妊娠合并肺动脉高压临床研究现状

<正>肺动脉高压(pulmonary hypertension,PH)是各种导致静息状态下经肺动脉导管测得的平均肺动脉压(mean pulmonary artery pressure,mP AP)≥25mmH g(1mmH g=0.133kP a)病理状态的统称,通常简称PH~([1])。但肺动脉导管检查创伤大,费用及技术要求高,临床不适宜初步诊断的进行,对有患PH可能性的患者,通常使用超声心动图进行初步判断,具体见表1~([1])。临床中,PH通常伴有肺血管阻力(pulmonary vascu-     

骨形态发生蛋白2型受体基因在肺动脉高压发病机制中的研究进展

<正>肺动脉高压(pulmonary arterial hypertension,PAH)是一种罕见的以肺末梢小动脉进行性重构、肺动脉内压力异常升高为特征的临床疾病~([1])。PAH诊断标准为静息状态下右心漂浮导管(right-heart catheterization,RHC)测定平均肺动脉压(mean pressure of pulmonary artery,mPAP)≥25mm Hg(1mm Hg=0.133kPa),肺毛细血管楔压(pulmonary capillary wedge pressure,PCWP)≤15 mm Hg,肺血管阻力     

肺动脉高压中炎性介质的研究进展

2013年尼斯第五届世界肺高血压(pulmonary hypertension,PH)论坛根据病因及发病机制将PH分为五大类,肺动脉高压(PAH)属于第一大类,其定义为静息状态下经右心导管(right heart catheterization,RHC)测得平均肺动脉压(mean pulmonary artery pressure,mPAP)≥25 mmHg(1 mmHg=0.133 kPa),且肺动脉楔压(pulmonary artery     

肺动脉高压的治疗进展

肺动脉高压（pulmonary artery hypertension,PAH）是以肺小动脉的血管痉挛、内膜增生和重塑为主要特征的一种疾病。一般认为,静息时平均肺动脉压（mean puhnonary arery pressure,MPAP）〉25mmHg（1mmHg=0．133kPa）或运动时MPAP〉30mmHg可定义为PAH。     

肺血管重构与磷酸二酯酶关系的新进展

肺动脉高压（pulmonary artery hypertension, PAH）是一大类以肺动脉压和肺循环阻力升高为特征的严重疾病。根据发病诱因可分为特发性PAH、家族性PAH、缺氧性PAH及结缔组织病引起的PAH;感染因素如艾滋病等引起的PAH;以及因先天性心脏病左向右分流引起的PAH;急、慢性肺动脉栓塞引起的PAH等。各类PAH的发病机制大部分未明,但其共同特征是肺动脉压及肺血管阻力升高、右心室后负荷增加,从而导致右心衰竭甚至死亡。不同发病原因的PAH进展过程中,都会出现肺血管收缩和肺血管重构相同的病理学特征。     

结缔组织生长因子和肺动脉高压

肺动脉高压(pulmonary artery hypertension,PAH)是以肺血管受损导致肺动脉压力升高为共同特征的疾病~([1]).参与PAH的体液因子较多,目前研究较多的有内皮素(endothelin-1,ET-1)、血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)、血小板衍生因子(platelet-derived growth factor,PDGF)等.     

西地那非抑制内皮素-1诱导人肺动脉平滑肌细胞增殖机制

动脉型肺动脉高压(pulmonary artery hypertension,PAH)主要病理生理变化是肺血管异常收缩、肺血管重构,肺动脉平滑肌细胞(pulmonary artery smooth muscle cells,PASMCs)增殖显著是肺血管重构的重要表现之一,细胞内Ca~(2+)是细胞增殖的分子基础,钙库操控性通道(SOC)是调节细胞内钙离子浓度([Ca~(2+)]i)的重要途径.TRPC1属于瞬时性感受器电位(transient receptor potential,TRP)家族蛋白,参与构成SOC并在人PASMCs中表达丰富.     

睡眠呼吸障碍与肺动脉高压

正肺动脉高压(pulmonary hypertension, PH)也被称为肺高血压,是由已知或未知原因引起的肺动脉压力异常升高的临床病理生理综合征。PH病因广泛,既可来源于肺血管自身病变,也可继发于其他心肺疾患。按照中国肺高血压诊断和治疗指南2018和2015年欧洲呼吸学会(European Respiratory Society,ERS)/欧洲心脏病学会(European Society of Cardiology,ESC)的PH指南~([1-2]),PH的血流动力学诊断标准为:海平面状态下、静息时右心导管测得肺动脉平均压(mean pulmonary artery pressure,mPAP)≥25 mmHg (1 mmHg=0.133 kPa)。动脉型PH(pulmonary arterial hypertension,PAH)指孤立性肺动脉压力升高,而左心房与肺静脉压力正常,主要是由于肺小动脉本身病变导致肺血管阻力增加。     

从肺动脉高压形成的病理生理机制看阿司匹林治疗的可能性

<正> 肺动脉高压(pulmonary arterial hypertension,PAH)是一种危及生命的疾病,其特点是肺动脉压力和肺血管阻力进行性升高,最终导致右心衰竭和死亡。PAH定义为肺动脉平均压≥25 mm Hg,肺毛细血管楔压≤15 mm Hg且肺血管阻力≥3个Woods单位。如果不治疗,PAH的预后很差,美国注册登记研究显示,未治疗的PAH患者在确诊后平均生存2.8年。肺血管的基本病理改变:(1)内膜增生;(2)中膜肥厚;(3)原位血栓形成。本文综述了PAH的主要病理生理学和分子生物学改变,及阿司匹林在抑制或改善这些主要病变中的重要作用,分析阿司匹林是否能够成为治疗PAH的手段之一。     

经胸超声心动图对肺动脉高压患者右心功能评价的研究进展

正肺动脉高压(pulmonary arterial hypertension, PAH)是一组以肺小动脉管壁进行性增厚、管腔狭窄和肺血管阻力(pulmonary vascular resistance,PVR)升高为特征的临床病理综合征~[1-3]。其血流动力学定义为:海平面、静息状态下,右心导管测量肺动脉平均压     

State of knowledge of helminth fauna of freshwater fishes of Poland

A total 89 fish and lamprey species has been recorded from Polish freshwater habitats. Twenty-seven of them (30.3%) have not been surveyed for parasitic helminthes. Some of the latter fishes are either rare or not easily accessible. Other live only in specific habitats in scattered localities. An important obstacle for studying parasite faunas of some fishes may be their status on an endangered species. Among the non-surveyed fishes, are those which have been relatively recently introduced to Poland or migrated there on their own. The present paper attempts to review all hitherto not studied helminthologically fish species, their habitats, localities and current protection status.     

高血压降压治疗目标的再认识

根据传统的高血压水平的定义,1993年WHO高血压治疗指南提出血压控制目标为<140/90mm Hg(1mm Hg=0.133kPa),但是并非所有患者都必须将血压降至同一水平,而应根据患者情况进行个体化治疗。Framingham进行的一项长达10～12年的心血管事件研究发现,第5年后,正常上限血压[收缩压(SBP     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.