不同剂量卡维地洛对急性心肌梗死大鼠左室重构及血流动力学的影响

目的比较不同剂量卡维地洛对大鼠急性心肌梗死(AMI)后左室重构及血流动力学的影响。方法选取AMI术后存活的SD大鼠随机分为AMI组、卡维地洛大剂量组[30mg/(kg.d)]、卡维地洛小剂量组[2mg/(kg.d)]。给药6周后用导管法行血流动力学测定和心脏组织病理分析。另设正常对照组及假手术组。结果与假手术组比,AMI组左室舒张末压(LVEDP)、各心室重量均显著增加,左室内压最大收缩和舒张速率(±dp/dtmax)显著降低。与AMI组比,大、小剂量卡维地洛组的LVEDP、心室重量均显著降低,±dp/dtmax显著升高。与卡维地洛大剂量组比,小剂量组LVEDP及左心室重量下降更明显。结论卡维地洛疗能有效抑制大鼠AMI左室重构并改善血流动力学,且小剂量卡维地洛组疗效优于大剂量组。     

葛瑞林对慢性心力衰竭模型大鼠TRX和ASK1表达影响的实验研究

目的探讨葛瑞林对慢性心力衰竭(CHF)模型大鼠心肌组织及血液中硫氧化还原蛋白(TRX)和凋亡信号调节激酶Ⅰ(ASK1)表达的影响。方法选取SD雄性大鼠88只,随机分为对照组、模型组、葛瑞林组以及阻断剂组,各22只。除对照组外均采用冠状动脉结扎法建立CHF模型,葛瑞林组和阻断剂组给予相应的药物治疗。对大鼠心脏功能[左室舒张末期内径(LVEDd)、左室收缩末期内径(LVEDs)、舒张末期左室后壁厚度(LVPW)、左室射血分数(LVEF)]、血流动力学指标[左室收缩压(LVSP)、左室舒张末压(LVEDP)、左室内压最大上升速率(+dp/dtmax)、左室内压最大下降速率(-dp/dtmax)]、血液和心肌组织TRX、ASK1水平进行检测。结果治疗后,与模型组比较:(1)葛瑞林组大鼠LVEDd、LVEDs水平较低,LVPW、LVEF水平较高(P0.05),阻断剂组大鼠LVEDd、LVEDs水平较高,LVPW、LVEF水平较低(P0.05);(2)葛瑞林组大鼠LVSP、+dp/dtmax、-dp/dtmax水平较高,LVEDP水平较低(P0.05),阻断剂组大鼠LVSP、+dp/dtmax、-dp/dtmax水平较低,LVEDP水平较高(P0.05);(3)葛瑞林组大鼠血液TRX水平较高,血液ASK1水平较低(P0.05),阻断剂组大鼠血液TRX水平较低,血液ASK1水平较高(P0.05);(4)葛瑞林组大鼠心肌组织TRX表达水平较高(P0.05),阻断剂组大鼠心肌组织TRX表达水平较低(P0.05);(5)葛瑞林组大鼠心肌组织ASK1表达水平较低(P0.05),阻断剂组大鼠心肌组织ASK1表达水平较高(P0.05)。结论葛瑞林能够明显提高CHF大鼠心脏功能,改善血流动力学指标,促进心肌组织及血液中TRX表达,抑制心肌组织及血液中ASK1表达。     

