静脉及口服美托洛尔对急性心肌梗死住院患者血压与心率的影响（中国心脏研究-Ⅱβ阻滞剂预试验报告）

目的评估β阻滞剂美托洛尔对急性心肌梗死(AMI)住院患者血压及心率的影响。方法入选发病24 h内可疑AMI的住院患者,且无研究药物明确禁忌证的。将入选对象随机分为β阻滞剂美托洛尔治疗组或相应安慰剂组。首先静脉注射美托洛尔或安慰剂5 mg,间隔2~3 min后,再注射5 mg,注射3次共15 mg;然后美托洛尔/安慰剂口服第1天为50 mg,4次/d;第3天起为200 mg,1次/d。疗程最长4周或出院。主要研究指标是血压、心率、其他不良反应、病死率及其他并发症。结果1999-11-2000-05,10家大中医院完成预试验研究236例,其中随机分到美托洛尔治疗组120例,安慰剂对照组116例。治疗前两组患者基础临床特征相似。当天进行静脉注射的美托洛尔与安慰剂组分别为100%与99.2%,完成3支静脉注射的为87.9%与95.8%;住院期提前停用的为24.4%与13.6%。治疗后,美托洛尔组低血压、心动过缓发生率均明显高于安慰剂组(P≤0.05~0.01);两组总病死率(7.8%vs 8.4%)相似(P=0.86),其他并发症也无明显差异。美托洛尔静注及口服后治疗组心率明显均低于对照组(P<0.01),血压略低于安慰剂组。结论美托洛尔早期治疗AMI住院患者低血压及心动过缓发生率较高。     

静脉及口服美托洛尔对急性心肌梗死住院患者血压与心率的影响(中国心脏研究-Ⅱβ阻滞剂预试验报告)

目的评估β阻滞剂美托洛尔对急性心肌梗死(AMI)住院患者血压及心率的影响.方法入选发病24 h内可疑AMI的住院患者,且无研究药物明确禁忌证的.将入选对象随机分为β阻滞剂美托洛尔治疗组或相应安慰剂组.首先静脉注射美托洛尔或安慰剂5 mg,间隔2～3 min后,再注射5 mg,注射3次共15 mg然后美托洛尔/安慰剂口服第1天为50 mg,4次/d;第3天起为200mg,1次/d.疗程最长4周或出院.主要研究指标是血压、心率、其他不良反应、病死率及其他并发症.结果 1999-11-2000-05,10家大中医院完成预试验研究236例,其中随机分到美托洛尔治疗组120例,安慰剂对照组116例.治疗前两组患者基础临床特征相似.当天进行静脉注射的美托洛尔与安慰剂组分别为100%与99.2%,完成3支静脉注射的为87.9%与95.8%;住院期提前停用的为24.4%与13.6%.治疗后,美托洛尔组低血压、心动过缓发生率均明显高于安慰剂组(P≤0.05～0.01);两组总病死率(7.8%vs 8.4%)相似(P=0.86),其他并发症也无明显差异.美托洛尔静注及口服后治疗组心率明显均低于对照组(P＜0.01),血压略低于安慰剂组.结论美托洛尔早期治疗AMI住院患者低血压及心动过缓发生率较高.     

普拉固早期强化治疗对急性心肌梗死患者压力和化学反射敏感性的影响

研究在急性心肌梗死(AMI)发作的早期,普拉固强化治疗对患者压力反射敏感性(BRS)和化学反射敏感性(ChRS)的影响。采用随机、单盲、空白对照方法,共入选84例AMI患者,均在入院后24h内随机分配至对照组(n=28),传统治疗组(普拉固组20mg/d,n=28),强化治疗组(普拉固组40mg/d,n=28)。3组主要基本资料具有可比性。分别在入院时、用药后4周检测血脂水平、BRS值、ChRS值及所有不良反应。结果:普拉固组20mg/d和40mg/d治疗4周后的患者较治疗前血脂指标均有明显改善;与对照组相比,2治疗组治疗后的血脂水平有显著改善(P<0.05);2治疗组间差异无显著性。4周后3组BRS值、ChRS值较入院时均有明显改善;与对照组相比,2治疗组治疗后的BRS值、ChRS值均有显著改善(7.34±2.26,6.87±0.53vs5.66±1.34;7.83±3.36,6.38±1.25vs5.28±1.12;P均<0.01);与传统治疗组相比,强化治疗组治疗后BRS值、ChRS值的差异亦有显著性。结论:普拉固早期强化干预能改善AMI的BRS、ChRS值,且具有剂量依赖性。     

