西地那非与前列腺素E1治疗猪肺动脉高压

目的 比较西地那非和前列腺素E1对幼猪肺动脉高压模型的影响.方法 体质量约5 kg实验用健康幼猪24只,用经气管内吸入胎粪法诱发幼猪产生肺动脉高压,2 h后建立急性缺氧性肺动脉高压模型.随机将幼猪分成4组:对照组,不给予任何药物治疗:西地那非组,静脉注射枸橼酸西地那非(2 mg/kg)、前列腺素E1组,持续静脉滴注前列腺素E120 ng/(kg·rain)至实验结束;合用组同时给予西地那非组和前列腺素E1.结果 吸入胎粪2 h后,记录动物的肺动脉压、肺血管阻力(pulmonary vascular resistance,PVR)和体循环血管阻力(systemic vascular resistance,SVR).发现肺动脉压、PVR和PVR/SVR均随时间明显增加.施加药物干预以后,西地那非组与合用组的上述指标均明显迅速下降,并且心输出量和心脏指数明显提高;前列腺素E1组肺动脉压、PVR以及PVR/SVR下降程度不如西地那非组明显,心输出量、心脏指数无改善:对照组的肺动脉压、PVR以及PVR/SVR无下降.结论 西地那非降低肺动脉压和肺血管阻力,改善心功能,同时对体循环血流动力学无不良影响;在本实验用量,西地那非扩张肺血管和降低肺血管阻力的作用比前列腺素E1强;两者联合应用没有发生协同降低肺动脉压作用.     

前列腺素E1治疗肺动脉高压进展

前列腺素E1具有强烈的扩血管 ,增加心肌收缩力 ,改善心肌缺血和左室功能的作用 ,应用日趋广泛 ,因其扩张肺血管 ,松弛小动脉平滑肌 ,降低肺毛细血管楔压的作用可治疗肺动脉高压。     

前列腺素E1联合氧疗对肺动脉高压的作用

前列腺素Ｅ＿１联合氧疗对肺动脉高压的作用郭振辉，叶曜芩，景炳文，罗文侗，宋志芳，邹霞英低氧性肺动脉高压（ＰＡＨ）存在着严重低氧血症，组织氧供（ＤＯ＿２）不足，并因ＰＡＨ的存在而产生肺心病。长期低流量氧疗可降低ＰＡＨ或延缓其进一步升高。我们曾应用不同剂...     

前列腺素E1治疗老年人慢性肺心病继发性肺动脉高压疗效观察

前列腺素Ｅ_１治疗老年人慢性肺心病继发性肺动脉高压疗效观察孙培宗，杜鹃，邢丽华，钟秀梅，郑秀荣，高维义前列腺素Ｅ１（ＰＧＥ１）是扩血管类前列腺素类物质，具有广泛的药理作用。现将我科观察的ＰＧＥ１对１２例老年人慢性肺心病继发性肺动脉高压的作用报道如下。?..     

西地那非治疗肺动脉高压

肺动脉高压是一种相对少见但有潜在致命危险的疾病,多年来缺乏有效治疗药物。最近,美国FDA批准西地那非口服制剂Revatio可用于治疗肺动脉高压,为肺动脉高压患者的治疗带来了新的希望。本文就西地那非治疗肺动脉高压的机理,临床疗效及安全性等作一综述。     

前列腺素E1对先心病合并重度肺动脉高压患者血流动力学的影响

先天性心脏病 (下称先心病 )合并重度肺动脉高压较难处理 ,所以对该病患者术前应用前列腺素 E1(PGE1)可降低其肺动脉压力 ,改善血流动力学指标 ,提高手术安全性 ,现报告如下。1　资料与方法1 .1　临床资料　本文 5 4例先心病合并重度肺动脉高压患者 ,男 3 0例、女 2 4例 ,年龄 1～ 5 8岁、平均 7± 1 4.6岁。其中室间隔缺损 2 6例 ,房间隔缺损 1 2例 ,动脉导管未闭 8例 ,其他 8例。心电图检查示双心室肥大 2 8例 ,右心室肥大 2 1例 ,左心室肥大 5例。X线检查示肺纹理增多 ,心影增大 ,其中 48例肺动脉段显著突出 ,右下肺动脉明显增宽。彩色…     

西地那非对肺动脉高压的作用

肺动脉高压是肺血管收缩、肺动脉内皮细胞和平滑肌细胞增殖以及原位血栓形成综合所致，由此引起肺血管阻力增加．肺动脉高压，最终导致右心衰竭而死亡的疾病。肺动脉高压不是一独立的疾病，而是一种病理生理状态，病因复杂。根据2003年9月召开的世界第三届肺动脉高压会议决定，仍基本维持Evian标准，肺动脉高压的诊断标准：肺动脉收缩压〉40mmHg（相当于多普勒超声检查三尖瓣血液反流速度〉310m／s），     