卡维地洛对大鼠急性心肌梗死后胶原网络重构的影响

目的研究卡维地洛、厄贝沙坦及二者合用对急性心肌梗死(AMI)大鼠胶原网络重构的影响。方法结扎左前降支建立雄性SD大鼠AMI模型,35只术后24h存活大鼠随机分为阳性对照组(n=8)、卡维地洛组(n=9,10mg·kg-1·d-1)、厄贝沙坦组(n=9,45mg·kg-1·d-1)和卡维地洛(10mg·kg-1·d-1)与厄贝沙坦(45mg·kg-1·d-1)合用组(n=9),另设假手术组(n=8)。治疗组直接灌胃给药干预8周后测定血流动力学参数及心功能。苦味酸天狼猩红染色心脏切片于偏振光显微镜下测量左心室梗死区及非梗死区总胶原容积分数(CVF)及、型CVF。结果AMI大鼠各组间梗死面积差异无显著性(40.02%～44.70%)。与假手术组相比,阳性对照组大鼠左心室舒张末压,左、右心室相对重量,左心室梗死和非梗死区、型CVF及总CVF均显著增加(P<0.05或P<0.01);平均血压、左心室收缩压(LVSP)、左心室内压最大上升和下降速率(±dp/dtmax)及其校正值(±dp/dtmax/LVSP)均显著降低(P<0.05或P<0.01)。与阳性对照组相比,3个治疗组左心室舒张末压,左、右心室相对重量,非梗死区总CVF及、型CVF均显著降低(P<0.05或P<0.01),但±dp/dtmax及±dp/dtmax/LVSP均显著升高(P均<0.01)。结论单用卡维地洛或厄贝沙坦与二者合用均能有效地减少左心室非梗死区胶原沉积,抑制大鼠AMI后的左心室重构,改善血流动力学和左心室功能。     

重组人生长激素对大鼠实验性心肌梗死后左室重构及心功能的影响

目的对比r-hGH和Valsartan对急性心肌梗死大鼠模型心功能,心肌梗死面积及左室重构的影响。方法通过结扎冠状动脉建立大鼠AMI模型,术后分空白对照,Valsartan和r-hGH三组。4周后通过心室内插管测定:心率(HR)、外周平均动脉压(MAP)、左室舒张压(LVDP)、左室舒张末期压(LVEDP)、左室收缩压(LVSP)、左室内压上升/下降最大速率(±dp/dt);测定左室心肌肥厚指数(LVW/BW);用TTC染色及图像分析测定左室心梗面积百分比。结果代表左心室收缩功能和舒张功能的多项指标LVSP, dp/dt,LVDP,-dp/dt:GH组>VALSARTAN组〉对照组(P<0.05)。代表左心室舒张功能的LVEDP:GH组、Valsartan组>对照组(P<0.05)、而GH组与Valsartan组比较差异无统计学意义。GH和Valsartan均有减慢心率,降低平均动脉压的作用,GH与Valsartan相比无差异。左心室心肌肥厚指数:Valsartan组相似文献   

曲美他嗪对慢性心力衰竭大鼠的心肾保护作用及其机制探究

目的探讨曲美他嗪对慢性心力衰竭(CHF)大鼠的心肾保护作用及其机制。方法将24只雄性Wistar大鼠随机分为对照组、模型组和实验组各8只。采用肾上腹主动脉缩窄法建立CHF模型,给予实验组大鼠曲美他嗪10mg/(kg·d)灌胃,给予模型组和对照组大鼠等量的生理盐水灌胃。3组大鼠均灌胃4周。比较3组大鼠的左室舒张末压(LVEDP)、左心室压力最大上升速率(+dp/dtmax)、左心室压力最大下降速率(-dp/dtmax);比较3组大鼠心肌组织在HE染色、肾组织在Masson染色下结构的变化;比较3组大鼠肾功能指标血尿素氮(BUN)、肌酐(Scr);采用蛋白质印迹法(Western bloting),比较3组大鼠肾组织基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)、α-平滑肌肌动蛋白(α-SMA)和转化生长因子-β(TGF-β)的蛋白表达。结果与模型组大鼠相比较,实验组大鼠的LVEDP明显降低,+dp/dtmax、-dp/dtmax明显升高(均P0.05);BUN、Scr明显降低(均P0.05);水肿比例明显减小,心肌纤维排列比较整齐,细胞肿胀程度明显减轻(P0.05);肾组织胶原纤维面积/视野面积的比值明显减小,肾小球毛细血管处胶原纤维增生明显减少(P0.05);MMP-2、MMP-9、α-SMA、TGF-β蛋白相对表达量明显降低(均P0.05)。结论曲美他嗪可以明显保护CHF大鼠的心肾功能,能够改善心肾组织结构。     