高血压病患者压力感受器敏感性

目的探讨高血压病患者压力感受器敏感性(BRS)情况及其可能影响因素。方法用全自动生化仪测定血脂、血糖,用倾斜方法同时记录血压和心率,BRS=(最低血压时RR间期-基础RR间期)/(最低血压-基础血压),用袖带对肱动脉加压后放气,测定肱动脉内径变化率的方法代表血流介导的内皮舒张功能。结果(1)高血压病患者的BRS明显小于正常对照组[(6.9±7.3vs13.9±3.6)ms/mmHg,P<0.01],亦明显小于肾性高血压组[(6.9±7.3vs12.2±6.2)ms/mmHg,P<0.01];高血压病BRS有随着高血压分级增高而下降趋势,1级患者BRS大于3级患者[(10.2±4.0vs5.4±4.8)ms/mmHg,P<0.01],2级患者BRS大于3级患者[(7.6±2.4vs5.4±4.8)ms/mmHg,P<0.01];(2)高血压病伴高脂血症患者BRS小于高血压病不伴高脂血症组[(2.2±4.7vs7.2±6.4)ms/mmHg,P<0.01];(3)高血压病患者血管内皮舒张功能与BRS相关(r=0.565,P<0.01),肾性高血压组内皮舒张功能与BRS相关(r=0.573,P<0.05),正常对照组内皮舒张功能与BRS相关(r=0.610,P<0.05)。结论(1)BRS功能降低可能是高血压病发病原因之一;(2)降脂治疗可通过升高BRS,改善高血压病患者的预后;(3)血管内皮舒张功能与BRS有关,可通过改善血管内皮舒张功能改善BRS。     

卡维地洛与美托洛尔对急性心肌梗死患者左室功能的影响

急性心肌梗死 (AMI)患者左室功能降低与病死率、致残率密切相关。本研究比较观察了卡维地洛与美托洛尔对AMI患者左室收缩与舒张功能的影响 ,现报告如下。1　对象与方法选择 2 0 0 0年 5月～ 2 0 0 3年 5月在吉林大学第一医院心内科住院及出院后门诊随访的AMI患者共 1 38例 ,排除入选时收缩压 <90mmHg( 1mmHg=0 .1 33kPa) ,心率 <5 0次 /min ;梗阻性肺疾病或哮喘 ;P R间期 >0 .2 4s,Ⅱ或Ⅲ度房室传导阻滞 ;killip 4级。将入选患者随机分美托洛尔组、卡维地洛组与对照组 ,前两组在症状开始 2 4h内分别口服美托洛尔 5 0mg ,bid ,与卡维地…     

氯沙坦、苯那普利及二者联合治疗高血压病的对比性研究

目的对比氯沙坦、苯那普利及二者联合治疗轻、中度原发性高血压(EH)的降压效果及耐受性.方法入选的轻、中度EH患者(坐位舒张压90～109 mmHg)经1周药物冲洗期及2周安慰剂期后,随机分为3组(1)L组,口服氯沙坦 50 mg/天;(2)B组,口服苯那普利 10 mg/天;(3)L+B组,口服氯沙坦 50 mg/天,苯那普利 10 mg/天.疗程8周.共入选病例67例,完成8周观察者63例,L组22例,B组20例,L+B组21例.于服安慰剂期末及治疗1、2、4、6、8周末测诊室血压、心率(HR)并记录不良反应.治疗前后测血浆肾素活性(PRA)、血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD)浓度.结果治疗8周后三组血压均下降,其中L组下降10.8±6.2/17.5±5.5 mmHg,总有效率59.1%;B组下降11.2±5.4/16.4±4.6 mmHg,总有效率65.0%;L+B组下降26.4±5.7/32.1±11.0 mmHg,总有效率95.2%.L+B组降压幅度最大,与L组、B组比较有统计学意义(P＜0.001).L组与B组的降压幅度及有效率无显著差异(P＞0.05).三组血浆ALD浓度在治疗后均下降,其中L+B组ALD下降较L组与B组显著(P＜0.001).氯沙坦组不良反应少.结论氯沙坦有明显降压作用,与苯那普利合用有叠加效应.     

