尼卡地平治疗高血压急症的Meta分析

目的：利用Meta分析方法评价尼卡地平治疗高血压急症的有效性和安全性,为临床用药提供参考。方法：以“尼卡地平”、“高血压急症”为检索词,计算机检索PubMed、ISI、EMbase光盘数据库、CBMdisc、CNKI、VIP数据库、万方数据库,纳入尼卡地平用于治疗高血压急症的随机对照试验,按照Meta分析方法,运用RevMan5．0软件对符合条件的纳入文献进行分析。结果：共纳入14篇文献,合计1010例患者。Meta分析结果显示,尼卡地平在降低收缩压（systolicbloodpressure,SBP）与舒张压（diastolicbloodpressure,DBP）这两方面的效果均好于硝普钠[MD=0．63,95％CI（0．25,1．01）,P=0．001;MD=0．35。95％CI（0．15,0．56）,P=0．0007],而与乌拉地尔、拉贝洛尔、酚妥拉明、硝酸甘油比较,差异无统计学意义。尼卡地平的不良反应发生率小于硝普钠[OR=0．55,95％CI（0．38,0．8）,P=0．002],与拉贝洛尔、乌拉地尔比较,差异无统计学意义。结论：尼卡地平治疗高血压急症疗效较好,安全性较高。     

培哚普利治疗高血压的临床疗效及安全性系统评价

目的:对培哚普利治疗高血压的疗效及安全性进行系统评价。方法:通过对Embase、Medline、Cochrane图书馆、PubMed及中国知网、万方、维普等中外数据库进行检索,筛选临床随机对照试验文献进行评价分析。按照文献质量评价标准严格评价文献,纳入高质量的研究文献。对培哚普利的疗效进行Meta分析,并对其安全性进行分析比较。结果:培哚普利具有良好的降压效果,与安慰剂、对照药物及常规降压药相比,其降压效果都有一定优势;且该药物的不良反应较少、症状较轻微。结论:培哚普利治疗高血压,临床疗效较好,安全性良好。     

卡维地洛治疗轻、中度原发性高血压的Meta分析

目的：回顾文献分析评价卡维地洛治疗轻、中度原发性高血压的有效性和安全性。方法：以拉贝洛尔为对照药，运用Meta分析方法，对8个采用随机盲法阳性药平行对照的独立临床试验结果进行定量合成分析。结果：卡维地洛组降压有效率略优于拉贝洛尔组，合并效应量OR为1．58，其95％CI为1．18～2．14，P〈0．01。剂量效应关系中，两组治疗的差别无统计学意义，合并效应量OR为1．42，其95％CI为0．98～2．08，P〉0.05。在降低心率上，两组在试验前后差别均有统计学意义，但是组间比较缺乏有效数据不能比较，需要进一步研究。两组间不良反应发生率无显著差异（P〉0．05）。卡维地洛组主要不良反应为头晕、头痛、嗜睡、乏力。结论：卡维地洛对轻、中度原发性高血压降压效果显著，是一种安全有效的抗高血压药物。     

复方利血平片治疗原发性高血压的有效性和安全性系统评价

目的:评价复方利血平片治疗原发性高血压的疗效和安全性。方法:计算机检索Cochrane Library、PubMed、Embase、中国生物医学文献数据库(CBM)、中国期刊全文数据库(CNKI)、维普中文科技期刊全文数据库(VIP),制定严格的纳入和排除标准,纳入复方利血平片对比常规降压药治疗原发性高血压的随机对照试验,对纳入的随机对照试验进行方法学质量评价和Meta分析。由2名研究员对原始研究独立进行质量评价和资料提取,采用RevMan5.0软件进行Meta分析,根据各原始研究间异质性大小选择随机/固定效应模型,并进行敏感性分析和亚组分析。结果:共纳入11个随机对照试验,其中4篇为中等质量,其余7篇均为低质量。Meta分析结果显示,复方利血平片组与常规降压药组间降压效果的总有效率差异有统计学意义[RR=0.80,95%CI(0.74,0.85),P<0.00001];2组不良反应均较少见且轻微,未观察到严重不良反应事件。结论:根据目前研究证据,复方利血平片的降压有效率不及其他常规降压药,但2组降压药均安全、有效。由于观察例数和时间有限,上述结论仍需更多设计严谨、大样本、多中心的随机对照试验进行证实和补充。     

