摘要
Acute lactic acidosis (ALA) and subclinical ruminal acidosis (SARA) are economically-important pathologies associated with poor adaptation of the ruminal ecosystem to diets high in soluble carbohydrates. Both pathologies result from an imbalance in the rate of production of fermentation acids relative to removal of these acids by absorption, flow of acids post-ruminally, and buffering of the acids by bicarbonate from the saliva and blood. In ALA, lactic acid accumulates, driving the pH of the ruminal fluid below 5.0, while subclinical acidosis is characterised by the accumulation of short-chain volatile fatty acids and a ruminal pH of 5.0–5.5. These reductions in ruminal fluid pH reflect changes in the profile and activity of the microbial populations, the buffering capacity of the ruminal fluid, and the absorptive capacity of the ruminal epithelium. The relative importance of the ruminal fluid (microbial and chemical properties) and the ruminal epithelium (absorptive capacity) is unknown. A novel ruminal transfaunation model was used to separate these two components of the pathologies. Four groups of sheep were formed by combining two ruminal fluid adaptions (adapted to high-energy density or low-energy density diets) and two ruminal epithelium adaptations (adapted to high-energy density and low-energy density diets). The four combinations of fluid and epithelium were then challenged with an intra-ruminal infusion of glucose to simulate conditions conducive to the development of acidosis. All groups developed acute acidosis in response to the glucose challenge and there were no differences between groups in the pattern of pH decline over a 24-h period. There was no difference between groups in ability to regulate rumen fluid pH, suggesting the major factor contributing to development of acidosis is rapid microbial fermentation of soluble carbohydrates irrespective of adaption of the epithelium or microbial populations. Modifications to the challenge protocol to more closely reflect normal dietary challenges would be a useful modification in future studies using this technique.
摘要译文
乳酸酸中毒（ALA）和亚临床瘤胃酸中毒（SARA）是与瘤胃生态系统对可溶性碳水化合物含量高的膳食不良适应有关的经济上重要的病理学。这两种病理都是由于发酵酸的生产速度相对于通过吸收去除这些酸的不平衡而产生的，在反刍后用酸的流动，并通过唾液和血液中的碳酸氢盐对酸进行缓冲。在ALA中，乳酸积聚，驱动瘤胃液的pH值低于5.0，而亚临床酸中毒的特征在于短链挥发性脂肪酸的积累和瘤胃pH 5.0-5.5。这些瘤胃液pH的降低反映了微生物群体的轮廓和活性的改变，瘤胃液的缓冲能力，和瘤胃上皮细胞的吸收能力。瘤胃液（微生物和化学性质）和瘤胃上皮细胞（吸收能力）的相对重要性未知。一种新型的瘤胃transfaunation模型被用来分离病理的这两个组成部分。（适应于高能量密度或低能量密度饮食）和两个瘤胃上皮适应（适应于高能量密度和低能量密度饮食）。然后用瘤胃内葡萄糖输注激发流体和上皮的四种组合，以模拟有助于酸中毒发展的条件。所有研究组在葡萄糖激发后出现急性酸中毒，24小时期间pH值下降模式组间没有差异。在调节瘤胃液pH值的能力方面没有区别，这表明引起酸中毒发展的主要因素是可溶性碳水化合物的快速微生物发酵，而不管上皮或微生物群体的适应性。对挑战方案进行修改以更密切地反映正常的饮食挑战将是使用此技术的未来研究中的有用修改。
Joshua PatrickFanning[1];Philip IanHynd;Peter DenysCockcroft[2];. The relative roles of the ruminal fluid and epithelium in the aetiology of ruminal acidosis[J]. Small Ruminant Research, 2018,162: 57-62