黄芪注射液联合川芎嗪治疗急性脑梗死临床观察

分别用黄芪联合川芎嗪（观察组）和维脑路通（对照组）治疗急性脑梗死（ACI）患者，比较其临床疗效及血液流变学参数。结果观察组总有效率高于对照组（P〈0．05）；两组血液流变学指标均改善，尤以观察组改善明显（P〈0．05）。提示黄芪注射液联合川芎嗪治疗ACI疗效优于维脑路通。     

常规抗痨治疗联合川芎嗪保肝的临床观察

抗结核治疗方案中的异烟肼(INH)、利福平(RFP)和吡嗪酰胺(PZA)都具有一定的肝毒性,联合用药不仅容易出现肝损伤,甚至可能发生急性肝坏死而危及生命.在抗结核治疗过程中能否有效预防抗结核药物性肝损伤(ATDH)的发生,关系到抗结核治疗的成败.我们对川芎嗪在抗结核治疗过程中预防药物性肝损伤的临床疗效进行观察.     

小剂量肝素联合川芎嗪注射液治疗肺心病的观察

目的：探讨小剂量肝素与川芎嗪注射液合用在肺心病治疗中的应用效果。方法：120例慢性肺心病急性加重期患者随机均分为对照组（常规治疗）和治疗组（常规治疗＋小剂量肝素与川芎嗪注射液）。结果：治疗组的疗效显著好于对照组（P〈0．01）。结论：小剂量肝素与川芎嗪注射液合用可提高慢性肺心病急性发作期患者的疗效。     

肾复康胶囊治疗急性肾小球肾炎和慢性肾小球肾炎急性发作(肾风)362例

1　对象与方法1.1　病例来源本课题观察病例来源于住院及门诊患者。1.2　性别与年龄共 36 2例患者 ,其中男性 2 17例 ,女性 14 5例 ,男女之比为 1.5 :1,最小年龄为 8岁 ,最大年龄为 87岁 ,2 0岁以下者为 17例 ,2 1～ 4 0岁者为 179例 ;4 1～ 6 0岁者为 12 9例 ,6 1岁以上者 37例。1.3　治疗方法服用吉林省力源药业股份有限公司生产的肾复康胶囊 ,每日 3次 ,每次 5粒。2　观察方法及疗效判定标准2 .1　疗程和证候分类全部病例均确定为一个月作为一个疗程 ,超过一个月者 ,为继续维持治疗 ,但不属本组观察病例。在证候分类上 ,一般以风邪客表证…     

还原型谷胱甘肽联合川芎嗪治疗酒精性肝病疗效观察

观察还原型谷胱甘肽联合川芎嗪治疗酒精性肝病的疗效。方法将62例酒精性肝病患者随机分为2组,对照组31例患者给予还原型谷胱甘肽1.2g静脉点滴,每天一次,30d为1疗程;治疗组31例患者在此基础上加用川芎嗪120mg静脉点滴,每天1次,30d为1疗程。观察两组患者肝功能、血清肝纤维化指标。结果治疗30d后,两组患者肝功能指标改善,血清肝纤维化指标明显下降(均P<0.05),治疗组疗效优于对照组(P<0.05)。结论还原型谷胱甘肽联合川芎嗪治疗酒精性肝病,疗效显著,且无不良反应发生。     

依那普利联合川芎嗪治疗肺源性心脏病急性加重期的临床疗效观察

目的观察依那普利联合川芎嗪治疗肺源性心脏病(肺心病)急性加重期的临床疗效。方法选取2013年1月—2014年4月都昌县人民医院收治的肺心病急性加重期患者78例,随机分为对照组和观察组,各39例。在常规治疗基础上,对照组患者给予依那普利治疗,观察组给予依那普利联合川芎嗪治疗,均治疗2周。比较两组患者治疗前后血液流变学指标及临床疗效。结果治疗前两组患者血浆黏度、全血黏度及红细胞比容比较,差异无统计学意义(P0.05);治疗后观察组患者上述指标均低于对照组(P0.05)。观察组患者总有效率为89.7%,高于对照组的69.2%(P0.05)。结论依那普利联合川芎嗪治疗肺心病急性加重期疗效确切,可有效改善患者血液流变学和心肺功能。     