高血压大鼠RAS阻断后心肌中MMP-2的蛋白表达

目的探讨高血压大鼠左室心肌中基质金属蛋白酶-2(MMP-2)蛋白表达的变化以及血管紧张素转化酶抑制剂(ACEI)、血管紧张素Ⅱ1型受体拮抗剂(AT1-ant)单独与联合治疗对高血压大鼠心肌中MMP-2蛋白表达影响。方法40只雄性8周龄的易卒中自发性高血压大鼠(SHRSP)随机分成5组(n=8)：SHRSP对照组、安慰剂组、缬沙坦组、苯那普利组及缬沙坦、苯那普利联用组。另外，取8只雄性8周龄的京都Wistar大鼠(WKY)作为对照。利用免疫组织化学的方法检测WKY以及SHRSP左室心肌中MMP-2蛋白的表达。结果SHRSP的收缩压(SBP)、左室重量指数(LVMI)、胶原容积分数(CVF)、血管周围胶原面积(PVCA)、左室心肌MMP-2蛋白表达较同龄的WKY显著增高。给予苯那普利、缬沙坦单独或联合治疗后SFIRSP的LVMI、CVF、PVCA、左室心肌MMP-2蛋白表达都显著降低。苯那普利、缬沙坦单独应用时的效果没有差异。而联合应用的效果更显著。结论SHRSP左室心肌中MMP-2蛋白表达增高，肾素血管紧张素系统(RAS)阻断后MMP-2蛋白表达显著减少；苯那普利、缬沙坦逆转高血压心室重塑的作用可能部分通过下调MMP-2蛋白表达而实现；苯那普利和缬沙坦都能降低SHRSP的血压以及逆转其左室重塑，而联合用药的作用更显著。     

氨甲酰化促红细胞生成素逆转慢性心力衰竭大鼠左室重构的研究

目的:探讨氨甲酰化促红细胞生成素(CEPO)对慢性心力衰竭(CHF)大鼠左心室重构的影响。方法:健康雄性Wistar大鼠90只,随机选取10只作为对照组,其余腹腔注射异丙肾上腺素(ISO)进行造模。5周后将造模成功者再分为CHF组和CEPO组,后者腹腔注射CEPO50μg/kg,2次/周,CHF组和对照组同期腹腔注射等量生理盐水,4周后检测各组大鼠血流动力学指标、血浆B型脑钠肽(BNP)水平,并计算左心室重量指数(LVW/BW)。结果:与对照组相比,CHF组左室内压峰值(LVSP)、左室内压上升/下降最大速率(±dp/dtmax)显著降低,左室舒张末压(LVEDP)显著升高(P<0.05),血浆BNP水平显著升高(P<0.05),LVW/BW也显著升高(P<0.05)。与CHF组相比,CEPO组LVSP、±dp/dtmax均显著升高,而LVEDP则显著降低(P<0.05),血浆BNP水平显著降低(P<0.01),LVW/BW也显著降低(P<0.05)。结论:CEPO可通过降低血浆BNP水平、减轻左心室重构来改善CHF大鼠的心功能。     

