肉鸡腹水症与自由基关系的研究进展

本文从腹水症发病的原因出发，阐述了自由基与腹水症的关系，患鸡的血清和组织中脂质过氧化物和抗氧化物酶类的变化情况。说明通过使用一些自由基清除剂来增强机体抗氧化系统的防御功能，来大大地降低肉鸡肺腹水症的发生。     

肉鸡腹水综合征发病学的氧应激机制及其防治

用高能高盐日粮结合环境因子诱发肉鸡腹水综合征,并在饲料中添加抗氧化性药物硒(Se)和中草药对其防治,检测体内自由基及其相关指标.结果显示腹水症高发鸡群肝组织FRs水平和血清丙二醛(MDA)含量明显升高,Se-GSH-Px活力显著降低(P＜0.05);在饲料中添加Se和中草药能显著降低腹水症的发病率和死亡率,并提高Se GSHPx活力、降低FRs水平和MDA含量,Se的作用强于中草药.结果提示缺氧引起的应激反应是肉仔鸡腹水综合征发病学的主要生理性因子,自由基在该病发生过程中起着重要作用;日粮中添加抗氧化药物硒和中草药能通过改善机体的抗氧化机能、清除体内过盛的FRs,从而起到预防和治疗腹水症的作用.     

法国亚麻籽添加抗氧化剂对蛋鸡生产水平和鸡蛋质量的影响

<正>动物自由基与疾病之间的关系已经成为现代医学和生命科学领域的一大热点。许多疾病的发生都与自由基的氧化破坏有关,而抗氧化剂则能减少或清除自由基,阻止或减轻自由基氧化应激的破坏〔1~2〕。在动物养殖过程中,由氧化应激导致的动物疾病有心脏病、肾脏病、腹水症、围产期疾病、胎衣不下、乳腺炎、消化道炎症等,已严重影响了畜牧业生产〔3~5〕。营养素及其代谢物与外源性抗氧化剂在自由基导致的重要生物损伤方面的修复、置换、     

饲料因子对肉鸡腹水症的影响

在肉鸡饲养中,许多国家都发生腹水症,该症是引起肉鸡死亡的主要原因之一。按过去的定义,腹水症是水在体内异常积留的疾病。现今,只有水在腹腔部位异常积留,才称为腹水症。肉鸡患腹水症,常伴有肝脏肥大和心膜水肿。腹水症死亡的肉鸡,必须在处理场作废弃物处理。通常,肉鸡在4～6周龄期间,腹水症的发生率最高。因此而带来的经济损失也最大。有关引起腹水症的病因,杂志上已发表了几篇综述文献。认为引起腹水症的原因有高地、氨、低温、肉鸡的过速生长、高能饲料、疫苗的副作用、呼吸道疾病、曲霉菌产生的毒素以及遗传的敏感性等因子,引起组织缺氧所造成。一旦发生腹水症,心脏的右心室肥大,功能     

一例肉鸡腹水综合征的病因分析及防治

通过对肉鸡腹水症的发病特点、病理变化和诱发原因的介绍,提出了肉鸡腹水症的综合防治措施,在做好控制预防措施的同时结合药物预防可有效的降低肉鸡腹水症的发病率和死亡率。从而减少了腹水症对肉鸡业造成的经济损失,最大提高饲养户的经济效益。     

养鸡技术讲座：第七十讲 肉鸡腹水症

养鸡技术讲座第七十讲肉鸡腹水症云南农业大学田允波当今严重危害肉鸡业的三大疾病是猝死症（ＳＤＳ）、腹水症（Ａｓｃｉｔｅｓ）和腿病（Ｅｌｂｅｒｔ，１９９０）。腹水症于１９４６年首次报道于美国，即雏火鸡腹水症。随后，腹水症很快成为一些高海拔（＞１５００ｍ）...     

邯郸市肉鸡腹水症的调查研究

肉鸡腹水症（ascites syndrome．AS）又称肺动脉高压综合征（pulmonary hypertension syndrome．PHS），是主要发生在快速生长期肉仔鸡的一种常见的代谢疾病。以明显腹腔积水，肺瘀血、水肿和心脏扩张、肥大、衰竭为特征。该病广泛分布于世界各地．我国肉鸡腹水症的平均发病率为4．5％．部分地区死亡率甚至高达20％．对养鸡业造成严重的危害。尽管人们对肉鸡腹水症进行了大量的研究．但腹水症仍是困扰肉鸡业的一大难题。近年来．邯郸市肉仔鸡养殖规模发展很快．肉鸡腹水症也经常出现。因此．笔者就邯郸市肉鸡腹水症发生情况进行了调查．进一步来分析肉鸡腹水症的发病原因及其防治措施。以指导生产实践。     

肉鸡腹水综合征

肉鸡腹水综合征李三星（河北农业大学牧医系，保定０７１００１）王敏（河北省食品公司养鸡场）肉鸡腹水综合征是一种腹腔大量潴留腹水为特征的疾病，根据其病型可分为肝型腹水症、肺型腹水症和心型腹水症。其发生原因有生长过快、中毒、缺氧、寒冷、高海拔、高温、细菌感...     

