Gentile A, Sconza S, Lorenz I, Otranto G, Rademacher G, Famigli-Bergamini P, Klee W
Veterinary Clinical Department, Faculty of Veterinary Medicine, University of Bologna, via Tolara di Sopra 50, 40064 Ozzano Emilia, Bologna, Italy.
J Vet Med A Physiol Pathol Clin Med. 2004 Mar;51(2):64-70. doi: 10.1111/j.1439-0442.2004.00600.x.
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.
为了验证犊牛瘤胃饮奶会导致D - 乳酸代谢性酸中毒这一假说,通过胃管向9头犊牛瘤胃内注入未经处理的全脂牛奶以诱发瘤胃酸中毒。每日强制喂入的液体量为3×1升。实验设计要求,如果观察到以下两种或更多症状,则停止瘤胃内给药:严重抑郁、估计脱水程度>10%、无吸吮反射、连续两次喂食无食欲、严重代谢性酸中毒且计算得出的实际碱剩余(ABE)<-15 mmol/L。该程序计划在实验第17天停止。瘤胃酸化迅速发生,并在首次给药后平均pH值从6.70(±0.48)降至4.90(±0.38)。随后几天pH值在4至5之间波动。瘤胃酸度在生化方面的特征是乳酸的两种异构体均显著增加。瘤胃内给药对犊牛的影响是有害的;9头犊牛中有8头出现急性病程。根据预先设定的临床标准,9头犊牛中有7头被停止瘤胃内喂食计划。除1头犊牛外,所有犊牛均发生严重的全身酸中毒。阴离子间隙增加表明存在净酸负荷。在所有犊牛中,发现D - 乳酸水平显著且迅速升高。相反,L - 乳酸从未偏离生理水平。这些观察结果证实,在幼龄犊牛和成牛中,瘤胃酸中毒可能导致临床表现为D - 乳酸代谢性酸中毒。