压宁定抢救高血压急症100例临床观察

高血压急症会给患者带来突然的危险,目前的降压药不是降压速度偏慢,就是副作用大或用药剂量不易掌握,选用压宁定治疗高血压急症,通过对100例高血压急症观察,该药具有明显的降压作用,适用于高血压脑病、高血压危象、高血压脑卒中及外科手术中的高血压治疗,具有起效快,效果确切,易掌握,副作用小,压宁定是高血压急症的首选药物。     

压宁定与拉贝洛尔治疗高血压急症疗效比较

运用压宁定与拉贝洛尔对34例高血压急症患者采取静脉注射方法,分别在不同时间内观察血压、心率变化。结果:两药在注射5min时血压下降较治疗前差异极显著(P<0.01)。不同之处:①两药降压的起效时间,压宁定3min,拉贝洛尔2min;②压宁定持续降压时间2h(P<0.01),拉贝洛尔至1 h有血压回升趋势,与用药5min比较,差异不显著(P>0.05)。③压宁定对心率轻度减慢,拉贝洛尔减慢心率幅度较大,治疗中出现两例缓慢性心律失常。笔者认为,压宁定降压效果好,无明显副作用,可作为治疗高血压急症首选药物。     

复方利血平氨苯蝶啶片治疗原发性高血压有效性及安全性的Meta分析

目的系统评价复方利血平氨苯蝶啶片(北京降压0号)治疗原发性高血压的有效性和安全性。方法检索PubMed、Cochrane、Web of Science、中国学术期刊全文数据库(CNKI)、维普数据库、万方数据库及百度学术数据库,中文检索词为复方利血平氨苯蝶啶片、降压零号、北京降压0号、高血压,英文检索词为com⁃pound reserpine and triamterene tablets、hypertension,筛选2000—2020年发表的研究复方利血平氨苯蝶啶片的安全性及有效性的随机对照试验。由2位研究员按纳入与排除标准独立筛选文献、提取资料和评价纳入研究的方法学质量后,采用Revman5.4软件进行Meta分析。结果最终纳入7项研究。Meta分析结果显示:在5项研究中,与其他降压药相比,复方利血平氨苯蝶啶片降压总有效率更高(OR=2.23,95%CI:1.32~3.75);不良反应发生率差异无统计学意义(OR=0.91,95%CI:0.68~1.22)。结论复方利血平氨苯蝶啶片治疗原发性高血压较其他降压药物降压效果与安全性均更可靠。     

静脉滴注拉贝洛尔治疗高血压急症的疗效和安全性

目的：评价静脉滴注拉贝洛尔治疗高血压急症的降压疗效及安全性。方法：31例高血压急症患者接受拉贝洛尔（1－4mg/min,iv gtt）治疗。结果：治疗前血压为23.2／16.5kPa,拉贝洛尔治疗2h后90％（28／31）患者平均血压下降15％－25％,治疗6h后血压控制在21.3／13.3kPa以下者为94％,拉贝洛尔降压起效快县无低血压现象发生。结论：静脉滴注拉贝洛尔治疗高血压急症有效、安全。     

厄贝沙坦治疗轻、中度高血压的疗效和安全性Meta分析

目的:采用Meta分析系统评价厄贝沙坦与其它降压药物治疗轻、中度高血压的临床疗效和安全性差异。方法:计算机检索中国学术期刊全文数据库、中文科技期刊数据库、万方数据资源系统和中国生物医学文献数据库(CBMdisc),在严格的文献质量评价基础上,应用Meta分析对纳入文献研究厄贝沙坦与其它降压药物治疗轻、中度高血压的有效率、安全性进行同质性检验及合并效应量的估计。结果:共纳入15篇文献,1528例患者。厄贝沙坦治疗轻、中度高血压的总有效率略优于其它降压药物,差异无统计学意义[合并OR=1.22,95%可信区间(0.95,1.58),Z=1.56,P=0.12];厄贝沙坦安全性优于其它降压药物,差异有统计学意义[合并OR=0.61,95%可信区间(0.44,0.85),χ2=2.89,P=0.004]。结论:厄贝沙坦治疗轻、中度高血压在疗效上与其它降压药物比较无显著性差异,但在安全性方面优于其它降压药物。     