氯沙坦联合依那普利对急性心肌梗死大鼠左室重塑的预防作用及相关机制

目的探究氯沙坦联合依那普利对急性心肌梗死大鼠左室重塑的预防作用及相关机制。方法选取SD大鼠60只,随机数字表法分为正常组、模型组、氯沙坦组、依那普利组和氯沙坦联合依那普利组(联合组),每组各12只。除正常组外,其余4组均构建急性心肌梗死模型。对比分析各组大鼠心功能指标[左心室射血分数(LVEF)、左室短轴缩短率(LVFS)和舒张末期左室心肌质量指数]、梗死面积、血流动力学指标[收缩压(SBP)、舒张压(DBP)、平均动脉压(MAP)、左室收缩压(LVSP)和左心室舒张末压(LVEDP)]、左室参数(左心室实际和相对重量)、左室功能指标[左室截面最短径(DMIN)和最长径(DMAX)]、心肌白细胞介素1β(IL-1β)和基质金属蛋白酶(MMP-9)mRNA表达水平、Ⅰ型和Ⅲ型胶原含量以及心肌组织中血管紧张素Ⅱ(AngⅡ)和心钠素的含量。结果模型组和氯沙坦组、依那普利组和联合组大鼠心肌梗死面积和心率比较,差异无统计学意义(P>0.05)。与正常组大鼠相比,模型组和氯沙坦组、依那普利组和联合组大鼠LVEF、LVFS和Lvmass(c)dI、SBP、DBP、MAP和LVSP值均降低(P<0.05),LVV、DMIN和DMAX以及左心室实际和相对重量均增加(P<0.05),IL-1β和MMP-9 mRNA表达水平、Ⅰ型和Ⅲ型胶原含量以及AngⅡ和心钠素含量升高(P<0.05),发生左室重塑。与模型组相比,氯沙坦组、依那普利组和联合组大鼠的LVEF、LVFS和Lvmass(c)dI、SBP、DBP、MAP和LVS P值均升高(P<0.05),LVV、DMIN和DMAX以及左心室实际和相对重量均减少(P<0.05),IL-1β和MMP-9 mRNA表达水平、Ⅰ型和Ⅲ型胶原含量以及AngⅡ和心钠素含量均降低(P<0.05)。结论氯沙坦联合依那普利能防治急性心肌梗死大鼠左室重塑和改善心功能,这可能与减少Ⅰ型和Ⅲ型胶原的增加量、抑制炎性细胞因子IL-1β的表达以及降低MMP-9活性有关。     

特异性COX-2抑制剂对压力负荷性心肌肥厚大鼠左心室重构的影响

目的观察特异性COX2抑制剂对大鼠慢性压力负荷性心肌肥厚过程中左室重构的影响。方法将SD大鼠随机分3组:模型对照组、模型组和实验组,模型组和实验组按腹主动脉缩窄致压力负荷性心肌肥厚制作大鼠模型。实验组加用特异性COX2抑制剂rofecoxib干预,20周用高频超声测定左心室结构和功能,心肌组织胶原Masson染色,测定总胶原容积百分比(CVF T)和无冠状动脉小血管视野胶原容积百分比(CVF NV)。结果模型组左室壁增厚,特别是室间隔增厚明显,左室重量增加(P<0.01),左室腔扩大。实验组左室舒张内径(LVDD)及LVM较模型组降低(P<0.01)。模型组CVF T和CVF NV明显增加(P<0.01),实验组则减少(P<0.01),与模型对照组无差异(P>0.05)。结论COX2参与了心肌胶原重塑的过程。特异性COX2抑制剂有抗心室重构作用,可能与抗心肌纤维化的作用有关。     

替米沙坦对实验性糖尿病心肌病大鼠心脏功能的影响

[目的]利用糖尿病心肌病大鼠模型来观察替米沙坦对糖尿病心肌病心脏功能的保护作用,探讨其与核因子-κB(NF-κB)表达的关系.[方法]采用SD大鼠一次性腹腔注射链脲佐菌素(STZ)55 mg/kg诱发糖尿病心肌病模型.替米沙坦20 mg/(kg·d)干预8周后,测定大鼠心功能、左心室重量指数,用免疫组化法观察心肌NF-κB表达量.[结果]糖尿病心肌病组大鼠左心室重量指数(LVMI)、左室舒张末期压(LVEDP)和室内压上升达最大速率所需时间(t-dp/dt)明显高于对照组(P＜0.05);左室收缩压(LVSP)、室内压最大上升速率(+dp/dtmax)、室内压最大下降速率(-dp/dtmax)明显低于对照组(P＜0.05);替米沙坦显著下调心肌NF-κB表达.[结论]替米沙坦能改善糖尿病大鼠心脏收缩和舒张功能,减轻心肌肥厚,对糖尿病大鼠心肌有保护作用.其机制之一可能与抑制NF-κB 表达有关.     

