静滴硝酸异山梨酯对充血性心力衰竭患者左室功能的影响

目的:观察硝酸异山梨酯注射液对充血性心力衰竭患者左室功能的影响。方法:30例充血性心力衰竭患者(男性18例,女性12例,年龄63±11岁),以硝酸异山梨酯注射液20mg加入5％葡萄糖液50ml中,按2.5mg/h滴速,每天维持8小时,连用7天。给药前、给药后进行超声心动图检查及心率、血压、心电图的检查。结果:经硝酸异山梨酯治疗后患者心率、血压均有降低,NST、∑ST明显降低;左心室收缩与舒张功能均有改善(P<0.01或P<0.05)。结论:短期静滴硝酸异山梨酯能改善充血性心力衰竭患者的左心收缩和舒张功能。     

贝那普利对慢性充血性心力衰竭患者左心室及血管内皮功能的影响

目的探讨贝那普利对慢性充血性心力衰竭患者左心室及血管内皮功能的影响。方法选取268例慢性充血性心力衰竭,随机分为常规治疗组130例采取常规治疗,贝那普利组138例采取常规治疗联合贝那普利治疗,观察两组治疗前后血管内皮功能测定、左室舒张末内径(LVDd)、左心室射血分数(LVEF)并进行比较。结果两组治疗后FMD、左室舒张末内径、射血分数比较差异有统计学意义(P<0.05)。结论慢性充血性心力衰竭应用贝那普利可以有效的逆转左室重塑,改善左心室功能、血管内皮功能,改善血流动力学,减轻心力衰竭,改善患者的生活质量。     

培哚普利与贝那普利治疗左心心力衰竭的比较

目的 :比较培哚普利与贝那普利治疗心力衰竭的疗效。方法 :培哚普利组 4 0例 (男性 2 7例 ,女性 13例 ,年龄 67a±s10a)应用培哚普利 4mg ,po ,qd .贝那普利组 4 0例 (男性 2 7例 ,女性 13例 ,年龄 71a± 9a)应用贝那普利 10mg ,po ,qd。 2组疗程均为 4wk。结果 :培哚普利组抗心力衰竭有效率为 82 % ,贝那普利组抗心力衰竭有效率为 80 % ,2组间差异无显著意义 (P >0 .0 5)。 2药均有减轻心肌缺血、改善左室收缩功能作用。 2组副作用均轻微。结论 :培哚普利和贝那普利抗心力衰竭作用相近     

沙利度胺对慢性充血性心力衰竭的影响

目的:探讨慢性充血性心力衰竭(CHF)病人应用沙度胺,治疗前后血浆心衰相关细胞因子水平及左室收缩功能变化。方法:将98例CHF病人(左室射血分数LVEF≤40％)随机分为2组,对照组常规应用治疗心衰药物,沙利度胺组在此基础上加用沙利度胺25～150mg·d-1,共用12wk,于治疗前后分别测定TNF-α,IL-6,超声心动图评价左室收缩功能。结果:CHF病人经沙利度胺治疗12wk后, TNF-α(p<0.01)、IL-6(P<0.05)水平均降低,且左室收缩功能显著改善(P<0.01)。结论:常规治疗慢性充血性心力衰竭基础上加用沙利度胺,安全易耐受,可显著改善CHF相关的临床症状和心功能。     

氯沙坦对慢性心力衰竭大鼠心室重塑和心功能保护作用的实验研究

目的研究氯沙坦(Los)对腹主动脉缩窄致慢性心力衰竭大鼠心室重塑和心功能的保护作用。方法SD大鼠40只,随机分为腹主动脉缩窄(COA)+Vehicle组,COA+Los组,假手术(Sham)+Vehicle组,Sham+Los组。药物干预8周后采用超声心动图和心室插管法评估心功能,计算左、右心室质量指数(LVMI、RVMI),比色法检测心肌羟脯氨酸(HYP)含量,酶联免疫吸附试验(ELISA)检测心肌Ⅰ型和Ⅲ型胶原含量和比值,放射免疫法(RIA)检测心肌血管紧张素Ⅱ(Ang Ⅱ)和醛固酮(ALD)水平。常规苏木素-伊红(HE)、Masson三色染色和透射电镜观察心肌组织形态学改变。结果与COA组相比,COA+Los组大鼠心功能和LVMI等指标明显好转,心肌HYP和Ⅰ型胶原含量降低,Ⅰ/Ⅲ型胶原比值降低;心肌Ang Ⅱ和ALD水平降低;心肌组织形态改变明显好转。结论Los通过阻断Ang Ⅱ与AT1-R结合,抑制心肌Ang Ⅱ和ALD生成,从而改善心肌肥厚和胶原重构所致心室重塑,提高心功能,延缓心力衰竭进展。     