西地那非治疗原发性肺动脉高压3例

例1:女性45岁,活动后气急1年,晕厥两次。心超测肺动脉收缩压97mmHg,右房右室增大。右心导管测肺动脉压为75/29mmHg,平均压47mmHg,血压95/62mmHg。诊断为原发性肺动脉高压(PPH),口服西地那非50mg,50min后测肺动脉压降至65/24mmHg,平均压降至38mmHg,但血压降至81/52mmHg,患者无明显症状。出院后口服西地那非25mg/bid,随访1周,症状有所改善,血压未见降低。 例2:女性47岁,头晕伴气急近10年。心超测肺动脉平均压85mmHg,多种药物治疗,效果不佳。行右心导管检查,提示在房间隔水平出现右向左分流,测肺动脉收缩压108mmHg,平均压65mmHg,口服西地那非50mg后,观察2h,肺动脉压均无明显变化。患者未出现不良反应。     

西拉普利与氨氯地平对高血压患者QT离散度与心律失常的疗效

目的:研究西拉普利与氨氯地平对原发性高血压患者QT间期离散度与心律失常的疗效。方法:2011年3月~2014年3月我院收治的120例原发性高血压合并室性心律失常的患者被纳入研究对象,随机均分为西拉普利组和氨氯地平组,两组均接受常规降压治疗,比较两组的血压、QT间期以及心律失常情况。结果:与氨氯地平组比较,西拉普利组患者的24h平均收缩压[(123.81±17.95)mmHg比(104.92±14.25)mmHg]、舒张压[(88.31±10.28)mmHg比(72.24±8.45)mmHg],24h平均收缩压变异度[(11.62±1.34)mmHg比(7.34±0.97)mmHg]、舒张压变异度[(9.47±1.18)mmHg比(5.13±0.72)mmHg],QT间期[(385.1±50.4)ms比(342.7±48.5)ms]、校正QT间期[(362.7±50.2)ms比(321.8±45.1)ms]、QT间期离散度[(34.1±5.1)ms比(22.5±3.7)ms]均明显降低(P<0.05或<0.01);室性心律失常分级明显优于氨氯地平组(P<0.05)。结论:对于高血压并发心律失常病人西拉普利治疗较氨氯地平降低血压,QT间期离散度和改善室性心律失常的疗效更好。     

美托洛尔和苯那普利对急性心肌梗死患者心率变异性的影响

目的：评价美托洛尔和苯那普利对急性心肌梗死（AMI）患者心率变异性的影响,方法：无合并症的AMI患者共49例,15例为美托洛尔组,15例为苯那普利组,19例为安慰剂组,于心肌梗死后5－7d及治疗30d后行24h动态心电图检查,观察心率变异性的时域指标和频域指标的变化,结果：心肌梗死后各组的心率变异性明显减低,美托洛尔和苯那普利治疗后,心率变异性的时域指标和频域指标均明显改善,结论,美托洛尔和苯那普利可以明显改善无合并症AMI患者的心率变异性。     

原发性高血压伴左心室肥厚患者Tp-Te间期初探

目的 探讨原发性高血压(EH)及伴左室肥厚患者T波峰-末(Tp - Te)间期.方法 根据血压将入选患者分为3组,血压对照组121例(血压≤139/89 mmHg),EH组126例(血压≥140/90 mmHg),高血压伴左室肥厚组16例.晨起空腹抽血,测血压,描记心电图.分规法测Tp - Te间期.结果 Tp - Te间期高血压组(103.3 ms±14.2 ms)与对照组(101.8 ms±12.8 ms)比较无统计学意义,而高血压伴左室肥厚组Tp- Te间期(112.0 ms±15.1 ms)延长,与高血压组及对照组比较有统计学意义(P＜0.05).结论 高血压伴左室肥厚患者Tp - Te间期延长,发生心脏事件的可能性增大.     

Effects of converting enzyme inhibition on baroreflex sensitivity in patients with myocardial infarction.