胰岛素治疗高血压动脉硬化性脑梗死的实验研究

目的：观察胰岛素（ Ｉｎｓ）对高血压动脉硬化大鼠脑梗死的疗效。方法：５０ 只肾血管性高血压大鼠（ Ｒ Ｈ Ｒ）复制成大脑中动脉闭塞（ Ｍ Ｃ Ａｏ）模型,随机分４ 组： Ａ 组１２ 只（ Ｉｎｓ ２１ Ｕ／ｋｇ）, Ｂ组１２ 只〔 Ｉｎｓ ２１ Ｕ／ｋｇ＋ ５０％ 葡萄糖（２ ｇ／ｋｇ）〕, Ｃ组 １２ 只〔 Ｉｎｓ ４５ Ｕ／ｋｇ＋ ５０％ 葡萄糖（４ ｇ／ｋｇ）〕和 Ｄ组 １４ 只（生理盐水 ４ ｍ ｌ／ｋｇ）。各组均于 Ｍ Ｃ Ａｏ 后即注射胰岛素, Ｍ Ｃ Ａｏ 后 ４ 小时和２４ 小时检查神经功能,２４ 小时处死大鼠取脑,测大脑体积和梗死灶体积。结果： Ａ 组的血糖较其他组有统计学意义的下降（ Ｐ均＜ ００１）, Ｃ组的神经功能障碍评级、梗死灶体积及其与大脑体积的百分比的减少都有统计学意义（ Ｐ 均＜ ００１）, Ａ、 Ｂ、 Ｄ组间比较则无差异（ Ｐ 均＞００５）。结论：胰岛素对缺血脑组织具有不依赖于其降糖作用的直接保护作用, Ｒ Ｈ Ｒ Ｍ Ｃ Ａｏ 后注射胰岛素在较高剂量时才显示疗效,这可能与高血压致脑血管发生病变有关。     

Increased resting heart rate and glucose metabolism in a community population

ObjectiveResting heart rate (RHR) independently predicts cardiovascular death. Increased RHR is related to chronic diseases, but community-based studies are rare. We investigated this population and factors related to RHR.MethodsIn total, 374 participants underwent medical examinations from March 2019 to December 2019. Participants were divided into groups with low RHR (LRHR; <65 beats/minute) and high RHR (HRHR; ≥65 beats/minute). RHR was judged using resting electrocardiogram at physical examination. We conducted laboratory examinations, including glycosylated hemoglobin (HbA1c), fasting plasma glucose (FPG), and blood lipids, among participants with chronic diseases. We used Cox proportional risk regression and multivariate analyses for the following covariates: previous chronic diseases, body mass index (BMI), smoking, blood lipids, and FPG.ResultsThe incidence of type 2 diabetes mellitus (T2DM) and HbA1c values were both significantly higher in the HRHR group than in the LRHR group. Spearman correlation analysis showed RHR had a positive correlation with low-density lipoprotein, BMI, FPG, and HbA1c (r = 0.104574, 0.117266, 0.116041, and 0.311761, respectively). Multiple linear regression analysis showed age, hypertension, T2DM, and HbA1c were factors influencing RHR.ConclusionRHR showed strong correlation with T2DM and HbA1c in our community population, suggesting that RHR may be a risk factor for cardiovascular disease.     