灯盏细辛治疗糖尿病周围神经病变系统评价

目的应用Meta分析方法了解灯盏细辛治疗糖尿病周围神经病变的临床疗效与安全性。方法①通过检索《中国医药数字化期刊群》（1998～2008年）中关于灯盏细辛治疗糖尿病周围神经病变的论文56篇,主题词包括灯盏细辛和糖尿病周围神经病变,并查阅原始文献。文献纳入标准：论文内容包含有灯盏细辛治疗糖尿病周围神经病变的对照研究;治疗效果根据患者的临床症状,膝、跟腱反射以及周围神经传导速度变化分为显效、有效和无效。②应用Meta分析方法对检索出的符合要求的12项研究进行同质性检验,计数资料采用四表格数据的Meta分析方法（Peto法）计算比值比（OR）和95%可信区间（CI）。结果最初纳入文献56篇,最终纳入Meta分析的文献12篇。①同质性检验结果：χ2＝9.77,自由度为11,P＞0.25。②两组疗效合并效应量的检验结果：灯盏细辛治疗组总有效率明显高于对照组［85.78%,57.01%,χ2＝39.35,P＜0.01（OR ＝3.21,95% CI：2.56～3.95）］。③治疗组仅13例（2.89%）患者出现轻微不良反应。结论灯盏细辛治疗糖尿病周围神经病变的临床疗效显著优于目前常用药物,且无明显不良反应。     

Intravenous labetalol in the management of resistant hypertensive emergency

A case of intravenous labetalol in the treatment of a resistant hypertensive emergency is reported. Although there have been several reports of the use of oral labetalol in resistant hypertension, no intravenous administration in hypertensive emergency resistant to other drugs has been reported to date. A 36-year-old black female with BP of 270/160 mm Hg with complaints greater than one month's duration of dizziness, severe headaches, blurred vision, shortness of breath, vomiting, palpitations, flushing, agitation, diarrhea, weakness, and weight loss, was treated successfully with intravenous labetalol after she failed to respond to other established parenteral antihypertensive drugs. The patient received labetalol 20 mg iv bolus, and then 20 mg every ten minutes until a cumulative dose of 200 mg was attained. Labetalol produced a prompt but smooth reduction in BP without any reflex tachycardia or other adverse effects. Intravenous labetalol may be safe and effective for the management of rapid BP control in hypertensive emergencies resistant to other parenteral antihypertensive agents.     

Effect of carvedilol on renal hemodynamics and renal excretory function in spontaneously hypertensive rats

The effects of the novel antihypertensive agent, carvedilol, on renal hemodynamics and excretory function have been investigated and compared with the effects of labetalol in conscious, spontaneously hypertensive rats. Sustained intravenous infusion of carvedilol or labetalol at a rate of 10 micrograms/kg/min resulted in a significant decrease in blood pressure which was equivalent in magnitude for both drugs. Carvedilol had no effect on renal hemodynamic parameters; glomerular filtration rate, renal blood flow, and filtration fraction were unchanged. In contrast, labetalol decreased the glomerular filtration rate by 13% (p less than 0.01) and the filtration fraction was reduced from 28 to 24%. Inasmuch as renal blood flow was unchanged and perfusion pressure was reduced, both compounds decreased renal vascular resistance. Urine flow decreased and osmolality increased with both carvedilol and labetalol. However, excretion of electrolytes was affected differently with the two compounds. While sodium and potassium excretion were significantly decreased with labetalol, sodium and potassium excretion remained stable during carvedilol infusion, which represents an important beneficial effect for a potent systemic vasodilator. We conclude, therefore, that carvedilol does not compromise the renal autoregulatory integrity in hypertensive rats, and that the antihypertensive activity of the compound is associated with an apparent 'renal sparing' effect, in that the decrease in blood pressure does not compromise the urinary excretion of sodium.     