BACKGROUND. Baroreflex sensitivity provides useful prognostic information in patients after acute myocardial infarction. However, no data are available about the effects of converting enzyme inhibition on this variable. OBJECTIVES. The aim of the study was to evaluate the effects of angiotensin-converting enzyme inhibition on baroreflex sensitivity in patients after uncomplicated myocardial infarction. METHODS. Twenty-five patients after uncomplicated myocardial infarction underwent baroreflex sensitivity evaluation 72 to 96 h after symptom onset and after 4 days of captopril therapy. Twenty additional patients with the same characteristics were evaluated at the same time intervals before and after placebo administration to identify spontaneous baroreflex sensitivity variations. Baroreflex sensitivity was assessed by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in the RR interval. RESULTS. The mean baroreflex sensitivity value increased after captopril administration from 6.5 +/- 4.2 to 11.8 +/- 6.1 ms/mm Hg (p less than 0.01) and in individual analyses increased by greater than 2 ms/mm Hg in 68% of patients. Mean plasma renin activity increased after captopril from 3.7 +/- 2.4 to 8.5 +/- 4.9 ng/ml per h (p less than 0.005). No difference was detectable in baroreflex sensitivity and plasma renin activity values according to the site of necrosis. In the control group, baroreflex sensitivity and plasma renin activity remained unchanged between the two studies. CONCLUSIONS. This study demonstrates that in patients with uncomplicated myocardial infarction, captopril significantly improves the chronotropic response to baroreceptor stimulation.     

Stability of the noninvasive baroreflex sensitivity assessment using cross-spectral analysis of heart rate and arterial blood pressure variabilities

BACKGROUND: Depressed baroreflex sensitivity (BRS), usually estimated using the invasive phenylephrine method or the nitroprusside test, is significantly and independently associated with an increased risk of malignant ventricular arrhythmias and sudden cardiac death in patients surviving acute myocardial infarction. Several investigators have compared the standard phenylephrine test and different noninvasive methods. HYPOTHESIS: This study evaluated the influence of different body positions with different breathing regimes on cross-spectral baroreflex indices (coherence between the spectral densities of blood pressure and cardiac cycle variabilities) in both low- and high-frequency bands. METHODS: The data were obtained in 103 patients (73 males, aged 53 +/- 12 years) with coronary artery disease and/or hypertension. Simultaneous electrocardiographic and noninvasive blood pressure recordings were obtained in each subject in both supine and sitting positions during both spontaneous and slow and fast controlled respiration (0.1 and 0.33 Hz). RESULTS: The results show a significant bias and disagreement between noninvasive baroreflex sensitivity (BRS) indices. The mean values of the baroreflex in low frequency ranged from 5.0 +/- 5.3 to 10.1 +/- 7.9 ms/mmHg, while in high frequency, the mean values ranged from 6.6 +/- 6.1 to 10.1 +/- 7.9 ms/mmHg. The limits of agreement ranged from +/-1.7 to +/-4.1 ms/mmHg with bias from -1.0 to +0.7 ms/mmHg. CONCLUSION: A comprehensive comparison of different methods shows that BRS estimated in low-frequency band in sitting position during spontaneous respiration is the most representative part of the global baroreflex gain.     

Cardiovagal response to acute mild exercise in young healthy subjects.

BACKGROUND: The aim of the present study was to investigate the effect of a single bout of mild exercise on autonomic nervous system activity in healthy subjects. METHODS AND RESULTS: The study group comprised 18 healthy males, aged between 20 and 24 years, who had not been training regularly for the last 3 months. A supine recording of systolic arterial pressure (SAP) and RR interval and the administration of the phenylephrine test were performed at baseline and repeated after a 60-min recovery period following treadmill exercise training for 30 min at 65% of maximal heart rate. Mean SAP and RR interval, heart rate variability (HRV) indices (the standard deviation of normal-to-normal RR intervals (SDNN), the square root of the mean of squared differences between successive intervals and the percentage of adjacent RR intervals differing more than 50 ms), noninvasive spectral baroreflex sensitivity (Spe-BRS) and phenylephrine baroreflex sensitivity (Phe-BRS) were assessed before and after training. Mean SAP measured after exercise was lower than baseline (120+/-12 mmHg vs 128+/-12 mmHg, p = 0.05). Spe-BRS and Phe-BRS increased significantly after exercise, from 11.8+/-6.1 ms/mmHg to 16.0+/-7.8 ms/mmHg (p = 0.034), and from 16.0+/-8.8 ms/mmHg to 21.9+/-9.3 ms/mmHg (p = 0.022), respectively. A parallel increase was also observed in SDNN (from 81+/-44 ms to 96+/-53 ms, p = 0.02), but the other HRV indices showed no significant differences between pre- and post-exercise. CONCLUSIONS: A single session of mild exercise performed by sedentary young men leads to significant autonomic nervous system improvement, which suggests that even mild physical activity is beneficial for neural cardiac regulation and should be recommended to sedentary healthy subjects.     