静息心率对慢性心力衰竭合并高血压患者心功能及预后的影响

目的 探讨静息心率(resting heart rate, RHR)与慢性心力衰竭合并高血压患者心功能及预后的关系。方法 2016年9月至2017年8月于保定市第一中心医院心内科因慢性心力衰竭住院的高血压患者250例,按入院RHR水平分为3组:RHR1组,RHR＜70次/min;RHR2组,70次/min≤RHR＜90次/min;RHR3组,RHR≥90次/ min。测量患者超声心动图参数,包括左心室舒张末期内径(left ventricular end diastolic diameter, LVEDD)和左心室射血分数 (left ventricular ejection fraction, LVEF),按照纽约心脏病协会(NYHA)分级情况对患者入院、出院及随访时的心功能进行评估并记录,对比各组之间各项指标及疗效的差异,并分析其相关性。结果 随着入院RHR的升高,LVEF呈现逐渐降低的趋势（P＜0.05）, 而LVEDD、B型脑钠肽(BNP)均逐渐升高,以RHR3 组最高（P＜0.05）;RHR1组、RHR2组出院疗效及随访疗效均优于RHR3组（P＜0.05）;RHR3组入院RHR水平与出院疗效呈负相关（r=-0.251, P均＜0.05）;RHR2组、RHR3组（入院-出院）RHR差值与出院疗效、随访疗效均呈正相关（其与出院疗效相关性r值分别为0.197、0.279, 其与随访疗效相关性的r值分别为0.214、0.321, P均＜0.05）。结论 对于慢性心力衰竭合并高血压的患者,静息心率水平越高,左心功能越差,出院疗效及随访疗效也越差,积极合理的控制RHR有助于改善预后。     

Effects of angiotensin-converting enzyme inhibition and calcium channel blockade on cardiac apoptosis in rats with 2K1C (two-kidney/one-clip) renovascular hypertension

Apoptosis plays a role in the regulation of heart mass and architecture, and might contribute to the cardiac remodelling seen in renovascular hypertension. It is not known whether the beneficial effects of angiotensin-converting enzyme (ACE) inhibition or calcium channel blockade on cardiac remodelling are linked to the modulation of apoptosis. To test this hypothesis, we established four groups of rats: (i) sham-operated controls, (ii) a group that underwent the two-kidney/one-clip (2K1C) procedure, (iii) a group with 2K1C treated for 12 weeks with quinapril (6 mg x day(-1) x kg(-1)), and (iv) a group with 2K1C treated for 12 weeks with diltiazem (24 mg x day(-1) x kg(-1)). Treatment started 2 weeks after clipping. Systolic blood pressure was reduced to a similar extent by quinapril and diltiazem (2K1C, 223+/-19 mmHg; 2K1C+quinapril, 149+/-15 mmHg; 2K1C+diltiazem, 160+/-40 mmHg; both P <0.01 compared with 2K1C alone). Left ventricular weight, interstitial fibrosis and perivascular fibrosis were reduced significantly by both drugs. The apoptotic index (apoptotic cells/total cell number) was increased 21.6-fold (P <0.01) after quinapril treatment as compared with the 2K1C group, but was not affected by calcium channel blockade. In conclusion, our study demonstrates that ACE inhibition, in contrast with calcium channel blockade, may cause regression of cardiac hypertrophy/remodelling in 2K1C renovascular hypertensive rats through enhanced apoptosis.     

Activity of Erythropoietin and Renin in Renal Venous Blood of Hypertensive Patients

Plasma activities of renin and erythropoietin were determined in the renal veins of the right and left kidneys of hypertensive patients. The patients were divided into the following groups either according to the origin of the hypertension (group 1: control or essential hypertension, group 2: renovascular hypertension) or according to the hormone levels (group 3: renin activity exceeding 10 ng/litre in at least one of the renal veins and group 4: erythropoietin activity higher than 4% 5 9Fe incorporation in at least one of the renal veins). In groups 1, 2 and 3 a statistically significant difference in renin activity was found between the kidney with the higher renin activity and that with the lower activity However, in group 4, the side, which showed elevated erythropoietin values also had higher renin activity as compared to the essential hypertensive group. Erythropoietin activity probably does not parallel the increased renin activity found in renovascular hypertension or in some cases of non-renovascular hypertension. However, in several cases of renal vascular alterations, both systems can be activated simultaneously.     