枸橼酸西地那非治疗原发性肺动脉高压1例

患者,女,36岁,因咳嗽、咯痰、易疲倦、气促伴双下肢水肿1个月入院。入院体检:BP108/80mmHg(1mmHg=0.133kPa),急性面容,高枕卧位,口唇发绀,颈静脉怒张,肝颈静脉回流征阳性,双肺底可闻及湿性啰音,叩诊心界向左扩大,心律齐,P2亢进,三尖瓣区可闻及3/6级收缩期吹风样杂音,肝脏在右肋     

前列腺素E1及卡托普利对先心病肺动脉高压患儿血浆ET—1水平的影响

为探讨前列腺素E     

前列地尔对先天性心脏病合并重度肺动脉高压的治疗作用

目的:观察前列地尔脂微球载体制剂对先天性心脏病合并重度肺动脉高压患儿的肺循环和体循环压力及阻力的影响作用。方法:将60例先天性心脏病合并重度肺动脉高压的患儿随机分为治疗组(30例)和对照组(30例)。治疗组于手术后使用前列地尔,以3~5ng·kg-1·min-1泵入,2h后停止,每天2次;对照组则使用酚妥拉明0.1mg/kg,每天2次。在用药前、后0.5、1、2h分别测量肺动脉压、主动脉压、肺毛细血管压力,以及肺循环阻力、体循环阻力和心率的数值。结果:①前列地尔和酚妥拉明均明显降低肺动脉压力(P<0.01);②前列地尔对体循环压力和心率影响不明显,而酚妥拉明使体循环压力下降,并明显加快心率(P均<0.01),对患者血流动力学影响较大。结论:前列地尔能选择性扩张肺血管从而降低肺动脉压力和肺血管阻力,且对体循环影响较小,副作用小。     

前列腺素E_1在先天性心脏病合并肺动脉高压的术前诊治作用

目的：本文目的是了解先天性心脏病（先心病）合并肺动脉高压患者，术前应用前列腺素Ｅ１（ＰＧＥ１）治疗后对其心肺功能的改善作用，为该病的诊治提供依据。方法：对２２例先心病合并严重肺动脉高压患者术前应用ＰＧＥ１治疗（ＰＧＥ１１００～２００ｎｇ·ｋｇ－１／ｍｉｎ，静脉滴注４～５ｈ／ｄ）４～７天。结果：对于肺低阻力组（平均全肺阻力７８．７０±２９．１６ｋＰａ·ｓ／Ｌ，用药后心前区杂音较前明显，动脉氧饱和度增加（Ｐ＜０．０５），肺血流受阻程度改善，右心射血分数增加（Ｐ＜０．０５）；对于肺高阻力组（平均全肺阻力２６５．３３±７６．９７ｋＰａ·ｓ／Ｌ，用药后除右心射血分数明显增加（Ｐ＜０．０５）外，其余各项指标改善不明显。结论：对于先心病合并肺动脉高压的患儿，应用ＰＧＥ１治疗，不但可判断肺血管病变性质，为手术适应证的选择提供参考；同时还可以改善患者的心肺功能，为手术做好准备。     

东茛菪碱联合前列腺素E1治疗肺心病并呼吸衰竭的临床研究

目的 探讨东莨菪碱联合前列腺素E1治疗肺心病并呼吸衰竭的疗效。方法 对72例肺心病并呼吸衰竭患者，随机分为2组，对照组37例，治疗组36例，治疗组在常规治疗基础上，应用东莨菪碱联合前列腺素E1，并对其结果进行分析。结果 治疗组3例，总有效率85．7％，对照组37例，总有效率45．9％，两组有效率有显著性差异（P〈0．01）。两组治疗1周后PaO2、PaCO2和SaO2与对照组相比均有显著性差异（P〈O．01）。结论 应用东莨菪碱联合前列腺素E1治疗肺心病并呼吸衰竭有显著疗效。     

Impact of Sildenafil Therapy on Pulmonary Arterial Hypertension in Adults with Congenital Heart Disease

Background : It has been demonstrated that sildenafil is effective in patients with pulmonary arterial hypertension (PAH). However, the impact of sildenafil on PAH in adults with congenital heart disease (CHD) has been less investigated. Objective : In this prospective, open‐label, uncontrolled and multicenter study, 60 patients with PAH related to CHD received oral sildenafil (75 mg/day) for 12 weeks. The enrolled patients underwent six‐minute walk test (SMWT) and cardiac catheterization at the beginning and the end of the 12 weeks. The primary end point was the changes in exercise capacity assessed by SMWT; the secondary end point included assessment of functional class, evaluation of cardiopulmonary hemodynamics, and clinical worsening (defined as death, transplantation, and rehospitalization for PAH). Drug safety and tolerability were also examined. Results : Oral sidenafil significantly increased SMWT distances (422.94 ± 76.95 m vs. 371.99 ± 78.73 m, P < 0.0001). There was also remarkable improvement in Borg dyspnea score (2.1 ± 1.32 vs. 2.57 ± 1.42, P= 0.0307). Moreover, significant improvements in World Healthy Organization (WHO) functional class and cardiopulmonary hemodynamics were also discovered (mean pulmonary artery pressure, P= 0.0002; cardiac index, P < 0.0001; pulmonary vascular resistance, P < 0.0001). Side effects in this study were mild and consistent with reported studies. None of the enrolled patients experienced significant clinical worsening. Conclusions : This study confirmed and extended previous studies. It suggested that oral sildenafil was safe and effective for the treatment of adult patients with CHD‐related PAH.     

