高钠所致肉用雏鸡肺动脉高压模型的心电图学研究

本试验用心电描记法对三组共２８５ 羽健康 Ａ Ａ 肉鸡从８ 日龄开始分别用含氯化钠０．０％ ,０．１５％ 、０．３０％ 的饮水所致肉用雏鸡肺动脉高压综合征（ Ｐｕｌｍ ｏｎａｒｙ ｈｙｐｅｒｔｅｎｓｉｏｎ Ｓｙｎｄｒｏｍ ｅ, Ｐ Ｈ Ｓ）进行了研究。结果表明：①试验组的右心室（ Ｒｉｇｈｔ Ｖｅｎｔｒｉｃｌｅ, Ｒ Ｖ） 和全心室（ Ｔｏｔａｌ Ｖｅｎｔｒｉｃｌｅ, Ｔ Ｖ）的重量比（ Ｒ Ｖ／ Ｔ Ｖ）较对照组显著增高;②回归分析表明Ⅱ、ａ Ｖ Ｅ 导联 Ｓ波波幅的变化与 Ｒ Ｖ／ Ｔ Ｖ 和（ Ｒ Ｖ／ Ｔ Ｖ）／ Ｂ Ｗ （ｂｏｄｙ ｗ ｅｉｇｈｔ）的变化呈强负相关（ Ｒ＝ － ０．７９８ 到－ ０．８１２）;平均组合向量（ Ｍｅａｎ Ｒｅｓｕｌｔａｎｔ ｖｅｃｔｏｒ, Ｍ Ｒ Ｖ）的变化与收稿日期：１９９９０５０４基金项目：国家自然科学基金和江苏省“九五”农业科技重点攻关资助项目 Ｒ Ｖ／ Ｔ Ｖ 和（ Ｒ Ｖ／ Ｔ Ｖ）／ Ｂ Ｗ 呈强正相关（ Ｒ＝ ＋ ０．７２３ 到＋ ０．７２８）;③对照组、试验Ⅰ组、试验Ⅱ组分别有 ０． ０％ , ６． ２５％ ,２８．７５％ 鸡发展成临床型腹水。因此心电图上的这些特征性变化可作为 Ｐ Ｈ Ｓ早期阶段的一个准确、可靠的指标。另外,     

饮水高钠诱发的肉鸡腹水综合征的血液流变学特征

为查明高钠饮水与肉鸡腹水综合征的病因学关系，将２４０只健康ＡＡ肉鸡随机均分为试验Ⅰ、Ⅱ和对照３个组，从８日龄起分别饮用含Ｎａ＋为０．０６％、０．１２％和０．００％的饮水，动态对比观察各组肉鸡临床表现、血液红细胞压积（ＰＣＶ）、红细胞变形性（ＥＤ）、右心室（ＲＶ）和全心室（ＴＶ）的重量比（ＲＶ／ＴＶ）。结果表明，高钠饮水可以诱发腹水综合征；肉鸡在摄入过量Ｎａ＋时，出现肺动脉高压（ＰＨ）、ＰＣＶ增加和ＥＤ下降等血液流变学特性的改变，促进了腹水综合征的形成。     

肉用仔鸡腹水综合征的发病原因及控制方法

肉用仔鸡腹水综合征（AS），又称肉鸡肺动脉高压综合征（PHS），是影响世界肉鸡养殖业的主要疾病之一。本病主要发生在冬春季节快速生长的４～７周龄肉鸡，以血液粘度升高、肺动脉高压、右心衰竭、肝脏淤血和腹腔积液为主症。目前认为，本病的发生与肉鸡生理机能本身、鸡舍环境低温、氨气、生长过快、饲料营养浓度太高、疫苗反应、呼吸系统疾病、曲霉菌病、遗传性过敏等因素有关。１肉仔鸡腹水综合征的发病原因肺动脉高压是AS发病机理的核心，引发的原因主要有：１．１缺氧１．１．１鸡舍通风不良，导致缺氧在冬季，鸡舍的通风换气受影响…     