The effect of spironolactone, cilazapril and their combination on albuminuria in patients with hypertension and diabetic nephropathy is independent of blood pressure reduction: a randomized controlled study.

OBJECTIVE: The effect of spironolactone, cilazapril and their combination on albuminuria was examined in a randomized prospective study in female patients with diabetes and hypertension. PATIENTS AND METHODS: Sixty female diabetic patients aged 45-70 years with blood pressure (BP) 140-180/90-110 mmHg, serum creatinine (sCr) < or = 160 micro mol/l, HbA(1c) < or = 10%, and albuminuria were treated by atenolol 12.5-75 mg/d and hydrochlorothiazide 6.25-25 mg/d. Titration-to-target helped to reach BP values < or = 135/85 mmHg in 46 patients after 12 weeks. These patients were randomized to spironolactone 100 mg/d or cilazapril 5 mg/d for 24 weeks. Then both groups received spironolactone 50 mg/d and cilazapril 2.5 mg/d for 24 weeks. BP was stabilized by tapering the dose of the initial agents. Urinary albumin/creatinine ratio (ACR), BP, K(+). sCr and HbA(1c) were assessed at baseline and at weeks 12, 16, 36 and 60. RESULTS: The average BP at week 12 was 128 +/- 4/81 +/- 3 mmHg and remained constant, in both groups, throughout the study. ACR declined on spironolactone from a median value (range) of 452 (124-1571) to 216 (64-875) mg/g (P = 0.001), and on cilazapril to 302 (90-975) mg/g (P = 0.001). The difference between spironolactone and cilazapril was significant (P = 0.002). Combined treatment resulted in a further modest decline in ACR. Serum creatinine was unaltered by spironolactone and rose slightly (121 to 126 micro mol/l, P = 0.02) on cilazapril. CONCLUSION: At the doses tested, spironolactone was superior to cilazapril in reducing albuminuria. Combined administration was more effective than either drug alone. These effects were independent of BP values. Hyperkalaemia was the main side-effect.     

Nocturnal home hemodialysis improves baroreflex effectiveness index of end-stage renal disease patients

BACKGROUND: In patients with end-stage renal disease receiving conventional hemodialysis, both the frequency with which brief rises or falls in systolic blood pressure initiate concordant changes in pulse interval (arterial baroreflex effectiveness index), and the gain of reflex heart rate responses to these stimuli (arterial baroreflex sensitivity) are diminished. In chronic renal failure, low baroreflex effectiveness index and baroreflex sensitivity are associated with increased rates of all-cause mortality and sudden death, respectively. Conversion to home nocturnal hemodialysis augments baroreflex sensitivity but its effects on baroreflex effectiveness index have not been reported. METHODS: In 20 consecutive hypertensive conventional hemodialysis patients training to transition to nocturnal hemodialysis (age 41 +/- 2 years; mean +/- standard error), baroreflex effectiveness index, baroreflex sensitivity (sequence method) and total arterial compliance (stroke volume/pulse pressure) were determined during quiet rest before and 2 months after conversion. RESULTS: With nocturnal hemodialysis, dialysis frequency doubled, the dose per session increased by 70% and antihypertensive medications were withdrawn (from 2.5 +/- 0.3 to 0.2 +/- 0.1 drugs/patient, P < 0.01) because systolic blood pressure fell (from 139 +/- 5 to 119 +/- 4 mmHg, P < 0.05). Baroreflex effectiveness index increased from (0.33 +/- 0.03 to 0.42 +/- 0.03, P = 0.01). Baroreflex sensitivity increased from 5.60 +/- 0.88 to 8.48 +/- 1.60 ms/mmHg (P < 0.05). Changes in total arterial compliance correlated with changes in baroreflex sensitivity (r = 0.63, P = 0.004) but not baroreflex effectiveness index (r = 0.05, P = 0.95), suggesting independent mechanisms for their attenuation and recovery in end-stage renal disease. CONCLUSION: Nocturnal hemodialysis increases baroreflex effectiveness index in addition to baroreflex sensitivity. The hypothesis that such changes might reduce cardiovascular event rates in this high-risk population merits prospective evaluation. More frequent engagement of the arterial baroreflex after conversion to nocturnal hemodialysis may improve short-term cardiovascular regulation.     

