共查询到18条相似文献，搜索用时 234 毫秒
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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… 相似文献
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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。 相似文献
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本试验用高选择性内皮素A受体拮抗剂BQ123处理低温肉鸡的方法,通过动态观察肺动脉压及肌型、部分肌型及非肌型肺小动脉数量的变化,探讨内源性内皮素在肺血管重塑中的作用。结果显示:30日龄时,低温组平均肺动脉压极显著高于常温组、低BQ123组及高BQ123组(P<0.01);低温组肌型及部分肌型肺小动脉的占位比均极显著高于常温组、低BQ123组及高BQ123组(P<0.01);低温组非肌型肺小动脉占位比极显著低于常温组、低BQ123组和高BQ123组(P<0.01),高BQ123组显著高于低BQ123组(P<0.05)。结果表明,BQ123可明显抑制低温肉鸡肺动脉高压和非肌型肺小动脉的肌型化的发生发展,因此认为内源性ET在低温诱发肺动脉高压肉鸡肺血管重塑的发生发展过程中起重要作用。 相似文献
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低温诱发肉鸡腹水综合征发生过程中肺血管重塑与肺动脉高压的关系 总被引：1，自引：0，他引：1
将160只15日龄雄性AA商品代肉鸡随机分为对照组((22±1.5)℃)和低温组((11±2)℃)。15~50日龄,每组每周随机取6只,以右心导管法直接测定肺动脉压(PAP),并取肺组织做石蜡切片进行Weigert-间苯二酚复红染色,分析肺血管重塑情况。50日龄时统计整个饲养过程中肉鸡腹水综合征(AS)发生率。结果显示,低温组肉鸡AS发生率(18.75%)极显著高于对照组(1.25%)(P<0.01);低温组肉鸡PAP从22日龄开始较对照组明显升高(P<0.01或P<0.05);20~50、50~100、100~200μm肺动脉结构分别从36、43、43日龄开始较对照组发生了明显的重塑(P<0.01或P<0.05)。结果表明,低温诱发肉鸡AS过程中出现了明显的PAP升高和肺血管重塑,且肺动脉高压(PH)促进了肺血管重塑,肺血管重塑加剧了PAP升高。 相似文献
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本试验旨在研究低温诱发肉鸡腹水综合征(AS)过程中平滑肌细胞增殖在肺血管重塑过程中的动态变化,初步探讨肺血管重塑的机制。160只15日龄雄性AA商品代肉鸡随机分为对照组(22℃±1.5℃)和低温组(11℃±2℃)。试验持续至50日龄,期间每周每组随机取6只,取肺组织做石蜡切片,Weigert-间苯二酚复红染色,观察并测定血管重塑情况;采用免疫组织化学方法检测肺动脉增殖细胞核抗原(PCNA)蛋白表达,并对其半定量化,分析平滑肌细胞增殖情况。50日龄时统计整个饲养过程中AS发生率。结果显示:(1)低温组肉鸡AS发生率(18.75%)极显著高于对照组(1.25%)(P<0.01);(2)低温组肉鸡直径20-50μm和50-150μm肺动脉结构从36日龄开始较对照组发生了明显的重塑(P<0.01或P<0.05);(3)低温组肉鸡直径20-50μm和50-150μm的肺动脉平滑肌细胞增殖指数分别从22日龄和36日龄开始极显著高于对照组(P<0.01)。结果表明:低温诱发肉鸡AS过程中肺动脉结构发生了明显的重塑,肺动脉平滑肌细胞发生了明显的增殖,并且平滑肌细胞增殖促进了肺血管重塑,在肉鸡AS发生发展过程中起着重要的作用。 相似文献
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通过动态观察肺动脉压、红细胞压积、腹水心脏指数、肺小动脉中膜厚度占外径百分值(mMTPA)及管壁面积/管总面积(WA/TA)的变化,探讨高选择性内皮素A受体拮抗剂BQ123对低温诱发肉鸡腹水综合征的预防作用。结果显示,BQ123能显著降低低温诱发肉鸡的肺动脉压、红细胞压积及腹水心脏指数(P0.05或P0.01);BQ123能显著减小低温诱发肉鸡的mMTPA及WA/TA(P0.05或P0.01)。结果表明,BQ123明显抑制了低温诱发肉鸡的肺动脉高压和肺血管重塑的形成和发展,对肉鸡腹水综合征具有明显的预防作用。 相似文献
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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。 相似文献
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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 总被引：10，自引：1，他引：9
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。 相似文献
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Pulmonary arterial remodelling is a pathological characteristic of pulmonary arterial hypertension (PAH), which contributes to the development of sustained pulmonary hypertension. The aim of this study was to investigate the effects of dietary Trifolium pratense isoflavones on pulmonary vascular remodelling in experimental broiler pulmonary hypertension syndrome. Exposure to sub‐thermoneutral environmental temperatures increased broiler's pulmonary hypertension syndrome incidence and raised expression levels of nitric oxide, endothelin and endothelial nitric oxide synthase. Dietary supplementation (20 mg/kg basal diet) with Trifolium pratense isoflavones reduced pulmonary hypertension syndrome incidence and improved pulmonary vascular remodelling without affecting growth performance. The beneficial effect likely came from isoflavone improved pulmonary vascular remodelling. Isoflavone induced inducible nitric oxide synthase expression, which led to increased nitric oxide level. The nitric oxide could mediate vasorelaxation in the lungs. At the same time, the expression of endothelin was downregulated by isoflavone. Dietary supplementation of Trifolium pratense isoflavone might be a potential therapeutic strategy for the treatment of pulmonary hypertension. 相似文献
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A 12-week-old, clinically normal Chihuahua was referred for investigation for a continuous heart murmur. Cardiac evaluation revealed an anatomically and haemodynamically typical left-to-right shunting patent ductus arteriosus. The continuous wave Doppler measurement of peak ductal jet velocity of 5.6 m/s was suggestive of a normal pulmonary to systemic arterial pressure ratio. The dog returned 16 days later with right heart failure and severe pulmonary hypertension. Marked reduction in left-to-right shunting was demonstrated and the ductal jet velocity had decreased to 2.5 m/s. Immediate ductus ligation, oxygen therapy before and after the operation, and administration of hydralazine failed to reduce