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早期限饲对肉鸡肺动脉高压综合征发病率、生产性能和腹脂率的影响 总被引：1，自引：0，他引：1
采用低温诱发肉鸡肺动脉高压综合征,对比观察不同的早期限饲方法对于常温和低温条件下PHS的发病率、肉鸡生产性能和腹脂率的影响。在试验1中,限饲处理组肉鸡分别于7￣14日龄或7￣21日龄每天给料8h,对照组肉鸡全程自由采食。在试验2中,限饲组肉鸡分别于7￣14日龄给予对照组肉鸡前1d饲料消耗量的60%或80%。结果表明:早期限饲能够降低肉鸡PHS的发病率,在低温条件下尤其明显;早期限饲改善了饲料效率,同时未对肉鸡的胴体品质产生显著的影响,且适当限饲不影响肉鸡的最终上市体重。这表明早期限饲是一种有效的控制肉鸡PHS的方法,值得在实际生产中推广应用。 相似文献
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早期限饲对肉鸡体内脂质过氧化作用和抗氧化酶活性的影响 总被引：3，自引：0，他引：3
采用低温诱发肉鸡腹水综合征(AS)，并观察早期限饲对常温和低温饲养时肉鸡AS的发病率、肉鸡体内脂质过氧化作用和抗氧化酶活性的影响。试验1，限饲处理组肉鸡分别于7～14日龄或7～21日龄每天给料8h，对照组肉鸡全程自由采食。试验2，限饲组肉鸡分别于7～14日龄给予对照组肉鸡前一天饲料消耗量的60％或80％，对照组肉鸡自由采食。试验过程中连续测定肉鸡血浆超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH—Px)、丙二醛(MDA)水平和腹水心脏指数(RV／TV值)。结果显示低温显著升高了肉鸡血浆MDA浓度，降低了血浆SOD和GSH—Px的活性；低温饲养肉鸡5～6周龄时的RV／TV值显著升高，AS的发病率显著增加。限饲处理显著降低了肉鸡血浆MDA含量，并且限饲处理肉鸡生长后期血浆中SOD和GSH—Px活性显著高于自由采食组肉鸡。所有的限饲处理均能降低肉鸡AS的发病率，并且早期限饲处理肉鸡42日龄的RV／TV值显著低于非限饲肉鸡。这表明早期限饲能够减轻肉鸡体内脂质过氧化作用，提高机体抗氧化酶的活性，从而降低AS的发病率。 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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低温诱发肉鸡肺动脉高压综合征（PHS）,动态观察限制光照对肉鸡PHS发病率及体内脂质过氧化作用的影响。将320羽1日龄肉鸡随机分为4组。常温组按常规饲养,24 h连续光照。3个低温组从14日龄起逐步降温诱发PHS,并于9～30日龄分别在夜间停止光照0、35、h。结果,低温组PHS发病率、右心全心比（RV/TV）、肺厚壁末梢血管百分率（%TWPV）和丙二醛（MDA）水平显著升高,而血浆超氧化物歧化酶（SOD）活性降低。限制光照组SOD活性升高而PHS发病率、RV/TV、TWPV和MDA显著降低。间歇光照组早期生长速度减慢,后期体质量得到补偿性增长,并在44日龄与连续光照组差异不显著。这一结果表明,减轻体内脂质过氧化作用,提高机体抗氧化酶活性并减轻以非肌型肺动脉肌型化为特征的肺血管重构,可能是限制光照使肉鸡PHS发病率降低的机理之一。 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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近年来国内外学者已对内鸡肺动脉高压综合征(腹水)的发病原因、病理过程和防治方法进行了广泛研究.限饲降低了肉鸡的生长率,减缓了体内的代谢过程,改善了缺氧状态,降低了肉鸡腹水的发病率.但是,限饲能否获得与非限饲肉鸡同样的体质量为此,利用冬天肉鸡腹水病为模型,动态观察限饲对内鸡腹水的发病率、体质量、饲料转化率的影响,从而为此病的发病机理和防治方法的研究提供理论依据. 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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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
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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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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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日粮中添加L—NAME对肉鸡腹水综合征发生的影响及其机理 总被引：6，自引：1，他引：5
应用低温环境和日粮中添加三碘甲腺原氨酸（3，3，5－triiodothyronine,T3)诱发肉鸡腹水综合征，同时通过日粮添加一氧化氮合酶抑制剂L－NAME，研究了抑制NO的合成对肉鸡肺动脉压及肉鸡腹水综合征发生的影响。180羽AA肉鸡随机等分为对照组（C）、试验组（A、B），参试鸡14日前按常规条件饲养。14日龄后C组鸡按常规条件饲养，A、B组鸡舍温按每日1－2℃逐步降至12℃，同时日粮中添加T3 1．5mg/kg以诱发腹水综合征。另外，B组肉鸡从14日龄起在日粮中添加100mg/kgL－NAME至试验结束。分别于3、4、5、6周龄测定各组肉鸡肺动脉平均压（mean pulmonary arterial pressure,mPAP)、红细胞压积、右心全心比、血浆一氧化氮（NO）和内皮素（endothelin-1,ET-1)水平并记录腹水综合征发病率。结果显示：低温添加T3处理后，A、B组肉鸡腹水综合征发病率增加，但B组高于A组；A、B组肉鸡mPAP从5周龄起高于C组（P＜0．05）；A、B组右心全心比的升高分别在6、5周龄时出现，B组右心全心比的升高比A组提前1周；B组 肉鸡血浆NO水平低于A组，差异不显著；A、B组肉鸡血浆ET－1水平高于C组（P＜0．05）；在6周龄时，A组肉鸡心率明显降低，B组肉鸡心率明显升高。随着肺动脉高压和右心肥大的出现，心率的升高可能促进了右心衰竭和肉鸡腹水综合征的发生。上述结果提示，抑制NO的合成可能促进了肉鸡肺动脉高压，右心肥大的形成和肉鸡腹水综合征的发生。 