卡维地洛对大鼠心室肌细胞Ito电流影响的实验研究

目的探讨卡维地洛对大鼠心室肌细胞瞬时外向钾电流(Ito)的作用.方法采用胶原酶酶解法分离得到大鼠单心室肌细胞;采用膜片钳全细胞技术记录灌流卡维地洛前后Ito电流的变化.结果灌流0.1 mM及1.0 mM卡维地洛后,Ito电流密度分别为(pA/pF)(5.06±1.98),(3.91±0.66),P＜0.05;不同去极化电压水平Ito电流值也有明显减小,Ⅰ-Ⅴ曲线向下方移位.结论卡维地洛对大鼠心室肌细胞Ito电流具有抑制作用,此抑制作用呈浓度依赖趋势.     

卡维地洛对慢性心力衰竭幼鼠心室重构的干预及作用机制

目的:探讨卡维地洛治疗幼鼠慢性心力衰竭(CHF)的疗效及作用机制.方法:采用腹主动脉缩窄术建立幼鼠CHF模型,术后4周随机分3组:假手术对照组、CHF组、卡维地洛组.直接灌胃给药,8周后行血流动力学、心肌病理分析、心肌细胞凋亡及其相关基因Bcl-2、p53蛋白表达水平和检测血清中脂质过氧化物(LPO)和超氧化物歧化酶(SOD)含量.结果:与假手术组比较,CHF组收缩压(SBP)、舒张压(DBP)、左室收缩压(LVSP)、左室舒张末压(LVEDP)、左右心室相对重量(LVRW,RVRW)、LPO、凋亡指数(AI)、p53基因蛋白表达水平显著升高(P<0.01),左室内压最大收缩率( dp/dtmax)、左室内压最大舒张率(-dp/dtmax)、SOD、Bcl-2基因蛋白表达水平均显著降低(P<0.01).与CHF组比较,卡维地洛组SBP、DBP、LVSP、LVEDP、LVRW、RVRW、LPO、AI、p53基因蛋白表达水平下降, dp/dtmax,-dp/dtmax,SOD,Bcl-2基因蛋白表达水平显著升高(P<0.01).结论:卡维地洛能有效抑制CHF幼鼠心室重构的发展,而抗凋亡、抗氧化、改善血流动力学是其治疗心室重构的重要机制.     

卡维地洛在心力衰竭治疗中的应用

作为治疗高血压的b受体阻断药卡维地洛,在临床上发现有抗心力衰竭作用,是获准FDA批准用于治疗心力衰竭的第一个b受体阻断药,本文就卡维地洛治疗心力衰竭做一综述。     

卡维地洛治疗充血性心力衰竭合并快速型心房纤颤的疗效观察

目的　观察卡维地洛治疗充血性心力衰竭 (CHF)合并快速型心房纤颤 (Af)的临床疗效。方法　将CHF并快速型Af患者 5 6例 ,随机分为治疗组、对照组各 2 8例。治疗组在常规治疗的基础上加用卡维地洛。对照组给予强心利尿等常规治疗。疗程均为 16周。结果　治疗组在临床疗效 (92 .86 % )、心电图疗效 (85 .72 % )以及心泵功能各项指标均明显优于对照组 (P <0 .0 1)。结论　卡维地洛治疗CHF并快速型Af,既能有效控制心室率 ,又能显著改善心功能。     

卡维地洛对扩张型心肌病患者运动时心率的影响

目的　研究有心衰的扩张型心肌病 (心功能NYHAⅡ级 )伴慢性持续性房颤患者在心衰治疗同时加用卡维地洛对心率控制的改善。方法　 2 4例扩张型心肌病伴房颤患者随机分成卡维地洛组 (Ⅰ组 ,12例 )和对照组 (Ⅱ组 ,12例 )。Ⅰ组在原有治疗基础上加用卡维地洛 ,开始剂量 3.12 5mg ,每日 1次 ,每 2周剂量加倍 1次 ,6周后目标剂量为12 .5mg ,每日 2次 ,并持续至研究结束 (共 12周 )。Ⅱ组维持原有的治疗不加任何其他药。结果　Ⅰ组患者静息心率下降 9%～ 35 % ,运动时最大心率下降 4 %～ 2 1% ,踏车运动总时间增加 1%～ 2 9% ,以上数据P =0 .0 0 1,室性异位心律也减少。Ⅱ组各项指标无变化。结论　在有心衰的扩张型心肌病伴房颤患者加用卡维地洛可以改善静息心率和运动时心率控制 ,从而提高运动耐受性。     

Influence of carvedilol and propranolol on coronary blood flow

A total of 17 patients with angiographically proven coronary artery disease and at least one stenosis blocking 70% of the left anterior descending or circumflex artery were included in a double-blind, randomized study. They received either 5 mg carvedilol or 6 mg propranolol intravenously. Heart rate, aortic pressure, mean coronary sinus pressure and coronary flow (thermodilution) were measured and coronary resistance and the rate-pressure product were calculated before and 25 min after injection. Carvedilol significantly (P < 0.05)=" lowered=" the=" heart=" rate=" (mean,=" 76=" to=" 69=" beats/min),=" aortic=" pressure=" (mean,=" 153/80–135/72=" mmhg),=" rate-pressure=" product=" (mean,=" 117–93=" mmhg/min),=" and=" coronary=" flow=" (mean,=" 114–94=" ml/min).=" coronary=" resistance=" (mean,=" 0.97–1.07=" mmhg=" ×=" min/ml)=" and=" coronary=" flow=" related=" to=" the=" rate-pressure=" product=" (mean,=" 1.0–1.02=" ml/mm=" hg)=" showed=" no=" significant=" change=" after=" carvedilol=" treatment.=" propranolol=" lowered=" the=" heart=" rate=" (mean,=">P < 0.05)=" and=" rate-pressure=" product=" (mean,=" 109–96=" mm.=" hg/min;=" not=" significant).=" aortic=" pressure=" (mean,=" 145/72–147/74=" mmhg),=" coronary=" flow=" (mean=" 109–101=" ml/min),=" coronary=" resistance=" (mean,=" 1.1–1.2=" mmhg=" ×=" min/ml),=" and=" coronary=" flow=" related=" to=" the=" rate-pressure=" product=" (mean,1.12–1.19=" ml/mmhg)=" showed=" no=" significant=" change=" after=" propranolol=" administration.=" following=" single=" application,=" carvedilol=" lowered=" the=" rate-pressure=" product=" more=" markedly=" than=" did=" propranolol=" on=" account=" of=" its=" acute=" blood-pressure-lowering=" effect.=" no=" differences=" in=" the=" hemodynamic=" effects=" of=" carvedilol=" and=" propranolol=" were=" found.=" neither=" drug=" seems=" to=" influence=" the=" adaption=" of=" coronary=" flow=" to=" myocardial=" oxygen=">     

