共查询到19条相似文献，搜索用时 406 毫秒
1.
采取分组对比的方法（对照组，肺动脉高压综合征（PHS）发病组，维生素C治疗组）分别检测试验鸡只肝组织、肠黏膜、心肌线粒体中的NO含量和NOS的活性。结果显示，对于发生PHS的快大型黄羽肉鸡，其肝脏、心肌和肠黏膜线粒体NO含量呈现先显著上升后显著下降的变化趋势（P〈0．05）。线粒体NOS活力的变化趋势则与NO一致。与对照组相比，维生素C治疗组各指标则呈现相反的变化，说明其能有效地阻止快大型黄羽肉鸡发生PHS这一过程。 相似文献
2.
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
3.
腹水综合征对肉鸡肝脏、心肌和肠黏膜线粒体抗氧化能力的影响 总被引：1，自引：1，他引：1
采取分组对比的方法（对照组，肉鸡腹水征发病组，治疗组）分别检测肝组织、肠黏膜、心肌线粒体中的MDA含量，SOD、GSH—PX的活性。结果显示，发生腹水综合征的肉鸡，其肝脏、心肌和肠黏膜线粒体MDA活力呈现先显著降低（1、2周时）、后显著提高（3、4、5周时）的变化趋势（P〈0．05）而与发病组线粒体MDA活力先降后升的动态变化趋势相反，治疗组线粒体MDA的活力则呈现先升后降的趋势，最终显著阻止了自由基的产生。线粒体SOD和GSH—Px活力的变化趋势则与MDA相反。提示：肉鸡腹水综合征显著诱导了肉鸡组织细胞和线粒体的脂质过氧化作用，显著降低了肉鸡组织细胞和线粒体的抗氧化能力；药物能有效地改善这一过程。 相似文献
4.
通过动物试验观察内毒素对肉鸡肠黏膜Na+-K+-ATPase活性影响及氨基胍的保护作用.30日龄黄羽肉鸡90只,随机分成内毒素处理组(LPS组,5mg/kg)、氨基胍治疗组(AG+ LPS组)和生理盐水对照组.每组分别在处理后1、3、5、7和9h时间点杀鸡取样.取肠黏膜匀浆,提取线粒体.检测肠黏膜线粒体Na+-K+-ATPase活性.LPS在3、5h时,显著增加了肉鸡肠黏膜线粒体Na+-K+-ATPase活力(P＜0.05),而在7、9h时,肠黏膜线粒体Na上-K+-ATPase活力却降至正常(P＞0.05).AG除了在5h时显著降低了肉鸡肠黏膜Na+-K+-ATPase活力外(P＜0.05),其余时间点均显著增加了肉鸡肠黏膜线粒体Na+-K+-ATPase活力(P＜0.05).由此推论:LPS诱导了线粒体的损伤,引起线粒体内Na+-K+-ATPase活性紊乱,能量代谢障碍,组织机能发生改变;AG对LPS具有明显的拮抗作用,对机体起到保护作用. 相似文献
5.
本研究采用30日龄黄羽肉鸡90只,随机分成内毒素处理组(LPS组,5mg/kg)、氨基胍治疗组(AG+LPS组)和生理盐水对照组。每组分别在处理后1、3、5、7h和9h时间点杀鸡取样。取肠黏膜、肝组织匀浆,提取线粒体。分别检测肠黏膜和肝脏线粒体复活体Ⅰ活性。结果显示,LPS在各时间段显著降低了肉鸡肠黏膜和肝脏线粒体复合体Ⅰ的活性(P<0.05)。注射AG 1h时,肉鸡肠黏膜和肝脏线粒体复合体Ⅰ的活性未发生变化(P>0.05),3h时却显著增加(P<0.05);5h、7h时,趋于正常(P>0.05);9h时,显著降低(P<0.05)。表明LPS诱导了线粒体的损伤,引起了线粒体内的复活体Ⅰ活性的紊乱,能量代谢障碍,组织机能发生改变;AG对LPS具有明显的颉颃作用,对机体起到保护作用。 相似文献
6.