Treatment of acute severe hypertension: current and newer agents

Approximately 72 million people in the US experience hypertension. Worldwide, hypertension may affect as many as 1 billion people and be responsible for approximately 7.1 million deaths per year. It is estimated that approximately 1% of patients with hypertension will, at some point, develop a hypertensive crisis. Hypertensive crises are further defined as either hypertensive emergencies or urgencies, depending on the degree of blood pressure elevation and presence of end-organ damage. Immediate reduction in blood pressure is required only in patients with acute end-organ damage (i.e. hypertensive emergency) and requires treatment with a titratable, short-acting, intravenous antihypertensive agent, while severe hypertension without acute end-organ damage (i.e. hypertensive urgency) is usually treated with oral antihypertensive agents.The primary goal of intervention in a hypertensive crisis is to safely reduce blood pressure. The appropriate therapeutic approach of each patient will depend on their clinical presentation. Patients with hypertensive emergencies are best treated in an intensive care unit with titratable, intravenous, hypotensive agents. Rapid-acting intravenous antihypertensive agents are available, including labetalol, esmolol, fenoldopam, nicardipine and sodium nitroprusside. Newer agents, such as clevidipine and fenoldopam, may hold considerable advantages to other available agents in the management of hypertensive crises. Sodium nitroprusside is an extremely toxic drug and its use in the treatment of hypertensive emergencies should be avoided. Similarly, nifedipine, nitroglycerin and hydralazine should not to be considered first-line therapies in the management of hypertensive crises because these agents are associated with significant toxicities and/or adverse effects.     

Autonomic and antihypertensive activity of oral amosulalol (YM-09538), a combined alpha- and beta-adrenoceptor blocking agent in conscious rats

The autonomic and antihypertensive activities of amosulalol (YM-09538) were studied in conscious rats. Single oral administration of amosulalol antagonized the phenylephrine-induced pressor and isoproterenol-induced positive chronotropic responses with DR10 values of 11.5 and 13.6 mg/kg in pithed rats, respectively, indicating that the compound inhibits both alpha 1- and beta 1-adrenoceptors to almost the same extent in agreement with previously reported results in vitro. Amosulalol was approximately 50 times less potent than prazosin and 12 times more potent than labetalol at alpha 1-adrenoceptors, and it was approximately as effective as labetalol and 2 times more potent than propranolol at beta 1-adrenoceptors. In spontaneously hypertensive rats (SHR), renal hypertensive rats and DOCA/salt hypertensive rats, a single oral administration of amosulalol (3-30 mg/kg) lowered acutely systolic blood pressure with a duration of over 6 hr and was found to be approximately 50 times less potent than prazosin and 3 times more potent than labetalol in lowering blood pressure. Propranolol did not cause such an immediate hypotensive effect. Amosulalol and labetalol did not increase heart rate, whereas prazosin induced a tachycardia in the hypertensive rats. Repeated oral administrations of amosulalol and labetalol (50 mg/kg/day, b.i.d., for 12 weeks) produced not only an antihypertensive effect without evidence of tolerance, but also reductions in plasma renin activity (PRA) and heart rate in SHR with established hypertension. We conclude that alpha-adrenoceptor blockade by amosulalol might account for its antihypertensive activity and that its beta-adrenoceptor blockade might inhibit reflexogenic increases in heart rate and PRA due to the reduction in blood pressure.     

降压药在老年高血压患者中的临床药学探析

目的：分析老年高血压患者降压药的临床应用情况,为临床工作提供借鉴。方法800例高血压患者的基本资料进行记录,包括患者的身高、体重、血压以及使用的降压药物等;记录患者的血压控制情况,观察不良反应,整理并回顾性分析。结果35.5%的患者使用缬沙坦,21.0%的患者使用氨氯地平;舒张压得到控制的患者占70.0%,收缩压得到控制的患者占51.0%;主要不良反应有踝部水肿、心动过缓、低钾血症、体位性低血压、干咳等。结论老年高血压患者,使用较多的药物为缬沙坦和氨氯地平,舒张压的控制比率要高于收缩压,同时,虽然有部分患者出现不良反应,但是降压药的使用基本符合规范。     

Bioavailability of labetalol increases with age.

The antihypertensive drug labetalol was administered orally and intravenously to ten hypertensive patients aged between 28 and 75 years. There was a significant increase with age in both bioavailability and half-life of labetalol. Clearance tended to be lower in the elderly subjects. First pass metabolism results in variable oral bioavailability of labetalol which is greater in the elderly and this should be borne in mind when using the drug in this age group.     

Pharmacokinetics, beta-adrenoceptor blockade and anti-hypertensive action of labetalol during chronic oral treatment.

