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硫肽菌素及相关抗生素对绵羊小麦诱导的乳酸酸中毒的控制

Control of wheat-induced lactic acidosis in sheep by thiopeptin and related antibiotics.

作者信息

Muir L A, Rickes E L, Duquette P F, Smith G E

出版信息

J Anim Sci. 1980 Mar;50(3):547-53. doi: 10.2527/jas1980.503547x.

Abstract

Thiopeptin, thiopeptin-like antibiotics and penicillin were shown previously to be highly active in vitro against Streptococcus bovis, the microorganism believed to be responsible for the initiation of ruminal lactic acidosis. The purpose of this work was to determine the efficacy of these antibiotics in preventing lactic acidosis in lambs challenged by intraruminal administration of ground wheat. Lambs, which were fasted and then given ground wheat at 40 g/kg body weight, showed dramatic increases in rumen and plasma lactate over the 30-hr experimental period. Rumen lactate increased from .2 to peak levels of approximately 150 mumoles/ml by 8 to 10 hr after wheat administration. Plasma lactate increased after rumen lactate was elevated and lambs succumbed when plasma levels exceeded 15 mumoles/ml. Ruminal volatile fatty acids were greatly reduced as rumen lactate increased. Over half of the lambs given ground wheat died within 30 hours. Thiopeptin given as a single dose completely prevented lactic acidosis by reducing rumen lactate 80 to 90%. In addition, thiopeptin permitted "normal" rumen fermentation to continue as indicated by a significant increase in volatile fatty acids. The minimum effective dose of thiopeptin to control acute lactic acidosis was .18 mg/kg body weight. Other members of the thiopeptin class, including sulfomycin, sporangiomycin, siomycin and taitomycin, prevented lactic acidosis in a manner similar to thiopeptin. Penicillin, however, inhibited ruminal volatile fatty acid production as well as lactate synthesis. In addition, the effective period for penicillin in the rumen was only 8 to 16 hr, after which lactate fermentation was reestablished. Thus, thiopeptin and thiopeptin-like antibiotics, but not penicillin, appear to provide prophylactic treatment against lactic acidosis in sheep.

摘要

硫肽菌素、类硫肽菌素抗生素和青霉素先前已被证明在体外对牛链球菌具有高度活性,牛链球菌被认为是引发瘤胃酸中毒的微生物。这项工作的目的是确定这些抗生素在预防经瘤胃内注射磨碎小麦而受到挑战的羔羊发生酸中毒方面的功效。禁食后以40克/千克体重给予磨碎小麦的羔羊,在30小时的实验期内瘤胃和血浆乳酸水平显著升高。小麦给药后8至10小时,瘤胃乳酸从0.2微摩尔/毫升增加到约150微摩尔/毫升的峰值水平。瘤胃乳酸升高后血浆乳酸增加,当血浆水平超过15微摩尔/毫升时羔羊死亡。随着瘤胃乳酸增加,瘤胃挥发性脂肪酸大大减少。超过一半接受磨碎小麦的羔羊在30小时内死亡。单次给药的硫肽菌素通过将瘤胃乳酸降低80%至90%完全预防了酸中毒。此外,如挥发性脂肪酸显著增加所示,硫肽菌素使“正常”的瘤胃发酵得以继续。控制急性酸中毒的硫肽菌素的最小有效剂量为0.18毫克/千克体重。硫肽菌素类的其他成员,包括磺胺霉素、孢霉素、西霉素和台霉素,以与硫肽菌素相似的方式预防了酸中毒。然而,青霉素抑制瘤胃挥发性脂肪酸的产生以及乳酸的合成。此外,青霉素在瘤胃中的有效期仅为8至16小时,此后乳酸发酵重新建立。因此,硫肽菌素和类硫肽菌素抗生素,而不是青霉素,似乎为绵羊的酸中毒提供了预防性治疗。

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