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1.
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   

2.
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   

3.
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   

4.
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   

5.

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   

6.
臧莹安  丁发源  王小龙 《中国家禽》2006,28(24):103-105
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   

7.
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   

8.
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   

9.
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   

10.
1. Three hundred and eighty 1-day-old Arbor Acres broilers were divided into control (A) and experimental (B, C, D, and E) groups. 2. After 14 d of age the experimental groups were subjected to a cool temperature challenge by lowering the temperature 1 to 2°C per day down to 12°C, and maintaining this temperature until 7 weeks of age. 3. At the same time, l.5 mg/kg 3,3,5-triiodothyronine (T 3 ) was added to the diet of groups D and E, and 500mg/kg ascorbic acid (vitamin C) to the diet of groups C and E. 4. The incidence of pulmonary hypertension syndrome (PHS), body weight gain and feed intake were measured weekly. Lung and blood samples were collected weekly from 10 birds per group beginning on d 14, and the percentage of thick-walled peripheral lung vessels (%TWPV) and packed cell volume (PCV) were determined. 5. The lower ambient temperature and diets supplemented with T 3 increased PHS incidence and % TWPV and decreased body weight gain. 6. There was an increase in PCV after 5 weeks of age under lower ambient temperature 3 and the PCV values 14 were also significantly increased by T 3 . 7. Vitamin C supplementation reduced PHS incidence and % TWPV but did not change packed cell volume, body, weight gain, feed intake, or feed conversion. 8. It is concluded that vitamin C reduced PHS and the associated muscularisation of pulmonary arterioles induced by exposing broilers to cool environmental temperatures and feeding them with T 3 .  相似文献   

11.
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   

12.
Oxidative stress is involved in the development of pulmonary hypertension syndrome (PHS) in broilers. l-Carnitine has an antiperoxidative effect and supplemental l-carnitine has been revealed to increase broiler heart weight. The present study was conducted to evaluate the effect of an addition of 100 mg/kg l-carnitine to the basal diets on PHS mortality in cold-exposed broilers. Two-hundred and forty mixed-sex broilers were equally assigned to three groups. The control group was reared in normal temperatures throughout the experiment. Starting on day 14 continuing until the end of the experiment, the other two groups were subjected to a step-down temperature programme (by lowering the temperature 1-2 degrees C per day down to 12-14 degrees C) with or without l-carnitine added to the basal diets. Cold exposure increased the right/total ventricle ratio (RV/TV) and plasma malondialdehyde (MDA), reduced superoxide dismutase (SOD) and led to pulmonary vascular remodelling in birds without feeding additional l-carnitine. Supplemental l-carnitine reduced plasma MDA, increased SOD, inhibited remodelling and postponed the occurrence of PHS for 1 week in cold-exposed broilers; nevertheless, it did not significantly influence the cumulative PHS mortality (p > 0.05). On days 24 and 32, birds fed supplemental l-carnitine had lower RV/TV and higher total ventricle/body weight (p < 0.05) but unchanged right ventricle/body weight ratios (p > 0.05) compared to their cold-exposed counterparts, indicating an increase in left ventricle weight. However, from day 39 on, their RV/TV ratios were suddenly increased (p < 0.05). It was suggested that the l-carnitine-induced increase in left heart weight might partially account for the postponed occurrence of pulmonary hypertension in the early stage by elevating cardiac output, which might, in turn, lead to the resulting increase in pulmonary pressure. In view of its complex effects on cardiopulmonary haemodynamics, l-carnitine supplementation may be impractical for reducing PHS.  相似文献   

13.
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   

14.
OBJECTIVE: The present study was conducted to examine the presence of protein kinase Calpha (PKCalpha) in the pulmonary arterioles of broilers during the development of pulmonary hypertension and pulmonary vascular remodelling. METHOD: One hundred and sixty day-old Avian-2000 broilers were divided equally into a control group and a cold temperature group. All the birds were reared in normal temperatures up to day 14, with the lighting schedule at 24 h per day. Thereafter, birds in the cold temperature group were subjected to low temperature by lowering 1-2 degrees C per day to 12-14 degrees C, and then kept constant until day 49, while birds in the control group were still brooded at normal temperatures. All the birds were fed a diet of pellets throughout the study. Samples of blood were taken from the wing vein, and of heart and lung collected after the birds were killed with an overdose of sodium pentobarbitial, at days 24, 32, 39 and 45 of age, respectively. Right ventricle to total ventricle ratio (RV/TV) and packed cell volume (PCV) were measured. Vessel wall area to vessel total area ratio (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA) was examined using computer-image analytic software. Expression of PKC in pulmonary muscular arterioles was assessed by immunohistochemistry and quantified by measuring optical density (OD) using computer-image analytic software. RESULTS: The incidence of pulmonary hypertension syndrome (PHS) was 12.5% in birds exposed to cold, and 3.75% in the control group (P<0.05). PCV in the cold temperature group was elevated after day 32 (P<0.05), and RV/TV ratio increased on day 45 (P<0.05). Both the WA/TA and mMTPA of birds subjected to cold were significantly elevated (P<0.05). The OD values were not significantly increased before day 32 (P>0.05), however, one week later (at day 39 of age), the difference between the two groups was significant (P<0.05). The increased PKCalpha expression was positively correlated with the values of mMTPA and WA/TA. CONCLUSION: PKCalpha expression was up-regulated during the development of pulmonary hypertension. The activation of PKCalpha might be involved in the development of pulmonary vascular remodelling.  相似文献   