Suppressive Effect of Prostaglandin E1 on Pulmonary Hypertension Induced by Monocrotaline in Rats

The effect of administering prostaglandin E₁ (PGE₁) on the extent of monocrotaline (MCT)-induced pulmonary hypertension and cytokine production [interleukins (IL) 1 and 6 and tumor necrosis factor (TNF)] by macrophages during MCT induction of pulmonary hypertension was studied. Right ventricle/left ventricle plus septum weight ratios (RV/LV + S) were used as an index of the development of pulmonary hypertension. Administering PGE₁ at a dose of 0.2 mg/kg/day for 4 weeks reduced significantly the RV/LV + S ratio from 0.428 ± 0.070 to 0.243 ± 0.059 (p < 0.01) and decreased the production of these cytokines: IL-1, from 4.675 ± 3.558 to 1.800 ± 0.722 units; IL-6, from 0.322 ± 0.121 to 0.060 ± 0.039 units; and TNF, from 0.578 ± 0.369 to 0.004 ± 0.004 units. In another series of experiments, a significant reduction of the RV/LV + S ratio was noted for only 1 week when we administered PGE₁ immediately after the injection of MCT. We confirmed that histopathologic improvements of lungs were noted by administering 0.2 mg/kg PGE₁ for 4 weeks. In another experiment, PGE₁ at a concentration of 2 μg/ml suppressed a rise in the cytosolic Ca²⁺ concentration of lipopolysaccharide-stimulated peritoneal macrophages of rats in vitro, suggesting that PGE₁ suppressed cytokine production by macrophages through the suppression of the Ca²⁺ influx. These results suggest that administering PGE₁ may be effective in the treatment of some forms of pulmonary hypertension in humans. Accepted for publication: 20 August 1998     

东莨菪碱联合前列腺素E1治疗肺心病并呼吸衰竭的临床研究

目的探讨东莨菪碱联合前列腺素E1治疗肺心病并呼吸衰竭的疗效。方法对72例肺心病并呼吸衰竭患者,随机分为2组,对照组37例,治疗组36例,治疗组在常规治疗基础上,应用东莨菪碱联合前列腺素E1,并对其结果进行分析。结果治疗组3例,总有效率85.7%,对照组37例,总有效率45.9%,两组有效率有显著性差异(P<0.01)。两组治疗1周后PaO2、PaCO2和SaO2与对照组相比均有显著性差异(P<0.01)。结论应用东莨菪碱联合前列腺素E1治疗肺心病并呼吸衰竭有显著疗效。     

The Extracellular Signal‐Regulated Kinase Is Involved in the Effects of Sildenafil on Pulmonary Vascular Remodeling

Pulmonary hypertension is a group of diseases comprising vascular constriction and obstructive changes of the pulmonary vasculature. Phosphodiesterase type 5 inhibitors, for example, sildenafil, can alleviate vascular remodeling in the monocrotaline pulmonary hypertension model in rats. We investigate the mechanisms of sildenafil on the pulmonary vascular remodeling of pulmonary hypertension induced by monocrotaline (MCT) in rats. Thirty Sprague‐Dawley rats (weighing 200–220 g) were administered with MCT abdominal cavity injection or equivalent volume of normal saline (NS) (which were treated as C group n = 10) to induce pulmonary hypertension model. Fourteen days later, 20 MCT treated rats were randomly fed with sildenafil (25mg/kg/day) or placebo as S, P group (10 rats for each group), respectively. Another 6 weeks later, mean pulmonary artery pressure (mPAP), index of right ventricular hypertrophy (RV/LV+S) of all animals were measured under general anesthesia. Pulmonary tissue was collected to investigate pathological features of pulmonary arteries and to measure protein expression of ERK₁/ERK₂ and MKP1. After 6 weeks, there were significant elevated mPAP and RV/LV+S in both P and S groups. The ratio of wall thickness to vessel diameter in pulmonary arteries with diameters <200 μm were increased in both P and S groups. But the ratio of wall thickness to vessel diameter was smaller in S group than that in P group. The phosphorylation level of ERK₁/ERK₂ were elevated in both P and S groups, but the level of phosphorlation ERK₁/ERK₂ were lower in S group than that in P group. Intriguingly, the expression level of MKP1 was significantly increased in both S and P groups, while it was higher in S group than that in P group. The Sildenafil can decrease mPAP and inhibit the progress of pulmonary vascular remodeling in pulmonary hypertension rats. The ERK‐MAP kinase signaling pathway might play a role during this process.