反刍动物瘤胃酸中毒机制解析及其营养调控措施

反刍动物瘤胃亚急性酸中毒(SARA)是现代集约化生产中常见的营养代谢病.“反刍动物SARA的发生和调控机制”是重要的科学问题,对其的进一步深入研究不仅在学术上有重要意义,而且对降低经济损失具有重要的现实意义.本文分析了国际上反刍动物瘤胃中毒研究的最新成果和进展,对其产生原因和机制以及预防措施进行了系统的阐述.本文深入探讨了引起瘤胃酸中毒的3个学说,“有机酸中毒学说”、“乳酸中毒学说”和“内毒素和组织胺中毒学说”;较为深入地解析了饲粮中碳水化合物组成、瘤胃微生物菌群及其代谢变化对瘤胃酸中毒发生的影响.同时,也对SARA的预防及其营养调控措施进行了论述,并提出通过科学合理的饲养管理,合理设计饲粮的碳水化合物组成,使用益生菌、缓冲剂、有机酸、硫胺素,接种疫苗,调控瘤胃内有机酸的产生和利用的途径来预防反刍动物瘤胃酸中毒的发生,以期为今后我国在预防瘤胃酸中毒方面的研究和生产应用提供参考.     

反刍动物瘤胃酸中毒研究进展

瘤胃酸中毒是危害反刍动物常见的一种代谢病.其产生的主要原因是反刍动物日粮中含有大量的易发酵的碳水化合物饲料或者日粮纤维含量较低,导致瘤胃产生酸性物质过多,引起瘤胃微生物区系失调和瘤胃功能紊乱而造成的.笔者就瘤胃酸中毒的影响因素、类型及营养调控等几方面进行了论述.     

反刍动物瘤胃酸中毒及其调控

瘤胃酸中毒是指反刍动物采食大量易发酵碳水化合物饲料后 ,瘤胃乳酸产生过多而引起瘤胃微生物区系失调和功能紊乱的一种代谢性疾病。该病在以高精料生产优质高档牛肉的国家较为常见 ,目前我国在肉牛后期肥育和高产奶牛的饲养中比较普遍。长期以来 ,我国养牛业过分强调耕牛使役和秸秆有效利用 ,忽视了高档牛肉的生产。随着人民生活水平的提高以及涉外宾馆的蓬勃发展 ,低质牛肉已不能完全满足人们的消费需求 ,而以高精料低蛋白日粮饲养的优质高档牛肉消费却急剧增长。基于我国国情 ,发展前期秸秆架子牛育成和后期高精料肥育不失为一种行之有效…     

牛瘤胃酸中毒综合防治与调控研究进展

近年来,养殖场饲草料配比不合理,过多的精料导致瘤胃微生物菌群失调,瘤胃代谢产物通过血液或淋巴管进入体内循环,引起瘤胃酸中毒.瘤胃酸中毒严重影响牛的生产性能,病死率较高,对牛群危害性较大.文章就瘤胃酸中毒的发病机制、临床症状、诊断治疗、药物预防、营养调控等方面进行阐述,旨在通过制定营养调控策略提高牛饲养精细化管理水平,降低酸中毒发病率,为保持牛群健康提供参考.     

奶牛亚急性瘤胃酸中毒调控措施

本文以奶牛亚急性瘤胃酸中毒的发生、危害及与日粮的关系为切入点,从营养和管理角度,结合国内外研究进展,探讨了降低奶牛亚急性瘤胃酸中毒发生率的措施。     

奶牛瘤胃酸中毒浅析

笔者针对1982年以来发生在南京农业大学实验牧场的44例病牛,在致死率,临床病症,发病率与月份,胎次,泌乳状况及饲料间的关系等方面进行了观察,其结果如下。一、材料和方法1982年1月至1988年12月在本校实验牧场所饲养的黑白花奶牛     

肉牛瘤胃酸中毒防治

在肉牛的养殖行业,瘤胃酸中毒是一种常见疾病,并且可能会导致肉牛的死亡,从而给养殖户造成经济损失.当肉牛进食过多的谷物,导致胃里剧烈发酵,并且生成大量的乳酸时,以及前胃出现功能的异常时,往往会导致该病的发生.为解决肉牛的瘤胃酸中毒问题,本文以肉牛养殖为例,对瘤胃酸中毒进行总结,分析了中毒的成因与症状,提出了综合防治的措施...     