本试验旨在研究基础日粮中添加谷氨酰胺替代饲用抗生素对黄羽肉鸡免疫器官指数及小肠黏膜免疫的影响。将180只1日龄体重相近、健康的黄羽肉鸡随机分为5个处理组,每个处理组3个重复,每个重复12只。阴性对照组饲喂基础日粮,阳性对照组在基础日粮中添加0.3 g/kg那西肽和0.25 g/kg硫酸黏杆菌素,试验Ⅰ、Ⅱ、Ⅲ组分别在基础日粮中添加1、2、3 g/kg谷氨酰胺。结果显示,试验Ⅰ、Ⅱ、Ⅲ组黄羽肉鸡免疫器官重量及免疫器官指数与阳性、阴性对照组相比差异均不显著(P＞0.05),且各试验组之间差异也不显著(P＞0.05)。45 d 时,试验Ⅰ、Ⅱ组黄羽肉鸡十二指肠、空肠肠黏膜蛋白质中溶菌酶的含量低于阳性对照组,但差异不显著(P＞0.05);与阳性对照组相比,试验Ⅰ、Ⅱ、Ⅲ组和阴性对照组的十二指肠内容物中细菌数量均显著提高(P＜0.05)。77 d时,试验Ⅰ、Ⅱ、Ⅲ组十二指肠、空肠、回肠肠黏膜蛋白质中溶菌酶的含量均与阳性对照组差异不显著(P＞0.05);十二指肠黏膜蛋白质中分泌型免疫球蛋白A的含量均低于阳性、阴性对照组;回肠内容物中乙酸、丙酸及总酸的浓度均低于阳性对照组,高于阴性对照组。因此,在基础日粮中添加谷氨酰胺替代饲用抗生素可能会提高黄羽肉鸡的细胞免疫水平,改善小肠黏膜免疫功能。 相似文献
7.
《中国家禽》2017,(10)
试验旨在研究饲粮不同硒水平对22~42日龄黄羽肉鸡生长性能、抗氧化指标的影响,从而确定快大型黄羽肉鸡饲养中期的最适硒水平。选用22日龄健康、发育良好的快大型岭南黄羽肉公雏鸡1 200只,根据体重随机分为5个组,每组6个重复,每个重复40只,试验组1(对照组)为基础日粮组(硒含量0.037 mg/kg),试验组2、3、4、5饲粮则在基础日粮中分别添加0.075、0.15、0.225、0.30 mg/kg硒,试验期为21 d。结果表明:饲粮添加不同水平硒对试验鸡生长性能无显著影响(P0.05);各硒添加组血浆、红细胞和肝脏谷胱甘肽过氧化物酶(GSH-Px)活力显著高于对照组(P0.05),饲粮添加不同水平硒对试验鸡血浆和肝脏丙二醛(MDA)含量无显著影响(P0.05)。综合考虑,22~42日龄黄羽肉鸡饲粮硒适宜水平为0.337 mg/kg。 相似文献
8.
为探讨NO和巯基在山羊内毒素血症发病机理中的作用,将48只山羊随机分为对照组、内毒素组、褪黑素保护组、褪黑素组。每组12只,分别在处理后3、6 h各宰杀6只提取心肌线粒体,检测心肌线粒体中的MDA的含量,总巯基(T-SH)的含量,蛋白巯基(PB-SH)的含量,非蛋白巯基(NP-SH)的含量,以及总一氧化氮合成酶(TNOS),分型一氧化氮合成酶(i NOS)的活性和一氧化氮(NO)水平的变化。结果显示,内毒素血症时山羊心肌线粒体中总巯基(T-SH)的含量,蛋白巯基(PB-SH)的含量,非蛋白巯基(NP-SH)的含量降低,MDA的含量,总一氧化氮合成酶(TNOS),分型一氧化氮合成酶(i NOS)的活性和一氧化氮(NO)水平升高。而褪黑素治疗组则情况明显好转。结果表明,由于NO过量生成而引起的脂质过氧化损伤在山羊内毒素血症发病机理中起着重要的作用,褪黑素可有效拮抗脂质过氧化造成的损伤。 相似文献
9.