Carvedilol blockade of alpha1- and beta-adrenoceptor induced inotropic responses in rats with congestive heart failure

Carvedilol is a combined alpha(1)- and beta-adrenoceptor antagonist. We investigated the ability of carvedilol to antagonize functional effects mediated through myocardial alpha(1)-adrenoceptors in failing vs. non-failing (sham-operated) control hearts and compared such antagonisms to those of myocardial beta-adrenoceptors. Congestive heart failure was induced in Wistar rats by coronary artery ligation. Papillary muscles experiments were performed. Carvedilol antagonized inotropic effects mediated through myocardial alpha(1)-adrenoceptors with similar potencies in failing (pK(i)=7.7 (95%, CI; 7.4-8.0)) and sham-operated hearts (pK(i)=7.9 (95%, CI; 7.6-8.1)). The potency for the alpha(1)-adrenoceptors was 10-30-fold lower than that for the beta-adrenoceptors. In failing hearts, the alpha(1)-adrenoceptor mediated response was similar in size to the attenuated beta-adrenoceptor mediated inotropic response. The beta-adrenoceptor mediated lusitropic effects were not, however, attenuated in failing compared to sham-operated hearts. A low degree of alpha(1)-adrenoceptor blockade in the myocardium may contribute to the beneficial effects of carvedilol in heart failure.     

Effect of amiodarone on dispersion of ventricular repolarization in a canine congestive heart failure model

相似文献   

Liguzinediol improved the heart function and inhibited myocardial cell apoptosis in rats with heart failure

Aim:

Liguzinediol is a novel derivative of ligustrazine isolated from the traditional Chinese medicine Chuanxiong (Ligusticum wallichii Franch), and produces significant positive inotropic effect in isolated rat hearts. In this study we investigated the effects of liguzinediol on a rat model of heart failure.

Methods:

To induce heart failure, male SD rats were injected with doxorubicin (DOX, 2 mg/kg, ip) once a week for 4 weeks. Then the rats were administered with liguzinediol (5, 10, 20 mg·kg⁻¹·d⁻¹, po) for 2 weeks. Hemodynamic examination was conducted to evaluate heart function. Myocardial cell apoptosis was examined morphologically. The expression of related genes and proteins were analyzed using immunohistochemical staining and Western blot assays, respectively.

Results:

Oral administration of liguzinediol dose-dependently improved the heart function in DOX-treated rats. Electron microscopy revealed that liguzinediol (10 mg·kg⁻¹·d⁻¹) markedly attenuated DOX-induced injury of cardiomyocytes, and decreased the number of apoptotic bodies in cardiomyocytes. Furthermore, liguzinediol significantly decreased Bax protein level, and increased Bcl-2 protein level in cardiomyocytes of DOX-treated rats, led to an increase in the ratio of Bcl-2/Bax. Moreover, liguzinediol significantly decreased the expression of both cleaved caspase-3 and NF-κB in cardiomyocytes of DOX-treated rats. Administration of digitalis (0.0225 mg·kg⁻¹·d⁻¹) also markedly improved the heart function and the morphology of cardiomyocytes in DOX-treated rats.

Conclusion:

Liguzinediol improves the heart function and inhibits myocardial cell apoptosis in the rat model of heart failure, which is associated with regulating Bcl-2, Bax, caspase-3 and NF-κB expression.     

老年充血性心力衰竭患者血清甲状腺激素的变化

目的：观察老年人充血性心力衰竭（CHF）患者血清甲状腺激素（TH）的改变,探讨TH与CHF病情和预后的关系。方法：观察组（60例）按NYNA心功能分级标准分类心力衰竭等级,用放射免疫法血清游离三碘甲状腺原氨酸（FT3）、游离甲状腺素（FT4）、促甲状腺素（TSH）各参数水平,并与对照组（30例）比较。结果：与对照组比较,FT3明显降低（P＜0．01）,FT4降低仅见于部分心功能Ⅳ级患者,而TSH无显著改变;心衰愈重FT3降低愈明显,两者呈正相关。结论：老年人CHF患者存在继发性TH代谢异常,FT3和（或）FT4降低可作为CHF患者病情和预后判断的指标。     