前列地尔联合川芎嗪注射液治疗急性脑梗死32例疗效观察

目的：观察前列地尔联合川芎嗪治疗急性脑梗死的临床疗效。方法将66例急性脑梗死患者按临床均衡顺序随机法分为对照组和治疗组各33例,两组均予以他汀类药物调脂、阿司匹林抗血小板聚集、调控血压及血糖、抗感染及降低颅内压等常规治疗。对照组给予奥扎格雷钠80mg、胞二磷胆碱注射液0.75g加入0.9％氯化钠250ml静脉点滴,1次/日,连用2周;治疗组在对照组治疗基础上加用前列地尔10ug加入0.9％氯化钠100ml联合川芎嗪注射液80mg加入0.9％氯化钠250ml静脉滴注,1次/日,连续2周。比较两组患者治疗前后临床疗效,神经功能缺损评分（NIHSS ）和Barthel指数及血液流变学指标值。结果治疗组与对照组总有效率分别为84.84％和57.58％,两组比较差异有统计学意义（ P＜0.05）。治疗后两组NIHSS和Barthel指数及全血高切黏度、血浆黏度、纤维蛋白原等指标比较,差异均有统计学意义（ P＜0.05）。结论前列地尔联合川芎嗪注射液治疗急性脑梗死可明显提高临床疗效。     

卡托普利联合川芎嗪治疗急性肾炎的临床疗效探讨

将2014年3月至2016年8月96例急性肾炎患者,盲选分成常规方法应用于对照组48例,卡托普利联合川芎嗪治疗方法应用于观察组48例患者。结果观察组各项指标与对照组更优,(P0.05)。血尿转阴率,观察组优于对照组77.08%、43.75%,(P0.05)。结论联合医治,疗效显著。     

硫辛酸联合川芎嗪治疗糖尿病周围神经病变疗效观察

目的观察硫辛酸联合川芎嗪治疗糖尿病周围神经病变(DPN)的临床疗效。方法将68例糖尿病周围神经病变患者随机分为两组。观察组患者36例给予硫辛酸与川芎嗪治疗,对照组患者32例给予川芎嗪治疗。两组疗程均为2周,比较两组患者的临床治疗效果以及治疗前后神经传导速度的变化。结果观察组患者症状、体征的改善显著优于对照组,差异有统计学意义(P0.05);治疗后观察组患者的神经传导速度显著提高,与对照组患者比较,差异有统计学(P0.05)。结论硫辛酸联合川芎嗪治疗2型糖尿病周围神经病变疗效显著,能明显改善患者症状、体征,提高患者周围神经传导速度,防止病情进一步发展,减轻患者痛苦,提高患者生活质量。     

氨溴索联合川芎嗪治疗特发性肺纤维化52例

目的观察氨溴索联合川芎嗪治疗特发性肺纤维化（IPF）的疗效。方法选取102例符合本次研究的患者,随机分为两组,对照组50例,予强的松口服治疗。治疗组52例,予氨溴索雾化吸人联合川芎嗪静脉滴注治疗。疗程均为8周。结果氨溴索雾化吸人联合川芎嗪静脉滴注疗效明显优于对照组。结论氨溴索雾化吸入联合川芎嗪静脉滴注治疗疗效确切,优于传统类固醇激素的治疗方法。     

美托洛尔联合卡托普利治疗慢性肺源性心脏病疗效观察

目的探析美托洛尔联合卡托普利治疗慢性肺源性心脏病的临床疗效。方法选择我院于2012年11月至2013年11月期间收治的40例慢性肺源性心脏病患者作为研究对象,随机分为观察组和对照组。两组患者首先均给予相应的常规治疗方法,具体包括确保充足的休息、合理氧疗、改善通气、控制感染、使用利尿剂和强心剂、纠正水和电解质平衡、并给予心肌能量药物等。观察组在此基础上联用美托洛尔和卡托普利进行治疗,比较两组患者的治疗有效率。结果观察组患者由于服用美托洛尔和卡托普利这两种药物,6例患者出现咳嗽症状,4例出现心动过缓,还有1例早期心衰加重,但是没有发生严重不良反应。在治疗有效率方面,观察组8例显效,9例有效,3例无效,总有效率为85.00%;对照组5例显效,8例有效,7例无效,总有效率为65.00%,两组之间的差异有显著统计学意义(P0.05)。结论美托洛尔联合卡托普利治疗慢性肺源性心脏病具有较大的安全保障,两药的联合发挥协同作用强化了治疗效果,患者的生活质量得到提高,同时复发率也明显降低,应用效果显著。     

Clinical experience with captopril in the treatment of severe drug-resistant hypertension

