氟西汀和5-羟色胺对肉鸡肺动脉平滑肌细胞增殖与凋亡的影响

为探讨5-羟色胺转载体(5-HTT)在肉鸡肺动脉高压综合征发病中的机制,采用MTT比色法、流式细胞术及Hoechst33258荧光染色法研究5-羟色胺(5-HT)和5-HTT抑制剂氟西汀对体外培养的肉鸡肺动脉平滑肌细胞(PASMC)增殖与凋亡的影响,发现氟西汀能够抑制5-HT促PASMC增殖的作用;氟西汀能明显促进PASMC的凋亡,但氟西汀和5-HT共同作用于细胞,PASMC凋亡率明显少于氟西汀单独处理组。表明5-HTT在调节肉鸡PASMC的增殖和凋亡方面起重要作用,有可能参与肺动脉高压肉鸡肺血管重构的形成。     

肉鸡和藏鸡肺动脉平滑肌中CaSR的表达

肉鸡肺动脉高压是以肺动脉压血管重构为特征的一种疾病,众多研究揭示肺血管重构是其中心环节之一。细胞内钙离子([Ca2+])浓度的升高是诱发并导致血管重构的重要机制,钙敏感受体(CaSR)在肺动脉平滑肌细胞内钙离子稳态失调及低氧性肺血管收缩和肺血管重构中起着重要的作用。应用免疫组化和Western blot方法研究了缺氧条件下CaSR在AA肉鸡和藏鸡肺动脉平滑肌组织中的表达情况,为肉鸡腹水综合征(PAH)的肺动脉重构提供新的证据。结果表明,肉鸡组有肺水肿发生,藏鸡组无肺水肿发生,缺氧条件下饲养的肉鸡肺动脉平滑肌CaSR表达明显高于藏鸡组(P0.05)。通过探讨CaSR在AA肉鸡和藏鸡肺动脉平滑肌组织中的表达情况,从新的角度阐明了肉鸡腹水综合征发生的分子机制。     

一氧化氮对肉鸡肺动脉高压综合征的影响

肺动脉压升高是肉鸡肺动脉高压综合征(PHS)的重要发病机制。近年来研究表明一氧化氮(NO)在PHS发生发展中发挥着重要作用。本文论述了NO对肉鸡PHS发病过程的影响。一氧化氮合酶(NOS)和NO活性在PHS早期升高而后期下降。NO具有强大的扩张血管的作用,但在PHS过程中,NO合成相对不足,导致肺血管舒缩失衡,引起肺动脉压升高。肺血管重构是肉鸡肺动脉高压综合征的重要病理学变化特征,而NO可促进肺小动脉平滑肌细胞凋亡,在一定程度上抑制肺血管重构的形成。NO作为自由基对机体造成的损伤也是引起PHS的原因之一。在肉鸡日粮中补充NO前体物L-精氨酸可以增加内源性NO的生成,有助于降低PHS的发病率。     

低温诱发肉鸡肺动脉高压中肺血管重塑的作用

采用低温处理肉仔鸡的方法,通过测定肺动脉压、肺小动脉中膜厚度占外径百分比及中膜面积与血管总面积比的变化,探讨肉鸡肺动脉高压的发生机制.结果表明:肺血管重塑在低温诱发肉鸡的肺动脉高压发生发展中起重要作用.     

红三叶异黄酮对肉鸡肺血管重构和平滑肌细胞凋亡的影响

为观察在低温环境下红三叶异黄酮对肉鸡肺血管重构和平滑肌细胞凋亡的影响,选取270只10日龄肉鸡,随机分为常温对照组(Ⅰ)、低温组(Ⅱ)和低温黄酮组(Ⅲ),每组6个重复,每个重复15只,Ⅰ组和Ⅱ组饲喂基础饲粮,Ⅲ组饲喂添加红三叶异黄酮20mg/kg的试验饲粮,分别于14,21,28,35,42日龄从各组随机抽取6只肉鸡,观察各组肉鸡肺血管病理形态学变化,检测Caspase-3和Bcl-2蛋白表达情况。结果表明,Ⅱ组肉鸡肺小动脉结构在28,35,42日龄比Ⅰ组肺小动脉管壁有不同程度增厚、管腔变窄,发生了明显的重构现象(P0.05或0.01)。Ⅲ组与Ⅱ组相比,在28,35,42日龄肺血管重构现象减轻(P0.05或0.01),肉鸡肺动脉高压综合征(PHS)发病率降低,血管平滑肌细胞Caspase-3蛋白阳性率增高,Bcl-2蛋白表达下降;表明红三叶异黄酮能有效减轻肉鸡肺血管重构,其机制可能与调节平滑肌细胞凋亡有关。     