心力衰竭合并室性心律失常的诊断和治疗进展

心力衰竭患者常合并室性心律失常,二者可以互为因果形成恶性循环,病情进展迅猛、病死率较高,严重影响患者的生活质量,是心力衰竭患者常见的死亡原因之一。临床治疗包括缓解症状、基础疾病治疗和诱因治疗、抗心律失常治疗、阻止或延缓心室重塑、防止心肌损害进一步加重等多个方面,最终达到改善症状和降低死亡率的目的。     

Effects of amiodarone on cardiac electrophysiology in right ventricular rapid pacing-induced heart failure dogs

ＥｆｅｃｔｓｏｆａｍｉｏｄａｒｏｎｅｏｎｃａｒｄｉａｃｅｌｅｃｔｒｏｐｈｙｓｉｏｌｏｇｙｉｎｒｉｇｈｔｖｅｎｔｒｉｃｕｌａｒｒａｐｉｄｐａｃｉｎｇｉｎｄｕｃｅｄｈｅａｒｔｆａｉｌｕｒｅｄｏｇｓＺＨＯＵＳｈｕＸｉａｎ１，ＺＨＡＮＧＸｕＭｉｎｇ，Ｗ...     

慢性心力衰竭患者射血分数与室性心律失常相关性分析

目的观察慢性心力衰竭（CHF）患者室性心律失常（Ventricular Arrhythmias,VA）发生情况,探讨VA与射血分数（Ejection Fraction,EF）的关系,并对室性心动过速的影响因素进行分析。方法选取我院258例CHF患者,按左室射血分数（LVEF）值分为A组（〈30％）、B组（30％～40％）、C组（40％～50％）及D组（〉50％）,比较各组间VA发生率及严重程度差异。分析心力衰竭患者室性心动过速发生的可能影响因素。结果各组间VA发生率的差异均有统计学意义,EF与VA的发生率呈负相关（r=-0．618,P〈0．01）。EF、左室舒张末期内径（LVDd）与心衰患者室性心动过速相关,OR值分别为0．247（P〈0．01）及2．690（P〈0．05）。结论CHF患者EF与VA发生呈负相关,EF是CHF患者室性心动过速发生的重要影响因素。     

Differential electrophysiologic and inotropic effects of phenylephrine in atrial and ventricular heart muscle preparations from rats

Summary Stimulation of ₁-adrenoceptors evokes a different pattern of inotropic responses in atrial and ventricular heart muscle preparations from rats. The inotropic effects are accompanied by different changes in membrane potential. In an attempt to clarify the question whether or to which extent these events are causally related, the effects of phenylephrine on force of contraction, transmembrane potential, Ca²⁺ current (I_Ca) and K⁺ currents were comparatively studied in either tissue.In atrial preparations, phenylephrine 10 mol/l caused an increase in force of contraction, a marked prolongation of the action potential duration and a depolarization of the membrane at rest. In the ventricle, however, the addition of phenylephrine 10 mol/l produced first a decline in force of contraction associated with a hyperpolarization of the membrane and a reduction in the action potential duration. These changes were followed by an increase in force,of contraction and a slight prolongation of the action potential, whereas the resting membrane potential remained increased. The hyperpolarization was eliminated in the presence of ouabain 100 mol/l.In enzymatically isolated atrial and ventricular myocytes, the whole-cell voltage clamp technique was used to study membrane currents on exposure to phenylephrine. Phenylephrine 30 mol/l did not affect the magnitude of I_Ca in either cell type. Transient and steady state K⁺ outward currents, however, were significantly diminished to a similar extent in atrial and in ventricular myocytes.It is concluded that the positive inotropic effect of ₁-adrenoceptor stimulation in the rat atrium is related to an increase in action potential duration and a decrease in resting membrane potential due to a decrease in K⁺ currents. In the ventricle, phenylephrine additionally activates the Na⁺/K⁺ pump thereby hyperpolarizing the membrane. The rapid onset of pump stimulation seems to overwhelm, in the beginning, the phenylephrine-induced decrease in K⁺ conductance and therefore to evoke a transient negative inotropic effect.It is assumed that phenylephrine can alter the intracellular Ca²⁺ concentration due to changes in the action potential duration. The way how Ca 2+ enters the cell remains speculative, since direct changes of Ica were not detected. The more complicated changes in membrane potential in the ventricle suggest that also other mechanisms for the positive inotropic response to phenylephrine must be considered. Send offprint requests to H. Nawrath at the above address     

Multiple muscarinic pathways mediate the suppression of voltage-gated Ca2+ channels in mouse intestinal smooth muscle cells

Background and purpose:

Stimulation of muscarinic receptors in intestinal smooth muscle cells results in suppression of voltage-gated Ca²⁺ channel currents (I_Ca). However, little is known about which receptor subtype(s) mediate this effect.