pulmonary hypertension, and the dog was euthanased. Histopathological examination of the lung showed pulmonary necrotising arteritis with acute and chronic arterial lesions. Chronic pulmonary vascular changes related to high flow have been associated with altered nitric oxide and endothelin responses. These changes may be responsible for the acute onset of pulmonary hypertension due to relatively minor vascular insults in some human and veterinary patients with left-to-right shunts. The potential for acute progression supports the recommendations for early ductus ligation and the prognostic importance of detecting pulmonary hypertension presurgically in patent ductus arteriosus patients. 相似文献
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This study was designed to determine whether calcium antagonists, diltiazem and nifedipine, can depress low temperature‐induced pulmonary hypertension (PH) in broilers (also known as ascites) and to characterize their efficacy on hemodynamics and pulmonary artery function. Chicks were randomly allocated into six experimental groups and orally administered with vehicle, 5.0 mg/kg body weight (BW)/12 h nifedipine or 15.0 mg/kg BW/12 h diltiazem from 16 to 43 days of age under low temperature. The mean pulmonary arterial pressure (mPAP), the ascites heart index (AHI), the erythrocyte packed cell volume (PCV) and the relative percentage of medial pulmonary artery thickness were examined on days 29, 36 and 43. The data showed that administration of diltiazem protected broilers from low temperature‐induced pulmonary hypertension and vascular remodeling. Although nifedipine prevented mPAP from increasing during the early stage, it did not suppress the development of PH during the late stage and did not keep heart rate (HR), PCV, AHI and the thickness of pulmonary small artery smooth muscle layer at the normal levels. Taken together, our results showed that diltiazem can effectively prevent low temperature‐induced pulmonary hypertension in broilers with fewer side‐effects and may be a potential compound for the prevention of this disease in poultry industry. 相似文献
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静脉注射纤维素粒子复制肉鸡肺动脉高压模型,观察肺小动脉中膜5-羟色胺(5-HT)表达和肺小动脉管壁病理形态学变化,探讨5-HT与肺血管重构的关系。80羽科宝肉鸡分为对照组(n=30)和试验组(n=50)。20日龄时,试验组每羽鸡静脉注射0.3 mL的纤维素悬液;对照组每羽鸡静脉注射等体积生理盐水。记录肺动脉高压综合征(PHS)发病率,并分别于21、28、35、42 d从各组随机抽样,测定右心室/全心室质量比(RV/TV)、红细胞压积(PCV)、血红蛋白(Hb)、肺小动脉管壁面积/管总面积(WA/TA)、平均中膜厚度(mMTPA)和肺厚壁末梢血管百分比(TWPV%);采用免疫组化方法标记5-HT,并用病理图像分析软件检测肺小动脉5-HT的量。结果表明:试验组肉鸡PHS发病率显著高于对照组(P<0.05);RV/TV值在35、42 d时显著升高(P<0.05);PCV在28、35 d时显著升高(P<0.05);Hb值在35 d时显著升高(P<0.05);血管mMTPA、WA/TA和TWPV%在35、42 d时均显著升高(P<0.05);肺小动脉5-HT含量升高,在各时间点均差异显著(P<0.05),且5-HT含量... 相似文献
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B Sustronck G Van Loon P Deprez E Muylle F Gasthuys L Foubert 《Research in veterinary science》1997,63(3):193
The effect of inhaling nitric oxide in the hypoxic pulmonary vascular response was measured in five calves anaesthetised with a combination of guaiacol, ketamine and xylazine. Alveolar hypoxia was induced by means of the inhalation of a gas mixture with an inspiratory oxygen fraction of 14–18 per cent. This alveolar hypoxia resulted in a pronounced pulmonary hypertension (mean pulmonary artery pressure in hypoxic animals : 30·2 mmHg). Inhalation of 20 and 40 ppm of nitric oxide significantly attenuated the hypoxia induced pulmonary hypertension. The effect ceased once nitric oxide administration was stopped. A concentration of 40 ppm of nitric oxide fully abolished the hypoxia induced pulmonary hypertension (mean pulmonary artery pressure during inhalation of 40 ppm nitric oxide : 22·8 mmHg). Inhalation of nitric oxide had no effect on systemic arterial blood pressure nor on systemic vascular resistance. It was concluded that inhalation of 20 or 40 ppm of nitric oxide prevented a selective pulmonary vasoconstriction during alveolar hypoxia in calves, which may be helpful in the treatment of acute respiratory disorders in calves. 相似文献
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Cardiac effects of pulmonary disease. 总被引：1，自引：0，他引：1
Fiona E Campbell 《Veterinary Clinics of North America: Small Animal Practice》2007,37(5):949-62, vii
