR was employed to investigate mRNA levels. The cellular distribution of CTGF was analysed by immunohistochemistry. RESULTS: Seven days after induction of myocardial infarction (MI) and HF in rats we found 2.3-fold and 1.9-fold increase of pulmonary transforming growth factor-beta1 and procollagen alpha1(I) mRNA levels, respectively, and typical morphological characteristics of pulmonary remodeling including interstitial fibrosis and medial thickening of pulmonary arteries. Pulmonary CTGF mRNA levels were substantially elevated in HF rats compared to sham-operated rats (4-fold; P<0.05) and corresponded with similar increase (3-fold; P<0.05) of pulmonary CTGF protein contents. Immunohistochemical analysis revealed increased pulmonary anti-CTGF immunoreactivity in HF, with immunostaining predominantly localized to alveolar macrophages and interstitial fibroblasts. Isolated alveolar macrophages from HF rats demonstrated substantial induction of CTGF mRNA expression (16-fold; p<0.05). Interestingly, platelets caused robust induction of CTGF mRNA expression in alveolar macrophages upon co-culture in vitro. CONCLUSION: Pulmonary CTGF was substantially increased in parallel with pulmonary remodeling in rats with HF. Our data indicate that alveolar macrophages are a major source of increased pulmonary CTGF in HF and that CTGF may be a player in the profibrotic mechanisms associated with HF.     

葡萄籽原花青素对糖尿病大鼠心肌糖基化终末产物受体和结缔组织生长因子的影响

目的 探讨葡萄籽原花青素(GSPE)对糖尿病大鼠心肌糖基化终末产物受体(RAGE)、核转录因子κB(NF-κB)和结缔组织生长因子(CTGF)的影响.方法 将链脲佐菌素诱导的糖尿病大鼠30只随机分为两组,糖尿病未治疗组(糖尿病1组)和糖尿病GSPE治疗组(糖尿病2组,每日给予GSPE 250 mg/kg灌胃)各15只;正常大鼠20只随机分为正常对照组(对照l组)和正常GSPE治疗组(对照2组,每日给予GSPE 250 mg/kg灌胃)各10只,24周后采血检测空腹血糖(FBG)、糖基化终末产物(AGEs),免疫组织化学染色和Western blot测定心肌NF-κB蛋白的表达,并应用Westernblot测定各组心肌RAGE和CTGF的蛋白表达变化.结果 糖尿病1组FBG、血清AGEs含量较对照1组显著升高(P＜0.05),经GSPE治疗后,血清AGEs含量显著降低(P＜0.05),而FBG降低差异无统计学意义;糖尿病1组心肌组织RAGE、NF-κB和CTGF蛋白表达较对照1组显著升高(P＜0.05),GSPE能够显著抑制RAGE、NF-κB和CTGF蛋白表达.结论 GSPE对糖尿病心肌病具有保护作用,其可能机制与抑制糖尿病大鼠AGEs-RAGE、NF-κB和CTGF的表达有关.     

Interactions between aldosterone and connective tissue growth factor in vascular and renal damage in spontaneously hypertensive rats

OBJECTIVE: The aim of the present study was to investigate possible inter-relationships between connective tissue growth factor (CTGF) and aldosterone in vascular and renal damage associated with hypertension. METHOD: Spontaneously hypertensive rats (SHR) were treated with two doses (100 and 30 mg/kg per day) of the mineralocorticoid receptor antagonist eplerenone, or with antihypertensive therapy (HHR) (20 mg/kg per day hydralazine + 7 mg/kg per day hydrochlorothiazide + 0.15 mg/kg per day reserpine). RESULTS: CTGF mRNA expression and protein levels in the aorta of SHR were upregulated (P < 0.05) compared with Wistar-Kyoto rats. Both doses of eplerenone similarly and significantly diminished CTGF upregulation, correlated with amelioration of aortic remodelling and endothelium-dependent relaxations. Only high-dose eplerenone and HHR significantly reduced arterial blood pressure. HHR treatment also diminished CTGF overexpression, suggesting a blood-pressure-mediated effect in CTGF regulation. This reduction, however, was lower (P < 0.05) than that produced by eplerenone (100 mg/kg per day). The direct effect of aldosterone on vascular smooth muscle cells was also studied. Incubation of cultured vascular smooth muscle cells with aldosterone increased CTGF production in a dose-related manner, but was reduced (P < 0.05) by the mineralocorticoid receptor antagonist spironolactone. Renal CTGF mRNA and protein levels were higher in SHR than in Wistar-Kyoto rats (P < 0.05), and were similarly diminished by all treatments (P < 0.05). CONCLUSIONS: These data show that aldosterone and haemodynamic stress from elevated blood pressure levels regulate vascular and renal CTGF in SHR. The results suggest that aldosterone, through CTGF stimulation, could participate in vascular and renal structural alterations associated with hypertension, describing a novel mechanism of aldosterone in hypertensive target organ damage.     

高血压左心室肥厚患者结缔组织生长因子和B型钠尿肽的变化及临床意义

目的观察原发性高血压左心室肥厚(left ventricular hypertrophy,LVH)患者结缔组织生长因子(CTGF)及B型钠尿肽(BNP)含量的变化并探讨其临床意义。方法选择120例高血压患者,分为LVH组62例和未合并LVH组(NLVH组)58例,另选择健康体检者30例为对照组。采用酶联免疫吸附法测定血清CTGF和血浆BNP的含量。采用彩色多普勒超声检查各组心脏舒张期室间隔厚度、左心室后壁厚度、左心室舒张末内径及LVEF。结果与对照组比较,NLVH组患者左心室质量指数明显升高(P<0.01),血清CTGF和血浆BNP比较,差异无统计学意义(P>0.05);LVH组血清CTGF和血浆BNP含量及左心室质量指数均明显升高,差异有统计学意义(P<0.01),且血清CTGF和血浆BNP含量与左心室质量指数呈正相关(r=0.51,r=0.64,P<0.01),NLVH组血清CTGF和血浆BNP含量与左心室质量指数比较差异无统计学意义(P>0.05)。结论血清CTGF和血浆BNP含量监测,对高血压LVH患者的诊治和预后判断具有重要临床意义。