Experimental approach:

The effect of carbachol on I_Ca was studied in single intestinal myocytes from M₂ or M₃ muscarinic receptor knockout (KO) and wild-type (WT) mice.

Key results:

In M₂KO cells, carbachol (100 µM) induced a sustained I_Ca suppression as seen in WT cells. However, this suppression was significantly smaller than that seen in WT cells. Carbachol also suppressed I_Ca in M₃KO cells, but with a phasic time course. In M₂/M₃-double KO cells, carbachol had no effect on I_Ca. The extent of the suppression in WT cells was greater than the sum of the I_Ca suppressions in M₂KO and M₃KO cells, indicating that it is not a simple mixture of M₂ and M₃ receptor responses. The G_i/o inhibitor, Pertussis toxin, abolished the I_Ca suppression in M₃KO cells, but not in M₂KO cells. In contrast, the G_q/11 inhibitor YM-254890 strongly inhibited only the I_Ca suppression in M₂KO cells. Suppression of I_Ca in WT cells was markedly reduced by either Pertussis toxin or YM-254890.

Conclusion and implications:

In intestinal myocytes, M₂ receptors mediate a phasic I_Ca suppression via G_i/o proteins, while M₃ receptors mediate a sustained I_Ca suppression via G_q/11 proteins. In addition, another pathway that requires both M₂/G_i/o and M₃/G_q/11 systems may be operative in inducing a sustained I_Ca suppression.     

法舒地尔对心力衰竭大鼠心室重塑干预与Rho GTPases活性的作用

目的:以升主动脉缩窄压力超负荷心力衰竭大鼠为研究对象,观察Rho激酶抑制剂法舒地尔对心室重塑和心肌组织Rho家族的小分子鸟苷酸三磷酸酶(Rho GTPases)活性的影响,并探讨两者之间的关系。方法:将雌性心力衰竭Wistar大鼠随机分2组(n=10),法舒地尔(5 mg·kg~(-1))组和模型组,同时制备假手术组;模型组、假手术组用等量生理盐水每日2次腹腔注射。测定治疗4 wk后组织Rho GTPases活性。结果:法舒地尔组左室重量-体重比明显下降(P<0.01),心室重构减轻,心肌组织Rho GTPases活性降低(P<0.01)。结论:Rho激酶抑制剂法舒地尔抑制左室重塑与心肌组织Rho GTPases活性有关。     

黄芪注射液治疗充血性心力衰竭的疗效观察

目的：观察黄芪注射液对充血性心力衰竭患者的临床疗效，方法：应用随机对比的方法对80例慢性充血性心力衰竭患者进行黄芪注射液和硝酸甘油的治疗对比，结果：应用黄芪注射液2周后，治疗组心功能改善率及总有效率分别为35％和80％，明显优于对照组（P＜0．05），两组治疗后的心输出量及心脏指数均较治疗前有明显改善（P＜0．05，P＜0．01），治疗组疗效更好，结论：黄芪注射液是治疗充血性心力衰竭的有效辅助药物。     

厄贝沙坦对高血压并发心力衰竭患者心功能的影响

目的 :观察血管紧张素Ⅱ受体阻滞剂厄贝沙坦的降压疗效和对心功能的影响。方法 :试验组 (n =4 0 )口服厄贝沙坦 15 0mg ,qd ,连用 4周 ;对照组 (n =36 )口服卡托普利 12 .5mg ,bid或tid ,连用 4周 ,用药期间仔细检查体格及心电图 ,给药前后行超声心动图计算射血分数 (EF)和E/A比值 ,评定心功能变化。结果 :试验组SBP和DBP都有明显降低 ,而对照组改变不明显 ,2组间比较差异非常显著 ;2组治疗后心功能都有明显改善 ,试验组总有效率为 80 % ,对照组为 6 1% ,2组比较差异有显著性 ;2组治疗后LVEF均升高 :试验组 0 .4 6± 0 .0 7vs 0 .4 1±0 .0 6 (P <0 .0 5 ) ,对照组 0 .4 2± 0 .0 6vs 0 .4 0± 0 .0 5 (P >0 .0 5 ) ;E/A比值升高 :试验组为 1.0 6± 0 .13vs 0 .5 8±0 .15 (P <0 .0 1) ,对照组 0 .76± 0 .12vs 0 .5 7± 0 .14 (P <0 .0 5 )。试验组好转更明显。结论 :厄贝沙坦有利于缓解心衰症状 ,改善其收缩功能和舒张功能 ;其疗效优于卡托普利。     

