共查询到20条相似文献，搜索用时 62 毫秒
1.
Jin-Chun Li Jia-Qiang Pan Guo-qing Huang Wei-Dong Sun Xiao-Long Wang 《Research in veterinary science》2010,88(1):116-121
Objective
The purpose of the present study was to characterize the relationship between platelet-derived growth factor β receptor (PDGF-β receptor) expression and pulmonary vascular remodeling found in broilers subjected to cold temperature beginning at 14 days of age.Method
One hundred and sixty-one-day-old mixed-sex Avian-2000 commercial broilers were randomly divided into a normal temperature group (control) and a cold temperature group (cold). All the birds were brooded in normal temperature up to day 14, with the lighting schedule at 24 h per day. Starting at day 14, birds in the cold group were moved to a pen in the cold house and subjected to low temperature, while birds in the control group were still brooded at normal temperature. On days 14, 23, 30, 37 and 44, the right/total ventricle weight ratio (RV/TV), packed cell volume (PCV), the vessel wall area to vessel total area ratio (WA/TA), mean media thickness in pulmonary arterioles (mMTPA) and the expression of PDGF-β receptor in pulmonary arterioles were measured, respectively. Cumulative pulmonary hypertension syndrome (PHS) morbidity was recorded in each group.Results
Cool ambient temperature increased PHS morbidity of broilers. The values of WA/TA and mMTPA were also increased significantly compared with control group. PCV values in the cold temperature group were elevated from days 30 to 44, and RV/TV ratios were increased on days 37 and 44. Cold exposure enhanced PDGF-β receptor expression in pulmonary arterioles, and the PDGF-β receptor expression was significantly correlated with pulmonary vascular remodeling that was dedicated by increased WA/TA and mMTPA.Conclusion
The results indicated that PDGF-β and its receptor were involved in the underlying mechanisms of pulmonary vascular remodeling in pulmonary hypertensive broilers. 相似文献2.
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
3.
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
4.
高钠所致肺动脉高压肉鸡肺细小动脉病理改变的图象分析 总被引：17，自引：3，他引：14
240羽健康AA肉鸡随机均分为试验1组，试验2组和对照组，从8日龄起分别饮用含Na^ 为0.06%、0.12%和0.0%的饮水，其它饲养管理条件相同，分别于12、19、30、34、39日龄抽取各组参试鸡，以右心室（Right ventricle,RV)与全心室（Total ventrcle,TV)的重量比（RV／TV）作为判定肺动脉高压的依据，用图象分析仪对肺细小动脉病理变化作定量检测。结果表明：34、39日龄时，试验1组和试验2组管壁面积／管总面积和中膜厚度占外径百分值明显大于对照组，肺小动脉密度明显低，其RV／TV值均大于0.25，表明试验组肉鸡发生了肺动脉高压。由此可见，由高钠引起肉鸡肺细小动脉血管重构的病变可能参与了肺动脉高压的形成过程。 相似文献
5.
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
6.
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
7.
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
8.
9.
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10.
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
11.
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
12.
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
13.
This article reviews recent nutritional approaches for counteracting the development of pulmonary hypertension syndrome (PHS; ascites) in broiler chickens especially when they are reared at high altitudes. High altitudes impose the sustained stress of hypobaric hypoxia, which reduces the availability of atmospheric oxygen to red blood cells passing through the lungs, thereby causing systemic arterial hypoxaemia (undersaturation of haemoglobin with oxygen), pulmonary arterial hypertension and PHS/ascites in susceptible broilers. Proper nutritional strategies are needed to reduce metabolic activity and prevent the development of ascites especially when modern broilers are reared in regions where the existing altitudes limit the availability of atmospheric oxygen. This article also addresses controversies with regard to broiler nutrition in relation to PHS. For example, the catabolism of protein from feed ingredients incurs increased oxygen consumption, suggesting that feeding reduced‐protein diets to broiler chickens may result in reduced PHS incidences. However, experimental and field data indicate that feeding reduced‐protein diets to broilers subjected to hypobaric hypoxia increases the development of PHS. Controversies on the nutrition of unsaturated fat in relation to PHS are also discussed. In conclusion, hypoxia, acidosis, vasoconstriction and enhanced metabolic rate are triggers of PHS. Feeding reduced‐protein diets might promote the susceptibility of broilers to PHS by decreased dietary intake of arginine, decreased uric acid production and increased lipogenesis. Feeding high‐protein diets, dietary arginine supplementation, partial substitution of sodium bicarbonate for sodium chloride, feeding low‐fat diets and effective feed restriction programmes can be considered as nutritional approaches to prevent PHS. 相似文献
14.
The effects of dietary flax oil and antioxidants on ascites and pulmonary hypertension in broilers using a low temperature model 总被引：4，自引：1，他引：3
1. Three experiments were conducted using a low temperature model to induce pulmonary hypertension (PH) and ascites in broiler chickens. Diets containing 25 g or 50 g flax oil/kg food and control diets with an equivalent amount of animal/vegetable (A/V) blend oil, with and without supplemental antioxidants (vitamin C and vitamin E) were used. The amount of PH was assessed by the ratio of right ventricle weight to total ventricle weight (RV/TV ratio). Birds were considered to suffer from pulmonary hypertension syndrome (PHS) if the RV/TV ratio was greater than 0.299. 2. In experiment 1, the test diets contained 50 g oil/kg food and were given during the grower period only. Birds fed on the flax oil diet tended to have a lower incidence of PHS, ascites and lower RV/TV ratios than birds fed on the control diet. However, when the flax oil diet was supplemented with antioxidants, the incidence of ascites, PHS, haematocrit and whole blood and plasma viscosity increased compared with birds fed on the flax oil diet without antioxidants. These effects were not seen in experiment 2, when the test diets containing 30 g oil/kg food (25 g flax oil plus 5 g A/V blend oil/kg food compared to 30 g A/V blend oil/kg food) were given during the grower period. However, in experiment 3, when the test diets containing 30 g oil/kg food were given from day 1 to week 8, birds fed on the control diet supplemented with antioxidants had a higher incidence of PHS than those fed on the control diet alone. 3. In all 3 experiments, there was no significant effect of dietary fat source or supplemental antioxidants on total food intake or food conversion. 4. We conclude that diets containing 50 g flax oil/kg food tend to reduce the incidence of PHS and ascites in broilers using a low temperature model but the results were not statistically significant. In some cases, supplementing diets with a combination of vitamin E and vitamin C increased the incidence of ascites and PHS. 相似文献
15.
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
16.
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
17.
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
18.
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
19.
20.
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