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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OBJECTIVE: The present study was conducted to investigate the effect of early feed restriction on protein kinase Calpha (PKCalpha) expression in pulmonary arterioles, which has been revealed to promote pulmonary vascular remodeling in pulmonary hypertensive broilers. METHODS: A total of 270day-old mixed sex commercial broilers were randomly distributed to a normal temperature control group (NT), a low temperature control group (LT) and a low temperature plus feed restriction group (LR). The PHS incidence, the right/total ventricular weight ratio (RV/TV), the vessel wall area/vessel total area ratio (WA/TA), the mean media thickness in pulmonary arterioles (mMTPA) and the expression of PKCalpha in the pulmonary arterioles were measured weekly. RESULTS: Low temperature treatment significantly increased the PHS mortality. The RV/TV, WA/TA and mMTPA values of group LT were significantly elevated compared with those of group NT on d 35 and 42. The LT chickens had increased PKCalpha expression compared with their NT counterparts on d 28 and afterwards. Feed restriction reduced the PHS mortality, RV/TV, WA/TA and mMTPA in cold-exposed broilers. The LR chickens had much lower PKCalpha expression in pulmonary arterioles than the LT chickens. CONCLUSION: Early time feed restriction inhibited pulmonary vascular remodeling in broilers, which might be partly attributed to reduced PKCalpha expression in pulmonary arterioles. 相似文献
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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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Two experiments were conducted to evaluate the effects of early feed restriction on lipid peroxidation, pulmonary vascular remodelling and ascites incidence in broilers under normal and low ambient temperature. In experiment 1, the restricted birds were fed 8h per day either from 7 to 14 d or from 7 to 21 d, while the controlled birds were fed ad libitum. In experiment 2, the restricted birds were fed 80 or 60% of the previous 24-h feed consumption of full-fed controls for 7 d from 7 to 14 d. On d 14, half of the birds in each treatment both in experiment 1 and experiment 2 were exposed to low ambient temperature to induce ascites. Body weight and feed conversion ratio were measured weekly. The incidences of ascites and other disease were recorded to determine ascites morbidity and total mortality. Blood samples were taken on d 14, 21, 28, 35 and 42 to measure the plasma malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). On d 42, samples were taken to determine the right/total ventricular weight ratio (RV/TV), vessel wall area/vessel total area ratio (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA). Low-temperature treatment increased plasma MDA concentration. When broilers were exposed to a cool environment for 3 weeks, plasma SOD and GSH-Px activity were decreased compared with normal-temperature chicks. RV/TV, WA/TA and mMTPA on d 42 were increased in birds exposed to cold, consistent with the increased pulmonary hypertension and ascites morbidity. Early feed restriction markedly decreased plasma MDA concentration. The plasma SOD and GSH-Px activity of feed-restricted birds were markedly higher than those fed ad libitum on d 35 and d 42. All early feed restriction treatments reduced ascites morbidity and total mortality. On d 42, the RV/TV, WA/TA and mMTPA of feed-restricted broilers were lower than that of the ad libitum-fed broilers. The results suggested that early feed restriction alleviated the lipid peroxidation, promoted the activity of enzymatic antioxidant and inhibited pulmonary vascular remodelling. These changes might be associated with reduced ascites incidence. 相似文献