Altered neuropeptide Y Y1 responses in mesenteric arteries in rats with congestive heart failure

The aim of the present study was to elucidate if the potentiating effect of neuropeptide Y on various vasoactive agents in vitro is (1) altered in mesenteric arteries from rats with congestive heart failure and (2) mediated by the neuropeptide Y Y₁ receptor. The direct vascular effects of neuropeptide Y and its modulating effects on the contractions induced by endothelin-1-, noradrenaline-, 5-hydroxytryptamine (5-HT)-, U46619-(9, 11-dideoxy-11, 9-epoxymethano-prostaglandin F₂) and ATP, and acetylcholine-induced dilatations were studied in the presence and absence of the neuropeptide Y Y₁ antagonist, BIBP3226 (BIBP3226{(R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]- -arginine-amide}). Neuropeptide Y, per se, had no vasoactive effect in the arteries. The potency of endothelin-1 was significantly decreased in congestive heart failure rats. Neuropeptide Y and neuropeptide Y-(13–36) potentiated the endothelin-1-induced contraction in congestive heart failure mesenteric arteries. In 20% of the congestive heart failure rats, sarafotoxin 6c induced a contraction of 31±4%. Neuropeptide Y also potentiated U46619- and noradrenaline-induced contractions but not 5-HT-induced contractions in congestive heart failure arteries. In sham-operated animals neuropeptide Y potentiated noradrenaline- and 5-HT-induced contractions. These potentiations were inhibited by BIBP3226. Acetylcholine induced an equipotent relaxation in both groups which was unaffected by neuropeptide Y. In conclusion, neuropeptide Y responses are altered in congestive heart failure rats. The potentiating effect differs between vasoactive substances. Neuropeptide Y Y₁ and non-neuropeptide Y₁ receptors are involved.     

超声心动图评价负荷量国产氨吡酮对心力衰竭病人左心功能的影响

本文用M型和脉冲多普勒超声心动图观察了30例心力衰竭病人静注国产氨吡酮对左心功能的影响.所有受检者氨吡酮(lmg·kg~(-1))iv过程中和用药后10min时所测的左心收缩和舒张功能均较用药前明显改善.每搏输出量增加了20％和18％;心排血量和心脏指数分别增加了23％、19％、和23％、23％;射血分数增加了32％和30％;平均周径纤维缩短率增加了50％和48％;左室舒张早期充盈速度增加了30％和21％.以上各项指标在用药中与用药后差异均无显著性,但两者与用药前差异均有显著性(p<0.05～0.001).用药中和用药后心率有轻度变化.但p>0.05 。     

扩张型心肌病心力衰竭病人卡维地洛治疗前后的冠脉血流储备评价

目的:利用无创腺苷激发经胸超声多普勒显像对卡维地洛治疗的扩张型心肌病心力衰竭病人冠脉血流储备(CFR)进行评价。方法:入选2004年6月至2005年6月因扩张型心肌病引起的慢性心力衰竭病人31例,在常规药物治疗基础上,加用卡维地洛至目标剂量或最大耐受剂量,治疗6mo。在卡维地洛治疗前后进行腺苷激发经胸超声多普勒显像检查,记录冠脉血流速度(CFV)及冠脉血流速度储备(CFVR),以CFVR评价CFR。结果:卡维地洛治疗前心力衰竭病人静息状态CFV与对照组无显著差别(P>0.05),最大冠脉扩张状态时CFV减低(P<0.05),CFVR较对照组明显下降(2.4±s0.3vs 3.2±0.4, P<0.05);治疗6mo后心力衰竭病人静息状态下CFV无明显改变(P>0.05)、最大充血状态时CFV升高(P<0.05),CFVR增加(2.7±0.3 vs 3.2±0.4,P<0.05);治疗后心力衰竭组CFV及CFVR与对照组比较仍有显著差别。结论:非选择性β受体阻滞剂卡维地洛能够改善扩张型心肌病心力衰竭病人的冠脉CFR,这可能也是β受体阻滞剂有效治疗扩张型心肌病的作用机制之一。