肉仔鸡腹水症的防治探究

肉仔鸡腹水症常见于周龄 4周的肉鸡,发病和季节、养殖环境等情况密切相关。患腹水症的肉仔鸡主要表现为腹腔中积聚大量的浆液,并存在多个脏器病理性变化的问题,致死率较高,故而肉仔鸡腹水症的防治工作尤为关键。     

特效腹水康防治肉仔鸡腹水症的效果观察

特效腹水康防治肉仔鸡腹水症的效果观察＠胡英杰＠王伟泽＠马国峰￥河北省石家庄华牧集团公司兽药厂特效腹水康防治肉仔鸡腹水症的效果观察胡英杰王伟泽马国峰（河北省石家庄华牧集团公司兽药厂,０５００６１）肉仔鸡腹水症是由多种致病因子引起的肉仔鸡慢性缺氧、代谢机能紊乱...     

Increased calcium deposits and decreased Ca2+-ATPase in right ventricular myocardium of ascitic broiler chickens

Right ventricular hypertrophy and failure is an important step in the development of ascites syndrome (AS) in broiler chickens. Cytoplasmic calcium concentration is a major regulator of cardiac contractile function and various physiological processes in cardiac muscle cells. The purpose of this study was to measure the right ventricular pressure and investigate the precise ultrastructural location of Ca(2+) and Ca(2+)-ATPase in the right ventricular myocardium of chickens with AS induced by low ambient temperature. The results showed that the right ventricular diastolic pressure of ascitic broilers was significantly higher than that of control broilers (P < 0.01), and the maximum change ratio of right intraventricular pressure (RV +/- dp/dt(max)) of ascitic broilers was significantly lower than that of the controls (P < 0.01). Extensively increased calcium deposits were observed in the right ventricular myocardium of ascitic broilers, whereas in the age-matched control broilers, calcium deposits were much less. The Ca(2+)-ATPase reactive products were obviously found on the sarcoplasmic reticulum and mitochondrial membrane of the control right ventricular myocardium, but rarely observed in the ascitic broilers. The data suggest that in ascitic broilers there is the right ventricular diastolic dysfunction, in which the overload of intracellular calcium and the decreased Ca(2+)-ATPase activity might be the important factors.     

Increased calcium deposits and decreased Ca-ATPase in erythrocytes of ascitic broiler chickens

The decrease of erythrocyte deformability may be one of the predisposing factors for pulmonary hypertension and ascites in broiler chickens. In mammals, the cytoplasmic calcium is a major regulator of erythrocyte deformability. In this study, the erythrocyte deformability was measured, and the precise locations of Ca²⁺ and Ca²⁺-ATPase in the erythrocytes were investigated in chickens with ascites syndrome induced by low ambient temperature. The results showed that ascitic broilers had higher filtration index of erythrocyte compared with control groups, indicating a decrease in erythrocyte deformability in ascitic broilers. The more calcium deposits were observed in the erythrocytes of ascitic broilers compared with those of the age-matched control birds. The Ca²⁺-ATPase reactive grains were significantly decreased on the erythrocyte membranes of ascitic broilers. Our data suggest that accumulation of intracellular calcium and inhibition of Ca²⁺-ATPase might be important factors for the reduced deformability of the erythrocytes of ascitic broilers.     

Pathogenesis of ascites in broilers raised at low altitude: aetiological considerations based on echocardiographic findings

This study reports novel insight into the aetiology of pulmonary hypertension and ascites in broiler chickens. The scope of measurements was focused on anatomical and functional parameters, and blood flow patterns in leghorns (resistant to ascites), fast-growing broilers (susceptible to ascites), broilers developing ascites, and ascitic broilers evaluated in vivo using echocardiography, and further examined in the context of postmortem findings. Both, in vivo observed features and postmortem findings, showed clear differences between broilers and leghorns, and between normal and ascitic broilers. Abnormalities in the heart chamber geometry and blood flow patterns were detected upon echocardiographic examination in all ascitic broilers. Right and left atrio-ventricular (AV) valve regurgitation were common findings in ascitic broilers and some apparently normal broilers, with left AV valve insufficiency being a predominant feature with respect to degree and frequency of occurrence. Blood flow disturbances were not detected in leghorns. Left ventricular fractional shortening (functional parameter) was considerably reduced (P < 0.01) in ascitic birds (mean: 21.7 +/- 2.0 SE) in comparison with normal broilers (mean: 39.1 +/- 3.6 SE), or leghorns (mean: 43.3 +/- 2.4 SE). The presented findings indicate that pathological and functional changes in the left ventricle and atrium play a significant role in the pathogenesis of ascites in broilers. Severe dilation of the left atrium and pulmonary veins seen on postmortem examination, as well as regurgitant blood flow in the left atrium, demonstrated by Doppler study in ascitic birds, provide evidence that chronically elevated pressure in the left atrium is involved in the aetiology of pulmonary hypertension and ascites in fast-growing broilers.     

Whole blood and plasma viscosity values in normal and ascitic broiler chickens.