反刍动物瘤胃内乳酸代谢与瘤胃酸中毒调控的研究进展

乳酸是反刍动物瘤胃内重要的中间代谢产物,在饲喂高精料的反刍动物瘤胃内乳酸累积过多可能会加速瘤胃酸中毒的进程。本文综述了瘤胃内乳酸代谢机制和影响因素,以及提高乳酸利用和添加硫胺素等预防瘤胃酸中毒的几种方式,旨在系统地总结反刍动物瘤胃内乳酸代谢机制,为瘤胃酸中毒的调控提供理论支撑。     

奶牛瘤胃酸中毒治疗失误

奶牛瘤胃酸中毒，是因采食或偷吃了大量精料及富含碳水化合物的饲料，而产生大量乳酸，被吸收入血后而引起的一种常见病。由于奶牛瘤胃的生理特点与马属动物胃的消化特点有所不同，因此往往误导一些兽医工作者，凡遇到有瘤胃积食或消化、反刍障碍时即连续大剂量的补给碱性药物，致使很多疾病不但没有治愈，反而导致发生碱中毒。此现象在兽医临床屡见不鲜。一旦导致碱中毒，治疗效果很不理想，特别是犊牛多取死亡经过。     

绵羊瘤胃酸中毒的诊疗

绵羊主要由于过食玉米、小麦等谷物饲料,于瘤胃内高度发酵,产生大量乳酸而致代谢性酸中毒.报告如下.     

D-Lactic acidosis in calves as a consequence of experimentally induced ruminal acidosis

In order to test the hypothesis that ruminal drinking in calves can lead to D-lactic metabolic acidosis, ruminal acidosis was induced in nine calves by intraruminal application of untreated whole milk via a stomach tube. The amount of the daily force-fed liquid was 3 x 1 l. The experimental design called for an end of intraruminal applications if two or more of the following signs were observed: severe depression, estimated degree of dehydration >10%, absence of sucking reflex, lack of appetite for two consecutive feedings, severe metabolic acidosis with calculated Actual Base Excess (ABE) <-15 mmol/l. The procedure was scheduled to be discontinued on the 17th day of experiment. The onset of ruminal acidification occurred rapidly, and mean pH value fell from 6.70 (+/-0.48) to 4.90 (+/-0.38) after the first application. The following days the pH values varied between 4 and 5. Rumen acidity was characterized biochemically by a significant increase in both isomers of lactic acid. The effects of the intraruminal administration on the calves were detrimental; eight of nine calves showed an acute disease process. According to the pre-established clinical standard, seven of nine calves were removed from the intraruminal feeding schedule. All but one of the calves developed severe systemic acidosis. The increase in anion gap demonstrated the net acid load. In all the calves D-lactate levels were found to show a significant and rapid increase. On the contrary, L-lactate never deviated from physiological levels. These observations confirm that, in young calves as in adult cattle, ruminal acidosis may lead to a clinically manifested D-lactic metabolic acidosis.     

反刍动物亚急性瘤胃酸中毒的营养调控

反刍动物饲喂高谷物日粮时常发生瘤胃酸中毒现象,本文针对反刍动物亚急性瘤胃酸中毒的营养调控进行综述.     

反刍动物瘤胃酸中毒发病机理的研究进展

关于瘤胃酸中毒的报道多集中于诊断、防治和调控方面,国内外对其发病机理虽有研究报道,但说法不一,存在争议。文中对其存在的不同观点作了简要综述,以期为进一步明确反刍动物瘤胃酸中毒发病机理提供依据。     

Pathomorphologic changes in the ruminal acidosis of sheep]

Acute and subacute and spontaneous rumen acidosis was experimentally induced in 20 sheep and two lambs after feeding of barley, maize or glycose. The inner organs of those animals then were examined for morphological changes. The changes recorded from experimental acidosis were analogous to those observed after spontaneous outbreaks. Hyperaemia and blood leakage were macroscopically observed underneath the rumen mucous membrane which could be easily pulled off. The same signs sometimes were manifest in the third and second stomach as well. Pronounced edemas and hyperaemia occurred in the lungs, meninges (pia mater), and brain, and blood leakage was recorded from the epicardium. The histological findings included epithelial desquamation, infiltration of lymphocytes and leucocytes into rumen and fourth stomach (subacute) hepatitis (in 60 per cent of all cases), physical degeneration in the kidneys, and focal myocarditis (in 50 per cent of all cases). There were hyperaemia, edematisation, and blood leakage in the lungs, perivascular and pericellular edema in the brain, and severe hyperaemia of the meninges (pia mater) and thyroid gland. Those morphological changes were persistent and characteristic. Their relevance to diagnosis of rumen acidosis in sheep is undenied, provided that due consideration is given at the same time to the case history and paraclinical indices.     