Thirty-three patients aged 12 to 77 years with severe hypertension uncontrolled on maximal combination therapy (mean arterial pressure on treatment 149 ± 4 mm Hg) were treated with captopril, 45 to 450 mg daily for up to 30 months. Renovascular lesions were present in 11 and other renal disease in a further 15, of whom 8 had undergone renal transplantation. Good control (mean blood pressure less than 110 mm Hg) was achieved in 11 patients and moderate control (mean blood pressure 110 to 130 mm Hg) in 13. Captopril was given with a diuretic agent in 13 patients, with a diuretic agent and a beta-adrenoreceptor blocker in 13, and with three or more other agents in 7, of whom 4 had undergone renal transplantation. Side effects of rash, fever and gastrointestinal symptoms were observed, but there were no adverse effects on renal function or leukocyte counts. Severe hyperkalemia (potassium level greater than 6.0 mmol/liter) occurred in four patients despite the use of furosemide and low potassium diet. There was no significant correlation between the long-term hypotensive response and the initial decrease in blood pressure during captopril therapy.     

Early treatment with captopril after acute myocardial infarction.

OBJECTIVES--To determine the effects of early treatment with captopril on haemodynamic function, neuroendocrine biochemistry, left ventricular structure, clinical outcome, and exercise capacity over one year from acute myocardial infarction. DESIGN--Randomised, double blind, placebo controlled comparison of captopril and placebo. SETTING--Coronary care units and cardiology departments of two university teaching hospitals in Glasgow. PATIENTS--99 haemodynamically stable patients with acute myocardial infarction, selected on clinical grounds as being at risk of late ventricular dilatation. INTERVENTION--Captopril or identical placebo started between six and 24 hours after start of symptoms and continued for 12 months. Target maintenance dose was 25 mg three times a day. MAIN OUTCOME MEASURES--(a) Acute haemodynamic effects of treatment; (b) neuroendocrine biochemistry from admission to two months; and (c) change in echocardiographic measures of left ventricular size, clinical outcome, and exercise capacity after 12 months of treatment with a separate analysis of the effects of one month of treatment withdrawal on left ventricular volumes. RESULTS--Captopril caused acute reductions in mean (SEM) pulmonary artery pressure (2.48 (0.69) mm Hg) and systemic vascular resistance (260 (103)) dyn.s.cm-5). Over the first 10 hours captopril reduced mean arterial pressure by 12.1 (2.4) mm Hg compared with 3.8 (1.9) mm Hg in the placebo group. No patient had to be withdrawn from the captopril group because of hypotension. From day 1 onwards systolic and diastolic arterial pressures in the captopril treated group were slightly but not significantly lower than on placebo. There was no difference in the incidence of ventricular or supraventricular arrhythmia with treatment. Captopril prevented the day 3 peak in angiotensin II that occurred in the placebo group (peak concentration (interquartile range): 10.1 (4.8-19.4) pg/ml v 16.8 (4.3-46.3) pg/ml)) but had no effect on atrial natriuretic factor, arginine vasopressin, or catecholamines. Plasma atrial natriuretic factor remained above normal in both groups at two months after infarction. After one year left ventricular volume indices had increased less on captopril than on placebo: left ventricular end systolic volume index 5.4 ml/m2 v 14.7 ml/m2 (95% confidence interval (95% CI) of difference -14.6 to -3.9; p = 0.0011); left ventricular end diastolic volume index 8.4 ml/m2 v 19.0 ml/m2 (95% CI of difference, -17.0 to -4.2; p = 0.0016). Withdrawal of captopril for one month did not affect ventricular volumes. There was no difference in exercise capacity. CONCLUSIONS--Captopril started between six and 24 hours after acute myocardial infarction is not associated with significant hypotension. It suppresses activation of the renin angiotensin system but has no effect on plasma concentrations of other neurohormones. Atrial natriuretic factor remains raised at two months after myocardial infarction. Captopril significantly decreases left ventricular dilatation. This effect is not lost after one month of treatment withdrawal and is thus due to an alteration of left ventricular structure and not to a short lived haemodynamic action of captopril. Long-term treatment with captopril does not result in improved aerobic exercise capacity after acute myocardial infarction.     

