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试验测定了常温和低温下限饲肉鸡和非限饲肉鸡体内一氧化氮(NO)含量、红细胞比容(PCV)和心脏指数的变化,以探讨早期限饲降低肉鸡肺动脉高压综合征(PHS)发病率的机理。试验结果显示低温下肉鸡的PCV值、心脏指数和PHS的发病率显著升高,NO水平在低温早期显著降低,然而随着低温时间的延长,低温处理组肉鸡的血浆NO水平反而代偿性升高。早期限饲显著降低了肉鸡生长早期的红细胞压积值,并显著降低了42日龄心脏指数和PHS的发病率。限饲鸡在限饲期间血浆NO水平显著降低,但其他阶段与非限饲鸡差异不显著。这提示早期限饲能够缓解肉鸡肺动脉高压和右心肥大的产生,其机理可能与NO和PCV改变所致的血流动力学变化有关。 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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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. 相似文献
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环境低温和T3对肉鸡内皮素、一氧化氮和肺动脉压的影响 总被引：4，自引：2，他引：2
20 0只 AA肉鸡随机等分为对照组 (C)和试验组 (T) ,C组和 14日龄前 T组鸡按常规饲养。 T组自 14日龄起舍温从 2 5℃起每天降 1～ 2℃逐渐降至 12℃ ,同时在日粮中按 1.5 m g/ kg的剂量添加三碘甲腺原氨酸 (T3 )以诱发肺动脉高压综合征 (PHS)。分别于 2 1、2 8、35、42、49日龄测定 2组肉鸡平均肺动脉压 (m PAP)、红细胞压积 (PCV)、右心全心比 (RV/ TV)、血浆内皮素 (ET- 1)及一氧化氮 (NO)水平 ,同时记录 PHS发病率。结果显示 ,试验组肉鸡 m PAP升高 ,PHS发病率增加 ;PCV、RV/ TV及血浆 ET- 1水平与对照组相比都显著升高 (P<0 .0 1) ;m PAP变化与血浆 ET- 1含量变化之间存在显著正相关 ,2组间血浆 NO水平无显著差异 (P>0 .0 5 ) ,但都出现随日龄增加血浆 NO水平升高的现象。 相似文献
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为了研究肉鸡肺动脉高压综合征(PHS)的抗病育种情况,试验采用静脉注射纤维素颗粒的方法诱发PHS,比较发病前后非易感组肉鸡和易感组肉鸡右心室与全心室重量比(RV/TV)值,心电图Ⅱ导联S波、R波和RS综合波波幅,红细胞比容(PCV),血红蛋白(HB)和血清蛋白含量。结果表明:静脉注射纤维素颗粒明显提高了肉鸡PHS的发病率。发病后腹水组肉鸡PCV、HB含量和RV/TV值升高,血清蛋白含量降低,心电图Ⅱ导联S波、R波和RS综合波波幅均升高,符合肉鸡PHS的特点;但发病前易感组肉鸡与非易感组肉鸡相比,PCV、HB含量、血清蛋白含量和心电图Ⅱ导联S波、R波和RS综合波波幅均无显著差异。 相似文献
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一氧化氮供体硝普钠降低肉鸡肺动脉压试验研究 总被引：1，自引：0，他引：1
AA肉鸡100羽，随机等分为对照组、试验组、试验组肉鸡自8日龄起给予含0．2％的钠离子的饮水以诱发肉鸡肺动脉高压综合征，按常规方法饲养。并通过右心导管法观察血管内注入硝普纳（Sodium Nitroprusside,SNP)前后两组肉鸡肺动脉平均压（Mean pulmonary arterial pressure,mPAP)变化，与此同时，还观察一氧化氮（Nitric Oxide,NO)与肉鸡肺动脉压间的关系。结果发现试验组肉鸡mPAP高于对照组（P＜0．01），注入SNP后试验组和对照组肉鸡血浆NO水平都显著升高（P＜0．01），而mPAP都显著降低（P＜0．01），试验组肉鸡mPAP降压幅度大于对照组（P＜0．05）。表明SNP可通过释放NO降低肉鸡mPAP。 相似文献
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PHS对快大型黄羽肉鸡线粒体NO代谢和Na+-K+-ATP酶活力的影响 总被引：1，自引：0，他引：1
采取分组对比的方法分别检测了对照组、PHS发病组（低温和日粮中添加1.5 mg/kg T3）、防治组（日粮中添加500 mg/kg Vc）快大型黄羽肉鸡肝组织、肠黏膜、心肌线粒体中的NO含量、NOS的活性和Na^＋-K^＋-ATP酶活力。结果显示,发生PHS的黄羽肉鸡,其肝脏、心肌和肠黏膜线粒体NO活力呈现先显著上升（至PHS处理后1、2周）后显著下降（3～5周）的变化趋势（P〈0.O5）。线粒体NOS活力和Na^＋-K^＋-ATP酶活力的变化趋势则与NO一致。提示：缺氧的早期,NOS活性升高从而使NO水平升高,NO水平升高舒张血管,缓解肺动脉高压,是机体的一种应激反应。随着缺氧时间的延续,机体NOS和NO合成相对不足,相应器官的功能受到损害,肺血管舒缩失衡出现肺动脉高压,进一步发生腹水。而Na^＋-K^＋-ATP酶活力的改变则使能量代谢发生障碍,ATP生成减少,引起了线粒体的损伤,进一步诱导了肉鸡PHS;日粮中添加500 mg/kg Vc对此过程具有明显的颉颃作用,对机体起到保护作用。 相似文献
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Xun Tan Jia-Qiang Pan Jin-Chun Li Yan-Juan Liu Wei-Dong Sun Xiao-Long Wang 《Research in veterinary science》2005,79(3):283-209
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
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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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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14.
Tan X Sun WD Li JC Pan JQ Liu YJ Wang JY Wang XL 《Veterinary journal (London, England : 1997)》2007,173(1):151-157