肉鸡肺动脉高压综合征自然病例肺细小动脉病理改变的图像分析

利用 ４ 只与缺氧有关的肉鸡肺动脉高压综合征 自然病鸡和 ４ 只 同品种、同龄健康肉 鸡,以右心室（ｒｉｇｈｔ ｖｅｎｔｒｉｃｌｅ, Ｒ Ｖ）与全心室（ｔｏｔａｌ ｖｅｎｔｒｉｃｌｅ, Ｔ Ｖ）的重量比（ Ｒ Ｖ／ Ｔ Ｖ）作为判定肺动脉高压的主要依据,用图像分析仪对 ２ 组肉鸡肺小动脉作了定量检测。结果显示,肺动脉高压综合征（ Ｐ Ｈ Ｓ）患鸡肺小动脉发生了以无肌细动脉肌型化、肌性动脉中膜平滑肌增厚、管壁肥厚为主要特征的血管重构现象,从而说明与缺氧相关的肉鸡肺动脉重构的病理变化可能参与了肉鸡肺动脉高压的形成过程。     

一氧化氮对肉鸡肺血管重塑影响的研究进展

肺血管重塑是肉鸡肺动脉高压综合征的重要病理学变化特征,虽然对其形成的机制尚未完全清楚,但众多细胞因子在其形成过程中起重要作用已得到共识。一氧化氮作为一种信号物质,在血管扩张、细胞增殖与凋亡、内皮素分泌与合成以及抗氧化等过程中发挥着重要的调控作用,显示了其在抑制肉鸡肺血管重塑、预防和治疗肺动脉高压发生方面有着广阔的应用前景。     

维拉帕米对环境低温诱发肉鸡肺动脉平滑肌细胞增殖的作用

环境低温诱发肉鸡腹水综合征(AS)发生过程中,肺血管发生明显重塑,并以肺动脉中膜增厚为主要特征。血管平滑肌细胞的数量将影响血管中膜的厚度[1]。故推测认为肉鸡肺动脉平滑肌细胞增殖在肺血管重塑过程中起着重要作用。研究认为细胞内的Ca2 是重要的细胞内第二信使,在细胞增殖过程中起着重要的作用。维拉帕米作为一种钙通道阻滞剂,可抑制Ca2 内流,使细胞内Ca2 水平降低,对肉鸡AS的发生有明显的预防作用[2]。但有关维拉帕米对环境低温诱发肉鸡AS过程中肺动脉血管平滑肌细胞增殖的作用,未见报道。增殖细胞核抗原(proliferating cell nucle…     

5-羟色胺转载体抑制剂对肺动脉高压肉鸡肺组织胶原蛋白含量的影响

5-羟色胺(5-HT)介导的肺血管重构是肉鸡肺动脉高压综合征(PHS)形成的重要病理机制,而5-羟色胺转载体抑制剂已被证明能够抑制肉鸡肺血管重构,降低PHS的发病率,但其机理尚不十分清楚.为了从肺组织胶原蛋白沉积的角度探讨5-羟色胺转载体抑制剂抑制肉鸡肺血管重构的机理.本试验采用翅静脉注射纤维素颗粒的模型诱发肉鸡PHS,分别给诱病肉鸡灌服两种5-羟色胺转载体抑制剂,即氟西汀(fluoxetine)和西酞普兰(citalopram).使用分光光度法测量肉鸡肺组织胶原蛋白含量,采用ELISA方法测量肺组织5-羟色胺浓度,观察各组肉鸡肺组织胶原蛋白含量和5-羟色胺浓度的差异.结果显示,发病组肉鸡肺组织5-羟色胺浓度和胶原蛋白含量高于正常对照组肉鸡,而氟西汀和西酞普兰均能降低PHS肉鸡肺组织胶原蛋白含量和5-羟色胺浓度,表明5-羟色胺转载体抑制剂能降低肺成纤维细胞合成胶原蛋白的能力,进而影响肺血管重构和PHS的发生.     