卡托普利对老年人急性心肌梗死的治疗及二级预防的作用

目的探讨老年人急性心肌梗死（心梗）卡托普利治疗对预后的意义。方法６３１例首次急性心梗后７２小时内入院无心源性休克老年患者中，３６１例早期及随访期持续卡托普利治疗（治疗组），２７０例常规治疗（对照组），比较两组住院期和随访期生存率的差异。结果住院期治疗组生存率（９２．２％）显著高于对照组（７８．９％，Ｐ＜０．００１），卡托普利对前壁心梗作用较下壁心梗明显。随访期（第９周～第５４个月末）第５４个月末治疗组累积生存率（９１．０％）显著高于对照组（７４．０％，Ｐ＜０．０１），心源性事件累积发生率（５５．０％）低于对照组（７２．０％，Ｐ＜０．０００１）。结论老年人急性心梗后早期及持续卡托普利治疗对其预后具有益作用     

阿托伐他汀联合阿司匹林治疗急性脑梗死患者的临床研究

目的 探讨阿托伐他汀联合阿司匹林治疗急性脑梗死患者的疗效及其对神经功能缺损、血脂、颈动脉斑块等影响.方法 选择急性脑梗死患者80例,随机分为阿托伐他汀联合阿司匹林治疗组40例.单用阿司匹林对照组40例,比较两组神经功能缺损程度及疗效,血脂、颈部血管超声的变化,并随访6个月,观察有无再发脑梗死.结果 治疗后三酰甘油(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、颈总动脉内径、斑块体积、阻力指数、搏动指数、神经功能缺损评分在治疗组分别为(1.36±0.33)mmol/L、(5.21±0.32)mmol/L、(1.20±0.10)mmol/L、(1.31±0.37)mmol/L、(6.43±0.71)mm、(40.39±8.94)mm3、(0.70±0.06)、(2.12±0.37)、(10.24±3.31)分,低于对照组[(1.77±0.80)mmol/L、(5.80±0.37)mmol/L、(1.43±0.16)mmol/L、(1.57±0.39)mmol/L、(6.67±0.47)mm、(54.26±8.25)mm3、0.82±0.08、2.18±0.54、(14.69±3.23)分],(均P<0.05或0.01);颈动脉内中膜厚度、收缩期峰值速度治疗组分别为(1.66±0.50)mm、(71.34±15.01)an/s,高于对照组[(1.50±0.68)(68.97±18.21)an/s](均P<0.01);治疗组总有效率92.5%,高于对照组75.0%(P<0.05),6个月内未见脑梗死复发.结论 阿托伐他汀联合阿司匹林治疗急性脑梗死有利于神经功能的恢复和改善预后,对缩小颈动脉粥样斑块体积、稳定斑块、降低血脂各项指标有较好的效果,对干预脑梗死的复发起到积极作用,可作为急性脑梗死治疗的联合药物.     

卡托普利对急性心肌梗死伴糖尿病患者的疗效观察

目的 观察糖尿病患者发生急性心肌梗死的临床特点及卡托普利对其的近期疗效。方法 本试验共纳入１４６６６例患者,分为糖尿病组和非糖尿病组,其中ＡＭＩ伴糖尿病患者１３７６例,多中心随机双盲安慰剂对照临床试验分为对照临床试验分为对照组７０７例,治疗组６６９例,口服卡托普利或安慰剂,治疗４周。结果 糖尿病ＡＭＩ组４周病死率为１４．７５％,明显高于非糖尿病ＡＭＩ８．８９％。     

Hemodynamic effects of captopril in acute infarct of the anterior myocardium

OBJECTIVE: Evaluation of haemodynamic effects after sublingual administration of 25 mg of captopril in patients with Acute Anterior Myocardial Infarction within the first 48 hours. DESIGN: Determination of basal parameters and 30 minutes after 25 mg of captopril. SETTING: Patients admitted in the ICU with Anterior Myocardial Infarction diagnosis. PATIENTS: 41 consecutive patients; 22 patients submitted to thrombolysis with streptokinase; 19 patients submitted to conventional therapy. RESULTS: A) In the whole group: No significant change in the HR, PAP, CI, SI, MAP, SVR, PR. RA and CWP were reduced. B) In thrombolysed patients: No significant change in HR, RA, PAP, CWP, MAP, SVR, PR. CI and SI were significantly increased. C) In non-thrombolysed patients: No significant change in HR, PAP, CI, SI, SVR, PR. RA, CWP and MAP were reduced. CONCLUSION: 1. We found no significant hypotension with sublingual captopril in Acute Myocardial Infarction. 2. Non-thrombolysed patients showed a greater reduction of arterial pressure. 3. Thrombolysed patients had significant increases in systolic function indices.