红三叶异黄酮对肉鸡肺血管重构和平滑肌细胞凋亡的影响

为观察在低温环境下红三叶异黄酮对肉鸡肺血管重构和平滑肌细胞凋亡的影响,选取270只10日龄肉鸡,随机分为常温对照组(Ⅰ)、低温组(Ⅱ)和低温黄酮组(Ⅲ),每组6个重复,每个重复15只,Ⅰ组和Ⅱ组饲喂基础饲粮,Ⅲ组饲喂添加红三叶异黄酮20mg/kg的试验饲粮,分别于14,21,28,35,42日龄从各组随机抽取6只肉鸡,观察各组肉鸡肺血管病理形态学变化,检测Caspase-3和Bcl-2蛋白表达情况。结果表明,Ⅱ组肉鸡肺小动脉结构在28,35,42日龄比Ⅰ组肺小动脉管壁有不同程度增厚、管腔变窄,发生了明显的重构现象(P0.05或0.01)。Ⅲ组与Ⅱ组相比,在28,35,42日龄肺血管重构现象减轻(P0.05或0.01),肉鸡肺动脉高压综合征(PHS)发病率降低,血管平滑肌细胞Caspase-3蛋白阳性率增高,Bcl-2蛋白表达下降;表明红三叶异黄酮能有效减轻肉鸡肺血管重构,其机制可能与调节平滑肌细胞凋亡有关。     

肉鸡腹水综合征的综合防治

肉鸡腹水综合征(AS)又称肉鸡肺动脉高压综合征,是由于生长过快的禽类在各种因素作用下出现相对性缺氧,导致机体呈现血液黏稠、血容量增加、肝肿大、肺淤血水肿及肺动脉高压,临床上以腹腔积液和右心室扩张、     

肉鸡和藏鸡肺动脉平滑肌中CaSR的表达

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。     

高钠所致肉用雏鸡肺动脉高压模型的心电图学研究

本试验用心电描记法对３组共２８５羽健康ＡＡ肉鸡从８日龄开始分别饮用含氯化钠０．０％、０．１５％、０．３０％的饮水所致内用雏鸡肺动脉高压综合征进行了研究,结果表明：（１）实验组的右心室和全心室的重量比（ＲＶ／ＴＶ）较对照组显著增坑。（２）回归分析表明ⅡａＶｐ导联波波幅的变化与ＲＶ／ＴＶ和的变化呈强负相关。（３）对照组、实验Ⅰ组、实验Ⅱ组分别有０．０１％,６．２５％,２８．７５％鸡发展成临床型腹水。因     

一氧化氮对肉鸡肺动脉高压综合征的影响

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。     

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

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。     

肉鸡腹水综合征的综合防制

肉鸡腹水综合征又称腹水症、"高海拔"症、肉鸡肺动脉高压综合征,是由多种致病因子引起的鸡慢性缺氧、代谢机能紊乱,临床上以腹腔积液和右心室扩张、全身瘀血为特征的一种非传染性疾病.     

低温诱发肉鸡肺动脉高压中肺血管重塑的作用

采用低温处理肉仔鸡的方法,通过测定肺动脉压、肺小动脉中膜厚度占外径百分比及中膜面积与血管总面积比的变化,探讨肉鸡肺动脉高压的发生机制.结果表明:肺血管重塑在低温诱发肉鸡的肺动脉高压发生发展中起重要作用.     

Activation of PKCalpha and pulmonary vascular remodelling in broilers

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.     

Expression of PDGF-β receptor in broilers with pulmonary hypertension induced by cold temperature and its association with pulmonary vascular remodeling

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.     

l-Arginine inhibiting pulmonary vascular remodelling is associated with promotion of apoptosis in pulmonary arterioles smooth muscle cells in broilers

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.     

Reduced PKCalpha expression in pulmonary arterioles of broiler chickens is associated with early feed restriction

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.     

L-Arginine inhibiting pulmonary vascular remodelling is associated with promotion of apoptosis in pulmonary arterioles smooth muscle cells in broilers

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.     

Changes in pulmonary arteriole protein kinase calpha expression associated with supplemental L-arginine in broilers during cool temperature exposure

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.     

The effect of dietary l-carnitine supplementation on pulmonary hypertension syndrome mortality in broilers exposed to low temperatures

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.     

The effects of dietary flax oil and antioxidants on ascites and pulmonary hypertension in broilers using a low temperature model

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.