This study investigated nitric oxide synthase (NOS) expression in the endothelium of pulmonary arterioles of broilers during the development of pulmonary hypertension syndrome (PHS). PHS was triggered by exposing broilers to sub-thermoneutral (cool) temperatures and an additional 1.0% L-arginine was added to the basal diet to evaluate the effects of supplemental L-arginine on nitric oxide (NO) production, endothelial NOS expression, and the incidence of PHS. Cumulative mortality from PHS, right/total ventricle weight ratios (RV/TV), and body weights were recorded. Plasma NO concentration and NOS expression in the endothelium of pulmonary arterioles with an outer diameter ranging from 100 to 200 microm were determined. Birds exposed to cool temperatures had increased pulmonary hypertension and PHS mortality and diminished endothelial NOS expression. Supplemental dietary L-arginine reduced PHS mortality and elicited higher NOS expression within the pulmonary endothelium coincident with elevated NO production. The results demonstrated that broilers developing PHS exhibited diminished NOS expression in the endothelium of their pulmonary arterioles. Supplemental L-arginine prevented the reduced expression of NOS in the pulmonary endothelium, which might contribute to the increased production of NO by the pulmonary vasculature. 相似文献
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Effect of L-NAME on pulmonary arterial pressure,plasma nitric oxide and pulmonary hypertension syndrome morbidity in broilers 总被引：4，自引：0，他引：4
1. Experiments were conducted to evaluate the effect of a synthetic inhibitor of nitric oxide (NO) synthase (L-NAME) on pulmonary arterial pressure (PAP) and pulmonary hypertension syndrome (PHS) morbidity in broilers. 2. In Experiment 1, broilers were infused intravenously with L-NAME, and the mean pulmonary arterial pressure (mean PAP) and plasma NO were measured at 0, 1, 2 and 4 h after the start of infusion. The mean PAP increased and plasma NO was reduced at 1 to 2 h in broilers treated with L-NAME. 3. In Experiment 2, 180 Arbor Acres broilers were evenly divided into three groups: a control group (group C), and two groups exposed to low environmental temperatures and fed a 3, 3, 5-triiodothyronine (T3) supplemented diet alone (group A) or also including 100 ppm L-NAME (group B). 4. The PHS morbidity of group A was higher than for group C but lower than for group B. Plasma endothelin-1 was higher in broilers in groups A and B than in group C. Plasma NO was not significantly lower in broilers of group B when compared with those in group A. 5. The right/total ventricular weight ratio (RV/TV) and mean PAP were higher in groups A and B than in group C, and the RV/TV ratio increased one week earlier in group B than in group A. 6. These results suggest that L-NAME increases broiler PAP by inhibiting the endogenous synthesis of NO, leading to pulmonary hypertension, right ventricular hypertrophy and the increased morbidity of PHS in broilers. 相似文献