1 beta-Adrenoceptor blockade, plasma labetalol concentrations and anti-hypertensive actions were investigated at 2 hourly intervals during the interdose period of chronic oral therapy in six hypertensive patients. 2 beta-adrenoceptor blockade varied during the inter-dose period and was maximal 2 and 4 h after the oral dose (P < 0.05). 3 Systolic pressure rose during the interdose period (P < 0.05). A significant correlation was found between the degree of beta-adrenoceptor blockade and the change in systolic pressure at 2 h after the oral dose. 4 Efficacy of labetalol as a beta-adrenoceptor antagonist and anti-hypertensive drug was assessed 2 h after an oral dose during chronic eight hourly dosage in sixteen hypertensive patients. Pharmacokinetics of labetalol were studied in the same patients. 5 Peak plasma labetalol concentration occurred 2 h after the oral dose and subsequently the plasma concentration declined monoexponentially. 6 The steady state concentration (CSS) of labetalol was correlated significantly with the daily oral dose in mg kg-1, the mid point labetalol concentration (Cmax+Cmin) divided by 2 and the isoprenaline dose ratio-1 at 2 h after the oral dose. 7 No correlation was found between the antihypertensive effect and the CSS ng ml-1 labetalol or between the isoprenaline dose ratio-1 and the CSS labetalol ng ml-1.     

Hemodynamic effects of labetalol in patients with combined hypertension and left ventricular failure

To investigate the safety of labetalol in the treatment of hypertension in patients with heart failure, sixteen hypertensive patients with a history of congestive heart failure and an ejection fraction at rest less than 45%, had measurements of ejection fraction and cardiac output by first pass radionuclide angiography at baseline, at the end of 2 weeks maintenance with labetalol (titrated to the effective antihypertensive dose of 200-1600 mg daily), and in the post-treatment placebo period. On labetalol, heart rate and blood pressure were significantly lower than placebo at rest and the ejection fraction was higher (30 vs 25%) (p less than 0.05). At maximal exercise on labetalol the heart rate and blood pressure were lower than at placebo maximal exercise (p less than 0.05) and the ejection fraction was higher (32 vs 27%) (p less than 0.01). Exercise tolerance was not changed by labetalol. No patient was discontinued from the study because of worsening heart failure. Dizziness was reported in 5 of 16 patients usually at one visit. Dyspnea that was reported in 4 of 16 patients improved with minor adjustments in digitalis or diuretic dose. In conclusion, labetalol reduces blood pressure in hypertensive patients with left ventricular dysfunction without reducing cardiac performance.     

Labetalol. A reappraisal of its pharmacology, pharmacokinetics and therapeutic use in hypertension and ischaemic heart disease

Since labetalol was first reviewed in the Journal (1978), its scope of therapeutic use has expanded and become better defined. Labetalol is an adrenoceptor blocking drug with combined alpha- and beta-blocking properties. These result in a more favourable haemodynamic profile for labetalol compared with 'pure' beta-blockers or pure alpha-blockers, but also contribute to a wider range, but not an overall increased incidence, of adverse effects. The drug is effective and well-tolerated in patients with all grades of hypertension, but is of particular value in special subgroups such as Black patients, the elderly and patients with renal hypertension. While comparative studies are not extensive, available data show that the drug reduces blood pressure to a similar extent, and in a similar proportion of patients, as 'pure' beta-blockers such as propranolol, pure alpha-blockers such as prazosin, calcium antagonists (nifedipine, verapamil), and centrally acting drugs (clonidine and methyldopa). Labetalol is very effective in hypertensive pregnant women and in hypertensive crises, where it provides good control of blood pressure without serious adverse effects, and where few therapeutic options exist. Few controlled studies have investigated the use of labetalol in deliberate induction of hypotension or prevention of hypertension during anaesthesia, and also in patients with ischaemic heart disease. However, available evidence suggests a role for labetalol in these indications and further studies should aid in clarification of its efficacy in these areas. Thus, with its broad scope of therapeutic use in hypertension labetalol remains an important therapeutic option, and the drug may well find an additional place in the treatment of myocardial ischaemia if further evidence confirms encouraging preliminary findings.     

Antihypertensive aminotetralins related to labetalol and medroxalol

A series of compounds was prepared in which the 1-methyl-3-phenylpropylamino moieties of the antihypertensive agents labetalol and medroxalol were replaced by 2-aminotetralins. Compounds containing a 6-methoxy and 6,7-methylenedioxy group in the aminotetralin were at least as active as labetalol in lowering the blood pressure of the spontaneously hypertensive rat (SHR). As determined by ligand binding, these compounds were comparable to labetalol as alpha 1-antagonists but were substantially weaker beta 1-antagonists.