Hindgut Acidosis

  • 文章类型: Journal Article
    这项初步研究的目的是生成数据以支持后肠酸中毒实验模型的开发,以进一步了解其与瘤胃酸中毒无关的系统性后果。对四头经乳造瘘的多胎荷斯坦奶牛(213±11DIM)进行了2个连续的实验期(P),由3d冲刷分开。从基线到最终测量的实验周期为96h,但扩展超过5个日历天(d0-4)。在P1和P2的前72小时(d0-3)中分别进行生理盐水和玉米淀粉(2.8kg/d)的厌恶输注。在输注结束后24h进行最终测量(d4)。通过比较P2与P1,将每头牛用作其自身的对照。在每次P的d2(输注开始后48小时)将CrEDTA脉冲剂量施用到皱胃中后,通过血液中的Cr外观来评估腔后肠通透性。P2期间的淀粉输注与乳蛋白产量增加(3.3%)和减少有关牛奶尿素氮(11%)。在P2期间,粪便干物质(DM)增加(8.8%),淀粉含量趋于增加(~2倍)。随着粪便pH值在淀粉输注过程中降低(1.3pH点),但在P1过程中保持恒定,因此每天都有一段时间的相互作用。虽然在P1期间检测不到粪便乳酸,但在淀粉输注期间始终增加。粪便碱性磷酸酶活性也随着淀粉输注而增加(约17倍)。Cr-EDTA给药后两小时,输注淀粉时血Cr浓度较高,导致小时相互作用治疗的趋势。此外,血D-乳酸增加(~2.5倍),血清铜降低(18%),和血尿素氮,胆固醇和钙呈下降趋势(9.4%,1.2%,和2.4%,分别),相对于P1。目前的结果表明,通过腔后淀粉输注成功诱导了后肠酸中毒,导致肠道损伤和肠道通透性增加。然而,未观察到全身性炎症的指征.本文描述的初步结果将需要在适当的动力研究中确认。
    The objective of this pilot study was to generate data to support the development of an experimental model of hindgut acidosis to further understand its systemic consequences independently of rumen acidosis. Four ruminally fistulated multiparous Holstein cows (213 ± 11 d in milk) were subjected to 2 consecutive experimental periods (P1 and P2), separated by a 3-d washout. Experimental periods were 96 h long from the baseline to the final measurements but expanded over 5 calendar days (d 0-4). Abomasal infusions of saline and corn starch (2.8 kg/d) were performed for the first 72 h (d 0-3) of P1 and P2, respectively. Final measurements were performed 24 h after the end of the infusions (d 4). Each cow was used as its own control by comparing P2 to P1. Postruminal-intestinal permeability was assessed by Cr appearance in blood after a pulse dose administration of Cr-EDTA into the abomasum on d 2 (48 h after infusion initiation) of each period. Starch infusion during P2 was associated with a milk protein yield increase (3.3%) and a decrease in milk urea nitrogen (11%). Fecal dry matter increased (8.8%), and starch content tended to increase (∼2 fold) during P2. There was a period-by-day interaction for fecal pH as it decreased during starch infusion (1.3 pH points) but remained constant during P1. Although fecal lactate was not detectable during P1, it consistently increased during starch infusion. Fecal alkaline phosphatase activity also increased (∼17 fold) in association with starch infusion. Two hours after Cr-EDTA administration, blood Cr concentration was higher during starch infusion, resulting in a tendency for a treatment-by-hour interaction. Furthermore, blood d-lactate increased (∼2.5 fold), serum Cu decreased (18%), and blood urea nitrogen, cholesterol, and Ca tended to decrease (9.4%, 1.2%, and 2.4%, respectively), relative to P1. The current results suggest that hindgut acidosis was successfully induced by postruminal starch infusion, leading to gut damage and increased intestinal permeability. However, indications of systemic inflammation were not observed. The herein described preliminary results will require confirmation in a properly powered study.
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