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The present study was conducted to examine the effect of supplemental L-arginine on pulmonary arteriole protein kinase Calpha (PKCalpha) expression in broilers exposed to cool temperature, to investigate further the molecular mechanisms of supplemental L-arginine on modulating pulmonary vascular functions in hypertensive broilers. Broilers were subjected to sub-thermoneutral (cool) temperature to induce pulmonary hypertension syndrome (PHS), and an additional 10 g/kg L-arginine was added to the basal diet to evaluate the effects of supplemental L-arginine on PHS mortality, plasma nitric oxide (NO) production and pulmonary arterioles PKCalpha expression. Supplemental L-arginine reduced PHS mortality but did not affect right/total ventricle (RV/TV) ratios in clinically healthy birds. Birds fed additional L-arginine had increased plasma NO and decreased PKCalpha protein expression in pulmonary arterioles; NO production was negatively correlated with PKCalpha expression. These results demonstrated that supplemental L-arginine diminished PKCalpha expression in birds exposed to cool temperature. It is suggested that NO-induced loss of PKCalpha expression might be partially responsible for its effects on dilating pulmonary vasculature and inhibiting pulmonary vascular remodelling in vivo. 相似文献
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To determine whether or not exposure to chronic hypoxia and subsequent development of pulmonary hypertension syndrome (PHS) induce alterations in endothelial nitric oxide (NO) production in broiler's pulmonary vascular bed of broilers, we studied the expression of nitric oxide synthase enzyme in pulmonary endothelial cells by a nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemical staining reaction. For this purpose, 60 broilers of three different ages (17, 30, and 42 days) were used. The animals were distributed in two groups: a) 30 healthy (nonhypertensive) broilers and b) 30 chicks with PHS. All broilers in group b had fewer NADPH-diaphorase-positive endothelial cells in arterioles than did the nonhypertensive broilers. These differences were highly significant (P < 0.01). These results demonstrate for, the first time in broilers, that hypoxia-induced pulmonary hypertension is associated with a decrease of endothelial-derived NO expression in pulmonary vessels. 相似文献
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肉鸡腹水综合征是造成商品肉鸡淘汰和死亡的一种重要疾病 ,发病原因包括遗传育种缺陷、饲养管理不善、饲养环境温度过低、环境氨气浓度过高和疾病因素 (包括传染病和中毒病 ) ,研究表明高海拔、低温环境缺氧是造成寒冷季节发病的最主要诱发因素 ,夏秋季节疾病因素成为主要诱发因素。目前认可的肉鸡腹水综合征发病机理有肠道高浓度氨假说和肺动脉高压假说 ,从不同侧面解释了发病机理。院收稿日期 :2 0 0 3- 0 4 - 2 1作者简介 :何 诚 (196 6 - ) ,男 ,宁夏中宁人 ,中国农业大学动物医学院副研究员 ,从事禽病病理生理研究工作。针对形成肺动脉高压的心输出量、肺血管阻力因素 ,国内外研究者观察了血液生化指标、血管舒张收缩因子、肺动脉压力、自由基清除、肺动脉形态等变化 ,试图支持肺动脉高压学说。最近研究发现发病因子造成肉鸡心脏和肺脏功能损伤是肉鸡腹水综合征的内在机制。针对不同的发病因素和发病环节 ,提出了改善心肺功能、降低肺动脉收缩阻力、消除自由基和活血化淤等新措施防治该病的发生 相似文献