Protective Role of Resting Heart Rate on All-Cause and Cardiovascular Disease Mortality

ObjectiveTo study the protective role of lower resting heart rate (RHR) in cardiovascular disease (CVD) and all-cause mortality.Patients and MethodsPatients (n=53,322) who received a baseline medical examination between January 1, 1974, and December 31, 2002, were recruited from the Cooper Clinic, Dallas, Texas. They completed a medical questionnaire and underwent clinical evaluation. Patients with CVD or cancer or who had less than 1 year of mortality follow-up were excluded from the study. Relative risks and 95% CIs for all-cause and CVD mortality across RHR categories were estimated using Cox proportional hazards models.ResultsHighest cardiorespiratory fitness with lower mortality was found in individuals with an RHR of less than 60 beats/min. Similarly, patients with a higher RHR (≥80 beats/min) were at greater risk for CVD and all-cause mortality compared with an RHR of less than 60 beats/min. This analysis was followed by stratification of the data by hypertension, where hypertensive individuals with high RHRs (≥80 beats/min) were found to be at greater risk for CVD and all-cause mortality compared with those with hypertension and lower RHRs (<60 beats/min). In addition, unfit individuals with high RHRs had the greatest risk of CVD and all-cause mortality. The unfit with low RHR group had a similar risk for CVD and all-cause mortality as the fit with high RHR group.ConclusionLower cardiorespiratory fitness levels and higher RHRs are linked to greater CVD and all-cause mortality.     

静息心率水平和血脂异常的关系研究

目的 探讨静息心率(RHR)水平和血脂异常的关系.方法 按照随机抽样的方法抽取样本,对772名健康查体者进行相关调查,其中包括RHR和血脂水平.将人群按RHR分为3组:＜70次/min组,70～80次/min组,≥80次/min组,并分析RHR水平与血脂异常之间的关系.结果 心率水平和甘油三酯(TG)及总胆固醇(TC)呈正相关(r值分别为0.136、0.110,P均＜0.05),高TG及高TC血症患病率随心率水平的升高呈明显的升高趋势(趋势χ2值分别为7.213、5.285,P均＜0.05),而RHR和低HDL-C及高LDL-C患病率之间无明显关系(趋势χ2值分别为3.562、4.149,P均＞0.05).采用Logistic回归模型校正了体重指数、性别、血肌酐、血尿酸、空腹血糖及年龄等因素后,以RHR＜70次/min组作为对照,70～80次/min组高TG血症患病率的OR值为1.540(95%CI:1.086～2.185,P=0.016),≥80次/min组 OR 值为1.640(95%CI:1.067～2.523,P=0.024);70～80次/min组高TC血症患病率的OR值为1.197(95%CI:0.749～1.913,P=0.453),≥80次/min组OR值为1.814(95%CI:1.036～3.177,P=0.037).结论 RHR和TG及TC呈正相关,与高TG及高TC血症的患病相关,且独立于体重指数、性别、血肌酐、血尿酸、空腹血糖及年龄等因素,而心率水平与HDL-C及LDL-C没有明显关系.     