Potential protective effects of thiamine supplementation on the ruminal epithelium damage during subacute ruminal acidosis

In ruminants, the ruminal epithelium not only has the function of absorbing nutrients but also is an important tissue to prevent harmful substances in the rumen from entering the blood circulation. Thus, the normal function of ruminal epithelium is critical for ruminants. However, subacute ruminal acidosis induced by high-concentrate diets often damages the barrier function of ruminal epithelium in ruminants. Recently, many studies have shown that dietary supplementation with thiamine is an effective method to alleviate subacute ruminal acidosis. In order to provide theoretical reference for the in-depth study of subacute ruminal acidosis and the application of thiamine in the future, this review introduces the effects of subacute ruminal acidosis on morphological structure, inflammatory response, and tight junction of ruminal epithelium. In addition, this paper summarizes the role of thiamine in maintaining ruminal epithelial function of ruminants during subacute ruminal acidosis challenge.     

Prevalence and consequences of subacute ruminal acidosis in German dairy herds

Background

The prevalence and the clinical consequences of subacute ruminal acidosis (SARA) in dairy cows are still poorly understood. In order to evaluate the prevalence of SARA, 26 German dairy farms were included in a field study. In each herd, between 11 and 14 lactating dairy cows were examined for their ruminal pH using rumenocentesis. Milk production data and farm management characteristics were recorded. Each farm was scored for lameness prevalence among lactating animals, and body condition score was recorded three times four to five weeks apart in all animals examined. Farms were grouped on basis of ruminal pH and compared for lameness, body condition, milk production parameters and style of management. Animals were grouped on basis of their measured ruminal pH and compared accordingly for milk production parameters and body condition score.

Results

Of 315 cows examined, 63 individuals (20%) exhibited a ruminal pH of ≤ 5.5 at time of rumenocentesis. Of 26 farms examined, eleven farms had three or more of their cows experiencing a ruminal pH of ≤ 5.5 and were classified as likely experiencing subacute ruminal acidosis. These farms tended to be bigger than the others and offered less lying space to the lactating cows. There was no clear tendency regarding lameness. Among individual cows, animals with a low ruminal pH of ≤ 5.5 were found to be in significantly poorer body condition than animals with higher pH values (p < 0,05).

Conclusions

The study shows 11 out of 26 of herds likely experiencing SARA. Bigger herds tend to be at a higher risk for SARA, while individuals with low ruminal pH tend to be lower in body condition. The study points to the importance of management in preventing SARA.     

奶牛亚急性瘤胃酸中毒的发生与危害

亚急性瘤胃酸中毒（SARA）是一个大多数牛场普遍存在的奶牛代谢性疾病。围产期、干物质采食量（DMI）过高、日粮配制差及采食模式变化过大等奶牛均易发生亚急性瘤胃酸中毒,继而造成干物质采食量下降、纤维素消化率降低、乳成分改变及引发腹泻等疾病。本文对奶牛亚急性瘤胃酸中毒的病因及危害等方面进行了简述。     

益生菌对奶牛亚急性瘤胃酸中毒的保护作用

亚急性瘤胃酸中毒对奶牛的生产性能有很大影响,使用益生菌来稳定奶牛分娩后-产奶过渡期瘤胃pH可以减轻这种代谢紊乱的症状。因此,本试验选择了体重(741±55)kg,产奶期在(212±19.5)d的奶牛4头,试验采用4×4拉丁方设计,共4种日粮:对照组饲喂基础日粮,处理1组为日粮添加0.5 g/d米曲菌,处理2组为日粮添加2.5 g/d米曲菌,处理3组为日粮添加2 g/d粪肠球菌和酿酒酵母菌的混合物。每组经过3 w的适应期、4 d酸中毒期以及3 d恢复期。结果显示:瘤胃最大pH范围在5.6～6.0,占比最高,与适应期和中毒期的结果相似。中毒期间,其他pH范围表现为显著差异(P <0.05)。中毒期,处理3组较对照组显著提高了瘤胃pH(P <0.05),同时处理3组瘤胃pH在5.6～6.0的占比也显著高于对照组(P <0.05)。日粮添加2.5 g/d米曲菌显著降低了产奶量(P <0.05)。奶牛遭受瘤胃酸中毒后,随着时间的推移,丙酸、丁酸和戊酸含量显著升高(P <0.05),而乙酸、异丁酸和异戊酸含量显著降低(P <0.05)。除了处理3组外,其他组瘤胃乳酸含量随时间的增加而升高(P <0.05)。饲喂12 d后,处理3组较对照组显著提高了乳酸含量(P <0.05)。瘤胃白球菌和大肠杆菌含量在饲喂2 h后显著升高(P <0.05),之后在6 h达到稳定。结论 :粪肠球菌和酿酒酵母菌复合物可以缓解奶牛亚急性瘤胃酸中毒的症状,米曲菌可以调控瘤胃pH,但高剂量米曲菌添加水平对瘤胃pH无显著影响。