15.
A reduced‐protein diet (designated as RPD) was prepared and its effects on growth performance and the development of pulmonary hypertension syndrome (PHS) were evaluated in broiler chickens compared to a normal‐protein diet (designated as NPD) or to the RPD supplemented with CoQ10 alone (30 mg/kg) or in combination with vitamin E (30 mg/kg CoQ10 + 100 mg/kg vitamin E). The RPD had 30 g/kg less crude protein compared to the NPD. A total of 208 1‐day‐old male broilers (Ross 308 strain) were used in a 42‐day trial. Serum concentrations of uric acid (UA) and nitric oxide (NO) significantly (p < 0.05) declined when chickens fed on the RPD. However, supplementing RPD with the antioxidants significantly (p < 0.05) increased the serum NO concentration. Although serum malondialdehyde (MDA) concentration was significantly (p < 0.05) higher in the RPD than the NDP, supplementing RPD with CoQ10 and CoQ10 + VE decreased serum MDA concentration to similar levels found in the NPD. Significant overexpression in GPX1 gene observed in the heart and lungs of broilers fed on the RPD, which was effectively restored by supplementation of CoQ10. The right to total ventricular weight ratio (RV:TV) was significantly (p < 0.05) increased in birds fed the RPD, which concurred with an increase in mortality from pulmonary hypertension syndrome (PHS). However, a significant decline in mortality from PHS was observed when birds on RPD received CoQ10 or CoQ10 + VE. In conclusion, antioxidant supplementation effectively improves pulmonary hypertensive response in broiler chicken fed of reduced‐protein diets.  相似文献   

16.
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   

17.
Nitric oxide (NO) is an endogenous gas that serves as a biologic messenger in many physiologic processes including neurotransmission, blood-pressure control, the immune system's ability to kill tumor cells, and wound healing. NO is produced after oxidation of L-arginine by a family of nitric oxide synthase (NOS) enzymes. Two of the NOS enzymes are present continuously and are thereby termed constitutive NOS. One of the enzymes, inducible NOS, is not typically expressed in resting cells and is induced by various substances including endotoxin, some cytokines, and microbial products. Thus, NO often has paradoxical activities. When NO is over- or underproduced, it can result in potentiation of disease states with disastrous results. This review discusses the biochemistry of NO, its functions in normal and disease states, and therapy for modulating NO production in disease states.  相似文献   

18.
19.
The objectives of this study were to investigate relationship of retained fetal membranes (RFM) to expression of NOS and NOS mRNA and to analyze pathohistological changes and the distribution of nitric oxide synthase (NOS) in foetal placentas of cows with RFM. Twenty cows were assigned to two groups, a control group (no retained fetal membranes, NRFM, n = 10) and a diseased group (RFM, n = 10). The endpoint method was used to detect the nitric oxide (NO) content and nitric oxide synthase (NOS) activity in foetal placental tissue fluid and the fluorescent quantitation PCR was used to measure the expression of NOS mRNA. Immunohistochemistry and hematoxylin-eosin staining were used to observe pathohistological changes. Tissue from RFM cows showed fibronecrosis of the chorionic villi, and a decreased number of trophoblastic cells. The majority of trophoblastic cells displayed vacuolar degeneration. Interstitium vessels were distended and congested. Expression of induced nitric oxide synthase (iNOS) protein and iNOS mRNA was significantly higher (P < 0.05) in the cytoplasm of placental villus trophoblastic cells in the RFM group. But expression of endothelial nitric oxide synthase (eNOS) protein and eNOS mRNA was significantly lower (P<0.05) in the RFM group. The NO content and NOS activity of cows with RFM were significantly higher (P < 0.05). A high expression of iNOS protein and iNOS mRNA in the cow foetal placenta could produce high content of NO, which might inhibit uterine contraction. So over expression of iNOS protein and iNOS mRNA might be an important agent of retained fetal membranes in cows, and it may be a potential diagnosis biomarker.  相似文献   

20.
1. There are few studies on the effect of dietary protein content on pulmonary hypertension syndrome (PHS) in broiler chickens. Conflicting results from these studies prevent a clear conclusion on the effects of reduced-protein diets on development of the syndrome.

2. To obtain an understanding of the mechanisms involved, the current study, conducted at a high altitude (2100?m above sea level), evaluated the effect of three treatments that varied only according to dietary protein (CP) levels. One treatment with dietary CP advocated by National Research Council (1994) acted as a control. Two reduced-protein diets were also prepared with CP reduced 20 and 40?g/kg relative to the CP of the control, which were designated as LCPD2 and LCPD4, respectively. A total of 180?d-old male broilers (Ross 308) were randomised across 15 floor pens measuring 1.5?m2 (12 birds per pen). Five such pens (replicates) were allotted to each dietary treatment. The protein treatments were applied from 1 to 42?d of age in which growth performance was measured and the mortality from PHS was monitored. At the end of trial (42?d), blood sampling was done and carcase characteristics were recorded.

3. Birds receiving LCPD4 gained more weight throughout the trial and had increased right ventricular weight ratio (RV:TV), relative liver weight, haematocrit, and heterophil: lymphocyte ratio at the end of the trial compared to the control. Plasma concentrations of nitric oxide (NO) and uric acid, however, were significantly lower in birds fed on LCPD4 than in those receiving the control diet.

4. Mortality from PHS was increased in birds fed the reduced-protein diets, which may have been associated with reduced concentration of plasma NO and increased haematocrit and RV:TV. In conclusion, feeding reduced-protein diets to broilers subjected to hypobaric hypoxia was associated with the development of PHS.  相似文献   

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