老年代谢综合征患者静息心率与靶器官损害

目的 探讨老年代谢综合征(SMS)患者静息心率(RHR)与靶器官损害(TOD)的关系.方法 采用病例对照研究方法,将215例SMS患者按RHR水平分为3组:RHR1组(55例):<60 次/min;RHR 2组(87例):70次/min≤RHR<80次/min,RHR3组(73例):RHR≥80次/min;设立正常对照组(60例):健康老年人.所有研究对象做以下检查:心电图、超声心动图、颈动脉超声、肌酐清除率(Ccr)以及尿微量白蛋白(MAU);部分SMS患者行冠状动脉造影和头颅CT.结果 ①与对照组相比,SMS各组的颈动脉内膜厚度(IMT)、颈动脉内径(CAD)、左心室质量指数(LVMI)以及MAU均升高,而左室射血分数(LVEF)、肌酐清除率(Ccr)降低(P<0.05或P<0.01).SMS各组随RHR增加,IMT、CAD、LVMI、MAU和冠状动脉造影评分逐渐增加,而LVEF、Ccr逐渐减少(P<0.05或P<0.01).②RHR与IMT、CAD、LVMI、MAU呈正相关(r分别为0.34、0.25、0.62和0.57,P<0.05或P<0.01),而与LVEF、Ccr呈负相关(r分别为-0.60和-0.52,均P<0.01).③非条件Logistic回归分析显示,RHR、收缩压(SBP)、舒张压(DBP)和脉压(PP)对心肌肥厚、冠心病、心力衰竭、脑卒中和肾功能损害有不同程度的影响(P<0.05或P<0.01),其中PP和RHR的作用更大.结论 RHR可能是SMS患者TOD的独立危险因素.控制RHR对SMS的发生发展具有重要意义.     

Effects of endothelin-A receptor antagonism on bilateral renal function in renovascular hypertensive rats

Recent studies indicated an enhanced expression of Endothelin (ET) in the kidney contralateral to the vascular clip in two-kidney, one-clip (2K-1C) Goldblatt hypertension. We proposed that the enhanced intrarenal ET production might be responsible for altered haemodynamic and excretory capability of the unclipped kidney (UK) of 2K-1C renovascular hypertensive rats. Therefore, we examined the changes in arterial pressure and split renal function in the clipped (CK) and UK simultaneously, in response to chronic administration of the selective ETA receptor blocker (A-127722), given orally at a dose of 30 mg/kg/day for 3 weeks starting from the beginning of the 4th week of clipping. Systolic pressure averaged 177 +/- 7 mmHg in control rats (n=15) and 164 +/- 9 mmHg in treated rats (n=16) and the difference was not statistically different. Glomerular filtration rate (GFR), renal plasma flow (RPF) and renal vascular resistance (RVR) in the UK were not different between control and treated groups. Data were then analyzed by classifying rats as moderate hypertensives (MAP < 180 mmHg), and severe hypertensives (MAP > 180 mmHg). In the moderately hypertensive group, average MAP was 143 +/- 5 mmHg and 138 +/- 4 mmHg in control (n=9) and treated (n=10) groups, respectively. In the severely hypertensive group, average MAP was 192 +/- 5 mmHg and 188 +/- 5 mmHg in control (n=6) and treated (n=6) groups, respectively. GFR and RPF were significantly improved in the UK of only the severely hypertensives who received the antagonist. However, the ET(A) antagonist blunted the sodium loss in both CK and UK of severely hypertensive rats. We conclude that ET(A) receptors do not play a role in the progression of hypertension in 2K-1C renovascular hypertensive rats. Yet, ET(A) receptors play an important role in altering renal hemodynamics of the unclipped kidneys in severe degrees of renovascular hypertension.     

Circadian renal rhythms influenced by implanted encapsulated hANP-producing cells in Goldblatt hypertensive rats

Renal excretion in experimental hypertensive rats implanted with encapsulated human atrial natriuretic peptide (hANP)-producing cells is circadian periodic. Chinese hamster ovary (CHO) cells transfected with the plasmid hANP-cDNA were encapsulated in biocompatible polycaprolactone capsules for intraperitoneal implantation into two-kidney, one-clip (2K1C) hypertensive rats. During a 12:12 light-dark cycle, as compared to control CHO cells, the implantation of encapsulated hANP-producing CHO cells was associated with an increase in the net excretion of water, sodium and potassium, and with a reversal of the advanced circadian phases related to renovascular hypertension in 2K1C rats. The increase in blood pressure postimplantation was delayed, and increases in renal blood flow, glomerular filtration rate, sodium output, urinary excretion and urinary cyclic GMP concentrations were also found. Implantation of encapsulated hANP-producing cells affects circadian rhythms in kidney excretion functions of 2K1C rats, and may be useful for the treatment of cardiovascular disease.