Efficacy and safety of carvedilol in renal hypertension A multicenter open trial

Carvedilol, a novel -blocker with a vasodilating action, was given either alone (monotherapy) or with diuretics (combination therapy) to 42 patients with renal hypertension. The hypotensive effect, safety, and optimal dose were investigated. In all, 23 untreated patients (16 men and 7 women; average age, 56.4 ± 2.5 years) made up the monotherapy group and 19 diuretic-treated patients (11 men and 8 women; average age, 56.4 ± 2.5 years) comprised the combined therapy group. All subjects had an initial blood pressure (BP) of > 160/95 mmHg and were started on 5 mg/day oral carvedilol. The dose was gradually increased to a maximum of 20 mg/day, or until either the BP was reduced to < 149/89=" mmhg=" or=" the=" reduction=" in=" mean=" bp=" was="> 13 mmHg compared with baseline levels. The total study period was 8 weeks. With monotherapy, the BP and heart rate decreased significantly from 167/102 to 150/94 mmHg and from 81 to 74 beats/min, respectively. With combined therapy, the BP and heart rate fell significantly from 176/103 to 142/85 mmHg and from 81 to 70 beats/min, respectively. Responders were defined as subjects with a BP of 149/89 mm Hg or those showing a fall of 13 mmHg in mean BE Responders accounted for 52.2% of the monotherapy group and 73.6% of the combination therapy group. Orthostatic hypotension was not seen in either group. Serum creatinine and blood urea nitrogen (BUN) levels were not altered by administration of carvedilol. Dizziness was noted by 1 of the 23 subjects in the monotherapy group. These results suggest that carvedilol is an effective and well-tolerated antihypertensive agent for the management of renal hypertension. We considered the optimal dose to be from 10 to 20 mg once daily, which is similar to that recommended for essential hypertension.     

卡维地洛治疗65例慢性心衰患者的目标剂量与耐受情况探讨

目的探讨卡维地洛治疗慢性心衰患者的目标剂量与耐受情况。方法慢性心衰患者65例作为研究对象，在常规心衰治疗措施基础上加用卡维地洛．起始剂量视心功能状态而定，目标剂量按心率目标、血压目标、心衰目标确定。结果卡维地洛平均维持量为6．25～50mg／d，平均（22．5±10．3）mg／d。达心率目标量和血压目标量无统计学差异（P〉0．05）；但心率目标量和血压目标量较心衰目标量显著偏低俨〈0．001）。结论卡维地洛在慢性心衰的治疗中是安全的，且较大剂量（接近目标剂量）时患者也能较好耐受；不同目标剂量确定方式存在差异．心衰目标剂量较心率目标与血压目标显著增大。     

Carvedilol in the failing heart.

Patients with chronic heart failure due to left ventricular systolic dysfunction of ischemic or nonischemic etiology have shown improvement in morbidity and mortality with carvedilol therapy. In patients with symptomatic (New York Heart Association class II-IV) heart failure, carvedilol improves left ventricular ejection fraction and clinical status, and slows disease progression, reducing the combined risk of mortality and hospitalization. Despite the overwhelming evidence for their benefit, there continues to be a large treatment gap between those who would derive benefit and those who actually receive the drug. In this article, the pharmacology, clinical trial evidence, and the potential differences between carvedilol and other beta blockers are discussed. Carvedilol provides powerful therapy in the treatment of chronic heart failure caused by a variety of etiologies and in a wide array of clinical settings.     

卡维地洛与琥珀酸美托洛尔治疗慢性收缩性心力衰竭的临床观察

目的： 分析卡维地洛与琥珀酸美托洛尔治疗慢性收缩性心力衰竭的临床疗效。方法： 选取于2009年1月-2011年1月在某院心内科接受治疗的慢性收缩性心力衰竭患者,随机分为A组和B组,其中A组应用卡维地洛进行治疗,B组应用琥珀酸美托洛尔进行治疗。待治疗24个月后随访两组患者的临床治疗效果、综合超声心动图主要指标、NT-proBNP的差异。结果： 共纳入267例收缩性心力衰竭患者,分析结果显示A组和B组治疗后左室射血分数、左室舒张末期内径及NT-proBNP明显改善,具有统计学意义（P<0.01）;与B组相比,A组对左心室射血分数的改善更加显著（P<0.05）,而对左室舒张末期内径和NT-proBNP的改善两组无统计学差异（P>0.05）。结论： 卡维地洛和琥珀酸美托洛尔均可明显改善慢性收缩性心力衰竭患者的心功能指标;与琥珀酸美托洛尔相比,卡维地洛能更显著提高慢性收缩性心力衰竭患者的左室射血分数。