Mechanism of lipid enhancement of alpha1-adrenoceptor pressor sensitivity in hypertension

OBJECTIVE AND DESIGN: Plasma lipids enhance alpha1-adrenoceptor pressor sensitivity, impair baroreflex function, and correlate with increased blood pressure. This clinical study was designed to determine whether the enhanced alpha1-pressor sensitivity induced by acute hyperlipidemia is primarily mediated by increased vascular alpha1 responsiveness, reduced baroreflex sensitivity (BRS) or both. METHOD: Regional alpha1-adrenoceptor vasoreactivity was measured using a graded brachial artery infusion of the alpha1 agonist, phenylephrine, in seven subjects with stage 1 hypertension. Forearm blood flow was estimated from venous occlusion plethysmography. The phenylephrine dose-forearm blood flow response curve was used to determine alpha1-vascular reactivity (slope of the dose-response curve) and sensitivity, EC50 (phenylephrine dose inducing 50% maximal response). BRS (ms/mmHg) was measured as the slope of the progressive rise in systolic blood pressure and the resultant lengthening in the subsequent R-R interval after systemic intravenous boluses of phenylephrine. Subsequently, plasma lipids were raised with a 1-h systemic co-infusion of intralipid and heparin, after which measurements of regional vasoreactivity and BRS were repeated. RESULTS: Mean arterial pressure was 109 +/- 4 versus 110 +/- 3 (P = NS), vasoreactivity was -0.71 +/- 0.10 versus -0.82 +/- 0.10 (P = NS) and log EC50 was 1.47 +/- 0.29 versus 1.52 +/- 0.34 nmol/l (P = NS) before and after raising non-esterified fatty acids, respectively. In contrast, mean BRS was acutely reduced from 8.2 +/- 2.1 to 6.2 +/- 1.8 ms/mmHg (P = 0.02) after the lipid infusion. CONCLUSIONS: These findings suggest that in hypertensive patients, the primary mechanism for short-term alpha1-pressor hypersensitivity in response to hyperlipidemia is via the acute impairment of BRS.     

Baroreflex sensitivity and its evolution during the first year after myocardial infarction

Experimental data have indicated that baroreflex sensitivity is often depressed in dogs after myocardial infarction and that this depression correlates strongly with subsequent mortality during episodes of acute myocardial ischemia. This finding has several clinical implications. The present study was undertaken with the objectives of assessing the potential existence of differences in baroreflex sensitivity between men with and without myocardial infarction and the time course during the 1st year after infarction of these potential changes in baroreflex sensitivity. Fifty-three subjects entered the study: 32 postinfarction patients and 21 control subjects. Baroreflex sensitivity was assessed by increasing mean blood pressure by aphenylephrine infusion (70 micrograms/ml) and recording the consequent RR interval changes. Baroreflex sensitivity, expressed as the slope of the regression line relating mean blood pressure to RR interval changes, was evaluated 18 days (n = 32), 3 months (n = 17) and 13 months (n = 10) after infarction. Baroreflex sensitivity was lower in the patients than in the control subjects (8.2 +/- 3.7 versus 12.3 +/- 2.9 ms/mm Hg, p = 0.0001). Moreover, 13 (41%) of 32 patients had a baroreflex slope less than 6.5 ms/mm Hg, which was 2 SD below the mean value of the control subjects. The internal control follow-up study showed that baroreflex sensitivity increased 3 months after infarction to values quite similar to those observed in the control subjects (11.1 +/- 5.3 versus 8.7 +/- 3.5 ms/mm Hg, p = 0.02). No further change was observed between 3 and 13 months after myocardial infarction. These data indicate that baroreflex sensitivity is lower in a proportion of postinfarction patients than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of vitamin C on baroreflex sensitivity in chronic heart failure

Chronic heart failure (CHF) reduces baroreflex sensitivity. Low baroreflex sensitivity, a risk factor for sudden death, could arise partly from CHF-dependent endothelial dysfunction. Vitamin C at high doses has a protective role against CHF-related endothelial damage. This study was conducted to investigate the effect of vitamin C on baroreflex sensitivity in CHF. A study group of 33 subjects with CHF secondary to postischemic dilated cardiomyopathy with an ejection fraction 相似文献   

Differential effects of angiotensin II and angiotensin-(1-7) at the nucleus tractus solitarii of transgenic rats with low brain angiotensinogen