日粮添加VE和VC对肺动脉高压综合征患鸡自由基代谢的影响 总被引：5，自引：4，他引：1
将380只AA商品肉鸡随机分为A组100只,B、C、D和E组各70只,14日龄前常规饲养。14日龄后,B、C、D和E组舍温按每日1～2℃由25℃、逐步降至12℃,同时日粮中按1．5mg／kg的剂量添加T3以诱发肺动脉高压综合征(PHS);C、D组在日粮中分别按500、100mg／kg的剂量添加维生素C和E;而E组同时添加维生素C和E,A组仍常规饲养,至试验结束。记录每周各组鸡群的PHS发病数、平均体质量和采食量,并每周每组取10只鸡采血和扑杀,测定其红细胞压积(PCV)、血浆、肺和肝组织的超氧化物歧化酶(SOD)及脂质过氧化物的降解产物丙二醛(MDA)浓度;取心脏测定其右心室和全心室质量比(RV／TV)。结果显示,环境低温和日粮添加T3极显著增加了肉鸡PHS的发病率(P＜0．01)。C、E组的肉鸡PHS发病率以及血浆、肺和肝组织的MDA值均极显著降低(P＜0．01),血浆、肺和肝组织的SOD值均极显著增加(P＜0．01),但增重、饲料转换率、血液PCV值和心脏指数RV／TV值未发生改变;D组5周龄后的血浆MDA值则极显著降低(P＜0．01)以及血浆、肺和肝组的SOD值极显著增加(P＜0．01),而肺和肝组织的MDA值和肉鸡PHS发病率未发生改变。由此表明,日粮添加维生素C明显阻断了低温和T3条件下肉鸡体内脂质过氧化过程,有效清除了体内自由基,显著增强了体内抗氧化能力,成功防制了肉鸡PHS的发生;日粮中同时添加维生素C和E使低温加T3条件下的肉鸡体内抗氧化能力进一步加强;但维生素C或／和E未能改变在环境低温和日粮添加T3诱病条件下肉鸡的增重和饲料转换率,而日粮中单独添加维生素E则使低温加T3条件下的肉鸡体内抗氧化能力有一定的增强作用,但并未改变肉鸡PHS的发病率。 相似文献
10.
青蒿素与青蒿水提液对感染柔嫩艾美耳球虫肉鸡的疗效评价 总被引：1，自引：0，他引：1
为评价青蒿素和青蒿水提液抗球虫的效果,选择体重相近20日龄黄羽肉鸡120只,随机分为健康组,病理组,青蒿组和青蒿素组4组.测定血清中一氧化氮(NO)和一氧化氮合酶(NOS)含量.结果表明,病理组抗球虫指数为52.7,青蒿组为172.6,青蒿素组为145.4;青蒿和青蒿素能够降低血清中NO和NOS含量.说明青蒿水提液和青... 相似文献
11.
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
12.
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
13.
静脉注射L-氨基胍对肉鸡肺动脉压及其相关指标的影响 总被引：1，自引：1，他引：1
按常规饲养条件饲养AA雄性肉鸡120羽，30日龄时随机分为试验组（T组）和对照组（C组）。T组肉鸡静脉注射L-AG（40mg／kg），C组肉鸡静脉注射生理盐水。分别在注射L-AG和生理盐水1、2、4h后测定平均肺动脉压（mPAP）、诱导型一氧化氮合酶（iNOS）活性、原生型一氧化氮舍酶（cNOS）活性、一氧化氮（NO）含量、红细胞压积（PCV）、电解质浓度、pH、超氧化物歧化酶（SOD）活性、过氧化氢酶（CAT）活性和丙二醛（MDA）含量。结果显示：（1）试验组mPAP、NO含量和iNOS活性均显著或极显著低于对照组（P〈0．05或P〈0．01）；（2）PCV和Ca^2＋在给药后2h和4h与对照组差异显著（P〈0．05）；（3）K^＋浓度在给药1h和2h后显著或极显著低于时照组（P〈0．05或P〈0．01）。结果表明，L-AG通过抑制iNOS活性，引起肉鸡肺动脉压的升高，从而推测iNOS具有调节肉鸡体内mPAP的作用并与肉鸡肺动脉高压综合征发生有着密切的联系。 相似文献
14.