Pulmonary hypertension (PHT) is the primary cardiac consequence of pulmonary disease. It develops as alveolar hypoxia of pulmonary disease, coupled with vasoactive and mitogenic substances released from pulmonary endothelial and vascular smooth muscle cells damaged by the primary disease process, mediates arterial vasoconstriction and vascular remodeling to raise pulmonary vascular resistance. Independent of the underlying pulmonary disease, PHT produces clinical signs of respiratory distress, exercise intolerance, syncope, and right heart failure. Diagnosis of PHT is made by estimation of pulmonary artery pressures by means of continuous-wave Doppler echocardiographic assessment of tricuspid or pulmonic regurgitant flow velocity. Treatment of PHT is directed at the underlying pulmonary disease but may also aim to attenuate pulmonary artery pressure and limit the clinical sequelae of PHT. No treatments are of proven benefit in veterinary patients; irrespective of the nature of the inciting pulmonary disease, the prognosis is often grave. 相似文献
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Objective
Pulmonary vascular remodelling is one of the important pathological bases of broiler pulmonary hypertension syndrome (PHS). Nitric oxide (NO) has been found to inhibit proliferation and to induce apoptosis in pulmonary artery smooth muscle cells (SMC) in mammals with pulmonary hypertension. The present study was conducted to evaluate the effects of NO precursor l-arginine on pulmonary vascular remodelling in broilers with pulmonary hypertension induced by cold exposure and to examine whether NO-induced apoptosis in pulmonary arteriole SMC is involved in the regulatory mechanisms.Methods
Two hundred and forty mixed-sex commercial broilers were equally assigned to three groups and reared in normal brooding temperatures before day 14. Starting on day 14 continuing until the end of the experiment, the control group was brooded in normal temperatures whereas the other two groups were subjected to low ambient temperatures with or without l-arginine added to the basal diets. Cumulative PHS mortality and body weight were recorded in each group. Right/total ventricle ratio (RV/TV), plasma NO concentration and pulmonary vascular morphological changes were analyzed. TdT-mediated dUTP-biotin nick-end labeling (TUNEL) assay was used to detect apoptosis in pulmonary arteriole SMC.Result
l-Arginine, in group A, had no effect on body weights under cold temperature condition. Birds kept in group B had increased PHS mortality, RV/TV ratio, vessel wall area/vessel total area ratios (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA) (P < 0.05). Percentages of apoptotic SMC in pulmonary arterioles in group B were not altered by cold exposure (P > 0.05). Supplemental dietary l-arginine in group A elevated plasma NO level (P < 0.05), reduced PHS mortality (P < 0.05), attenuated pulmonary vascular remodelling and increased the percentages of apoptotic SMC (P < 0.05) when compared with the group B.Conclusion
Supplemental l-arginine partially inhibited pulmonary vascular remodelling that occurred secondary to increased pulmonary pressure; NO-induced apoptosis in arteriole SMC might contribute to its regulatory effect on pulmonary vascular structural changes. 相似文献18.
1. The aim of the study was to determine if H2S is involved in the development of hypoxia-induced pulmonary hypertension in broilers, a condition frequently observed in a variety of cardiac and pulmonary diseases. 2. Two-week-old broilers were reared under normoxic conditions or exposed to normobaric hypoxia (6?h/day) with tissue levels of H2S adjusted by administering sodium hydrosulfide (NaHS, 10?µmol/kg body weight/day). Mean pulmonary arterial pressure, right ventricular mass, plasma and tissue H2S levels, the expression of cystathionine-β-synthase (CSE) and vascular remodeling were determined at 35?d of age. 3. Exposure to hypoxia-induced pulmonary arterial hypertension was characterized by elevated pulmonary pressure, right ventricular hypertrophy and vascular remodeling. This was accompanied by decreased expression of CSE and decreased concentrations of plasma and tissue H2S. 4. Hypoxia-induced pulmonary hypertension was significantly reduced by administration of NaHS but this protective effect was largely abolished by D, L-propargylglycerine, an inhibitor of CSE. 5. The results indicate that H2S is involved in the development of hypoxia-induced pulmonary hypertension. Supplementing NaHS or H2S could be a strategy for reducing hypoxia-induced hypertension in broilers. 相似文献