OBJECTIVES : In this study, we investigated the effects of angiotensin II and angiotensin-(1-7) at the nucleus tractus solitarii (nTS) in transgenic rats with a severe deficit in brain angiotensinogen production, TGR(ASrAOGEN) (TGR). METHODS : Angiotensin II (10 pmol), angiotensin-(1-7) (10 pmol) or NaCl (0.9%/50 nl) were microinjected into the nTS of urethane-anaesthetized TGR (n = 36) and Sprague Dawley (SD) (n = 34) rats. Mean arterial pressure (MAP) and heart rate were measured via a femoral artery catheter and the baroreflex control of heart rate was evaluated after increases in MAP induced by phenylephrine (baroreflex bradycardia). RESULTS : Angiotensin II microinjections into the nTS of the TGR induced a higher decrease in MAP and heart rate (-37 +/- 5 mmHg and -69 +/- 12 b.p.m., respectively) in comparison to SD rats (-18 +/- 1 mmHg and -43 +/- 5 b.p.m., respectively). In contrast, changes after angiotensin-(1-7) microinjections into the nTS of TGR (-6 +/- 1 mmHg and -13 +/- 4 b.p.m.) were significantly smaller than that induced in SD (-11 +/- 2 mmHg and -24 +/- 6 b.p.m.). The baseline baroreflex sensitivity to phenylephrine of TGR was accentuated in comparison to SD rats (0.70 +/- 0.06 versus 0.44 +/- 0.03 ms/mmHg). Angiotensin II microinjection into the nTS produced similar attenuation in the baroreflex bradycardia in both SD (0.28 +/- 0.07 versus 0.5 +/- 0.07 ms/mmHg, before injection) and TGR (0.44 +/- 0.1 versus 0.82 +/- 0.1 ms/mmHg, before injection). In contrast, angiotensin-(1-7) microinjection elicited a facilitation of the baroreflex bradycardia in SD (0.68 +/- 0.12 versus 0.41 +/- 0.03 ms/mmHg, before injection), while in TGR, angiotensin-(1-7) induced an attenuation of baroreflex bradycardia (0.34 +/- 0.07 ms/mmHg versus 0.55 +/- 0.05 ms/mmHg, before injection). CONCLUSIONS : These results indicate that a permanent inhibition of angiotensinogen synthesis in the brain can lead to an increase in the sensitivity of the baroreflex control of heart rate (baroreflex bradycardia) and an increase in angiotensin II responsiveness at the nTS. However, the nTS effect of angiotensin-(1-7) was significantly attenuated in these transgenic rats. These data further indicate that the decrease in brain angiotensins in the transgenic rats may be functionally relevant and support the concept of differential regulatory mechanisms for the effects of the two angiotensin peptides.     

Acute aldosterone antagonism improves cardiac vagal control in humans

OBJECTIVES: We have examined the acute effects (<45 min) of aldosterone antagonism on heart rate variability and baroreflex sensitivity, markers of cardiac vagal control, in 13 healthy subjects. BACKGROUND: Evidence for the beneficial effects of aldosterone antagonists comes from studies showing increased survival rates following their addition to standard heart failure therapy. Many mechanisms have been suggested for this action, including effects upon the autonomic nervous system. METHODS: Heart rate variability and baroreflex sensitivity were examined 30 min following the administration of potassium canrenoate (intravenous) (aldosterone antagonist) or saline (control). RESULTS: Active treatment reduced resting heart rate (-6 +/- 1 beats/min [mean +/- standard error mean]) compared to control (0 +/- 1 beat/min) (p < 0.001) and increased measures of high frequency (HF) heart rate variability. Root mean square of successive RR interval differences increased by 21 +/- 5 ms versus -6 +/- 5 ms control (p < 0.001); HF power increased by 1,369 +/- 674 ms(2)with aldosterone antagonism compared to -255 +/- 431 ms(2) following saline infusion (p < 0.01). Baroreflex sensitivity (alpha-HF) was increased after active treatment (+4 +/- 2 ms/mm Hg vs. 0 +/- 1 ms/mm Hg control [p < 0.05]). No changes in plasma potassium levels were observed. CONCLUSIONS: These results provide evidence that aldosterone antagonists acutely improve cardiac vagal control, irrespective of any diuretic effects, and may in part explain their beneficial effects in treatment of heart failure.