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
15.
饲粮维生素E水平对43～63日龄黄羽肉鸡肉品质和抗氧化功能的影响 总被引：1，自引：0，他引：1
本试验旨在研究饲粮维生素E水平对43 ～ 63日龄黄羽肉鸡肉品质和抗氧化功能的影响.选用1 440只43日龄岭南黄羽肉公鸡,采用单因子随机分组试验设计,共设6个处理,每个处理6个重复,每个重复40只鸡.试验采用玉米淀粉-豆粕型基础饲粮,各处理饲粮营养水平除维生素E水平不同外,其他均相同.空白对照组饲喂未添加维生素E的基础饲粮,其余各处理饲粮中分别添加5、10、20、40、80 mg/kg维生素E.试验期21 d,试鸡地面平养,自由采食颗粒料和自由饮水.结果表明:1)饲粮中维生素E添加水平对试鸡生长性能和胴体品质无显著性影响(P＞0.05).2)胸肌肉色的L*、a*、b *值和肌肉嫩度也未受饲粮维生素E添加水平显著影响(P＞0.05).添加各水平维生素E均显著提高了宰后45 min胸肌pH(P ＜0.05),添加5、10、40、80 mg/kg维生素E均显著提高了宰后24 h胸肌pH(P ＜0.05).添加20、40 mg/kg维生素E显著降低了宰后45 min胸肌滴水损失,添加5、10、40、80 mg/kg维生素E显著降低了宰后48 h胸肌滴水损失(P＜0.05).3)饲粮中添加不同水平维生素E对试鸡血清中丙二醛(MDA)含量和总超氧化物歧化酶(T-SOD)活性无显著性影响(P＞0.05),添加10、20 mg/kg维生素E使试鸡血清中谷胱甘肽过氧化物酶(GSH-Px)活性分别比对照组提高了27.51％、30.57％(P＜0.05).添加各水平维生素E均使试鸡肝脏中GSH-Px活性显著提高(P＜0.05),添加20、40、80 mg/kg维生素E均显著降低了肝脏中MDA含量(P＜0.05),显著提高了肝脏中α-生育酚含量和肌肉中T-SOD活性(P＜0.05).以上试验结果提示,饲粮中添加维生素E可提高43～63日龄黄羽肉鸡机体抗氧化功能,改善肉品质,且添加20 mg/kg效果较好. 相似文献
16.
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
17.
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.
肺动脉高压综合征发病过程中肉鸡血清和肺脏iNOS和cNOS活性变化 总被引：1，自引：0，他引：1
常规饲养条件喂养的大群AA肉鸡，按临床症状分为肺动脉高压组（M组），肺动脉高压腹水组（S组）和正常对照组（C组）。分别测定21、28、35和42日龄S组、M组和C组肉鸡的腹水心脏指数（AHI）、全心与体重比（WH／BW）、平均肺动脉高压（mPAP）、血清一氧化氮（NO）水平、肺脏和血清cNOS和iNOS活性。试验结果表明：（1）S组和M组全心与体重比值（TV／BW）以及S组血清NO水平均从28日龄起显著或极显著高于C组（P〈O．01或P〈0．05）；（2）S组肺组织cNOS水平显著或极显著低于C组（P〈0．01或P〈0．05）；（3）S组肺组织iNOS在21、35和42日龄显著或极显著高于C组（P〈0．01或P〈0．05）；（4）S组从28日龄起血清中cNOS和iNOS与C组差异显著或极显著（P〈0．01或P〈0．05）；（5）正常对照组肉鸡血清中iNOS活性在21、35和42日龄均显著或极显著低于血清中cNOS活性（P〈0．01或P〈0．05）。此研究结果提示cNOS和iNOS活性的变化与PHS发病机理有着密切的关系，并在其中发挥着重要的作用。 相似文献
19.
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