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瘤胃模拟技术中短暂酸中毒的诱导

Induction of a transient acidosis in the rumen simulation technique.

作者信息

Eger M, Riede S, Breves G

机构信息

Department of Physiology, University of Veterinary Medicine Hannover, Hannover, Germany.

出版信息

J Anim Physiol Anim Nutr (Berl). 2018 Feb;102(1):94-102. doi: 10.1111/jpn.12662. Epub 2017 Mar 16.

Abstract

Feeding high concentrate diets to cattle results in an enhanced production of short-chain fatty acids by the micro-organisms in the rumen. Excessive fermentation might result in subclinical or clinical rumen acidosis, characterized by low pH, alterations in the microbial community and lactate production. Here, we provide an in vitro model of a severe rumen acidosis. A transient acidosis was induced in the rumen simulation technique by lowering bicarbonate, dihydrogen phosphate and hydrogen phosphate concentrations in the artificial saliva while providing a concentrate-to-forage ratio of 70:30. The experiment consisted of an equilibration period of 7 days, a first control period of 5 days, the acidosis period of 5 days and a second control period of 5 days. During acidosis induction, pH decreased stepwise until it ranged below 5.0 at the last day of acidosis (day 17). This was accompanied by an increase in lactate production reaching 11.3 mm at day 17. The daily production of acetate, propionate and butyrate was reduced at the end of the acidosis period. Gas production (methane and carbon dioxide) and NH -N concentration reached a minimum 2 days after terminating the acidosis challenge. While the initial pH was already restored 1 day after acidosis, alterations in the mentioned fermentation parameters lasted longer. However, by the end of the experiment, all parameters had recovered. An acidosis-induced alteration in the microbial community of bacteria and archaea was revealed by single-strand conformation polymorphism. For bacteria, the pre-acidotic community could be re-established within 5 days, however, not for archaea. This study provides an in vitro model for a transient rumen acidosis including biochemical and microbial changes, which might be used for testing feeding strategies or feed additives influencing rumen acidosis.

摘要

给牛饲喂高浓缩日粮会导致瘤胃中的微生物增加短链脂肪酸的产生。过度发酵可能会导致亚临床或临床瘤胃酸中毒,其特征为低pH值、微生物群落改变和乳酸生成。在此,我们提供了一种严重瘤胃酸中毒的体外模型。通过在人工唾液中降低碳酸氢盐、磷酸二氢盐和磷酸氢盐的浓度,同时提供70:30的精粗比,在瘤胃模拟技术中诱导短暂的酸中毒。实验包括7天的平衡期、5天的第一个对照期、5天的酸中毒期和5天的第二个对照期。在酸中毒诱导期间,pH值逐步下降,直到酸中毒最后一天(第17天)降至5.0以下。这伴随着乳酸生成的增加,在第17天达到11.3 mmol。在酸中毒期结束时,乙酸、丙酸和丁酸的日产量降低。气体产生(甲烷和二氧化碳)和NH₃-N浓度在终止酸中毒挑战后2天达到最低值。虽然酸中毒后1天初始pH值已恢复,但上述发酵参数的改变持续时间更长。然而,到实验结束时,所有参数都已恢复。通过单链构象多态性揭示了酸中毒诱导的细菌和古菌微生物群落的改变。对于细菌,酸中毒前的群落可在5天内重新建立,然而古菌则不能。本研究提供了一种包括生化和微生物变化的短暂瘤胃酸中毒体外模型,可用于测试影响瘤胃酸中毒的饲养策略或饲料添加剂。

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