1. Whole blood and plasma viscosity values in normal and ascitic broiler chickens were measured. 2. The mean blood viscosity value in ascitic broilers was greater than that of the controls. There was a small but significant difference in the opposite direction between plasma viscosity values of the respective groups of birds. 3. Although the haematocrit and arterial pressure index values in the ascitic birds were raised, there was a fall in the concentration of total plasma protein. 4. The data suggest that the raised viscosity in the ascitic birds was caused by a polycythemia and not by any influence of plasma protein. 5. The cumulative effect of these factors, such as raised blood viscosity values and larger deformed red cells flowing through constricted lung arterioles, may contribute to the pulmonary hypertension and ascites seen in some young commercial broilers.     

Erythropoiesis regulation during the development of ascites syndrome in broiler chickens: a possible role of corticosterone

The ascites syndrome in broiler chickens is attributed to metabolic burdening, which results from intensive genetic selection for rapid growth coupled with exposure to extreme environmental conditions, such as low ambient temperature. These conditions impose on the broilers difficulties in fulfilling tissue demands for oxygen, and the birds exhibit a decrease in blood oxygen saturation and high hematocrit values. It is unknown whether the increase in hematocrit results from alteration in erythropoiesis or from fluid exudation out of the blood system to the abdominal cavity. The present study was conducted to examine the association between abnormal stress response and erythropoiesis process in ascitic broilers. Ascitic chickens revealed a uniquely continuous stress response: expressing an increase (P < or = 0.05) in plasma corticosterone concentration 2 to 3 wk before death. At 5 wk of age, ascitic broilers exhibited an increase (P < 0.05) in hematocrit, blood cell count, and packed cells and blood volumes, with no significant change in plasma volume. These results confirm an accelerated erythropoiesis process in ascitic birds. Increased blood cell production in ascitic birds was matched by an increase (P < 0.05) in the proportion of immature red blood cells (23%) in comparison with broilers that remained healthy (7%), and by decreased (P < 0.05) hemoglobin content relative to red blood cells. We conclude that continually increased corticosterone concentrations, as an inducer of erythropoiesis proliferation and differentiation arrest, in ascitic chickens, resulted in increased production of red blood cells (partially immature) with decreased hemoglobin content; this decrease in hemoglobin might have contributed to enhanced development of hypoxemia and to aggravation of the syndrome.     

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。     

Vascular remodeling and its role in the pathogenesis of ascites in fast growing commercial broilers

This study examined the putative role of blood vessel pathology in the development of ascites in broilers. Major blood vessels (aorta, brachiocephalic arteries, pulmonary arteries, and vena cava) from normal commercial male broiler chickens, and broilers that developed congestive heart failure (CHF) with or without ascites were subjected to gross and microscopic examination.On cross-section, grossly, the arteries from normal broilers and those showing dilated cardiomyopathy without ascites appeared circular, with firm wall tone characteristic of the normal artery. In contrast, the arteries from ascitic broilers appeared flaccid and lacked elasticity, which was evidenced by collapsing, ellipsoid cross-sectional arterial lumen owing to the structural weakness of the arterial walls. Microscopically, ascitic broilers showed thinning or occasionally total loss of elastic elements in the arterial wall, and reduced network density of the structural matrix of the vascular wall, as well as increased thickness of fibers in vena cava.The structural changes seen in the major arteries from ascitic broilers are maladaptive, and as such would definitively impose an increased hemodynamic burden on the already failing heart pump. The changes in veins are indicative of pathological remodeling conducive to increased permeability of the vascular wall, particularly in the situation when a poorly distensible structure is further subjected to wall stress associated with increased pressure and volume overload. Taken together, increased hemodynamic burden and reduced structural density of the venous wall constitute conditions conducive for seepage and accumulation of ascitic fluid.     

微生物源性抗氧化剂对大鼠繁殖损伤的修复作用研究

本研究以脂多糖(LPS)作为自由基的诱发剂,微生物源性抗氧化剂作为自由基的清除剂,探讨自由基对大鼠繁殖性能的损伤及抗氧化剂的修复作用。将64只70日龄SD大鼠随机分成4组,每组16只,雌雄对半。对照组和损伤模型组饲喂基础日粮,抗氧化剂组和损伤修复组饲喂基础日粮并添加0.8 mL/d.只微生物源性抗氧化剂。损伤模型组和损伤修复组腹腔注射1 mg/kg LPS,对照组和抗氧化剂组注射等量的生理盐水,研究微生物源性抗氧化剂对雌鼠和雄鼠繁殖性能的影响。结果表明,注射LPS的雌鼠雌二醇浓度下降,受孕率降低,雄鼠精子数目、精子活动率和a级精子数显著降低。日粮中添加微生物源性抗氧化剂使雌鼠生育综合指数明显提高,血清中雌二醇含量升高,雄鼠精子数目增加,精子运动能力增强,断奶时仔鼠的数量和存活率提高。与损伤模型组相比,损伤修复组可一定程度提高大鼠的生育状况。结果提示,注射LPS导致大鼠产生氧化应激,对机体生殖机能造成损伤,微生物源性抗氧化剂具有提高大鼠繁殖性能并一定程度修复繁殖损伤的作用。