内皮素在肉鸡腹水综合征肺动脉高压中的病理学意义

肉鸡腹水综合征是当今世界各国肉鸡养殖业的一大难题 ,是造成肉仔鸡淘汰、死亡的重要原因之一。在许多国家 ,寒冷季节肉鸡腹水综合征造成的经济损失已经超过了传染病。对于我国肉鸡饲养业而言 ,大部分的肉鸡饲养集中于北方地区 ,每年饲养期有一半时间处于寒冷时期 ,因此肉鸡腹水综合征成为冬春季节危害最为严重的疾病之一。肉鸡腹水综合征的发病涉及环境、营养、遗传、饲养管理等多方面因素 ,目前普遍认为缺氧性肺动脉高压是肉鸡腹水综合征病理机制的中心环节 ,而肺血管收缩和肺血管结构重建为缺氧性肺动脉高压的特征。研究表明 ,肺及肺血管…     

Relationship of pulmonary arterial pressure to pulmonary haemorrhage in exercising horses

Exercise-induced pulmonary haemorrhage (EIPH) is characterised by blood in the airways after strenuous exercise and results from stress failure of the pulmonary capillaries. The purpose of this experiment was to establish a threshold value of transmural pulmonary arterial pressure at which haemorrhage occurs in the exercising horse. Five geldings, age 4-14 years, were run in random order once every 2 weeks at 1 of 4 speeds (9, 11, 13, 15 m/s); one day with no run was used as a control. Heart rate, pulmonary arterial pressure and oesophageal pressure were recorded for the duration of the run. Transmural pulmonary arterial pressure was estimated by electronic subtraction of the oesophageal pressure from the intravascular pulmonary arterial pressure. Within 1 h of the run, bronchoalveolar lavage was performed and the red and white blood cells in the fluid were quantified. Red cell counts in the lavage fluid from horses running at 9, 11 and 13 m/s were not significantly different from the control value, but after runs at 15 m/s, red cell counts were significantly (P<0.05) higher. White cell counts were not different from control values at any speed. Analysis of red cell count vs. transmural pulmonary arterial pressure indicated that haemorrhage occurs at approximately 95 mmHg. Red cell lysis in the lavage fluid was also apparent at transmural pulmonary arterial pressures above 90 mmHg. We conclude that, in the exercising horse, a pulmonary arterial pressure threshold exists above which haemorrhage occurs, and that pressure is often exceeded during high speed sprint exercise.     

Diagnosis of pulmonary hypertension

Pulmonary hypertension may complicate a variety of congenital or acquired cardiac and pulmonary conditions. This vascular disorder results from conditions that lead to a chronic increase in left atrial pressure, increased pulmonary blood flow, or increased pulmonary vascular resistance. Definitive diagnosis requires cardiac catheterization and detection of systolic and mean pulmonary artery pressures exceeding 30 and 20 mm Hg, respectively. Clinical signs and historical complaints reflect underlying cardiac or pulmonary conditions, although syncope may be a predominant finding. Radiographic changes are nonspecific; however, right ventricular enlargement and enlarged pulmonary arteries should increase suspicion for the disorder. Estimates of pulmonary arterial pressure may be obtained through Doppler echocardiography. This requires detection of a high-velocity regurgitant jet across the tricuspid or pulmonic valve. Further investigation is required to determine how pulmonary hypertension impacts therapy and prognosis for dogs and cats with cardiac and pulmonary diseases.     

Diagnosis of pulmonary thromboembolism in a cat using echocardiography and pulmonary scintigraphy

A 10-year-old male cat was presented with sudden onset of respiratory difficulties. Clinical examinatlon revealed an acute dyspnoea with cyanosis associated with a left systolic heart murmur. Standard thoracic radiographs excluded pulmonary oedema and showed very few pulmonary changes given the intensity of the respiratory compromlse. Echocardiographic examination revealed hypertrophic cardiomyopathy and a thrombus In the right pulmonary artery. Pulmonary sclntlgraphy confirmed a pulmonary thromboembolism with hypovascularisatlon of the left cranial lobe and of the ventral segment of the right lobe. Conservative treatment was instituted using an antibiotic (doxycycllne), anticoagulants (heparin, coumadine) and a calcium lnhlbitor (diltiazem). The cat was given absolute rest. The general condition of the animal improved.     

Exercise-induced pulmonary hemorrhage

This article addresses many aspects of exercise-induced pulmonary hemorrhage (EIPH). Reports of the prevalence, effect on performance, and the clinical signs and means of diagnosis of EIPH are included. Radiologic and scintigraphic findings in horses with EIPH are reported. Pathogenesis and treatment are discussed.