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盐酸、乙酸、丁酸和丙酸对马胃非腺部溃疡发病机制的影响。

Effects of hydrochloric, acetic, butyric, and propionic acids on pathogenesis of ulcers in the nonglandular portion of the stomach of horses.

作者信息

Nadeau Jenifer A, Andrews Frank M, Patton Clark S, Argenzio Robert A, Mathew Alan G, Saxton Arnold M

机构信息

Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.

出版信息

Am J Vet Res. 2003 Apr;64(4):404-12. doi: 10.2460/ajvr.2003.64.404.

Abstract

OBJECTIVE

To identify the pathogenesis of gastric ulcers by comparing injury to the nonglandular gastric mucosa of horses caused by hydrochloric acid (HCl) or volatile fatty acids (VFAs).

SAMPLE POPULATION

Gastric tissues from 30 horses.

PROCEDURE

Nonglandular gastric mucosa was studied by use of Ussing chambers. Short-circuit current (Isc) and potential difference were measured and electrical resistance calculated for tissues after addition of HCl and VFAs to normal Ringer's solution (NRS). Tissues were examined histologically.

RESULTS

Mucosa exposed to HCl in NRS (pH, 1.5) had a significant decrease in Isc, compared with Isc for mucosa exposed to NRS at pH 4.0 or 7.0. Also, exposure to 60mM acetic, propionic, and butyric acids (pH, 4.0 or 1.5) caused an immediate significant decrease in Isc. Recovery of sodium transport was detected only in samples exposed to acetic acid at pH 4.0. Recovery of sodium transport was not seen in other mucosal samples exposed to VFAs at pH < or = 4.0.

CONCLUSIONS AND CLINICAL RELEVANCE

Acetic, butyric, and propionic acids and, to a lesser extent, HCl caused decreases in mucosal barrier function of the nonglandular portion of the equine stomach. Because of their lipid solubility at pH < or = 4.0, undissociated VFAs penetrate cells in the nonglandular gastric mucosa, which causes acidification of cellular contents, inhibition of sodium transport, and cellular swelling. Results indicate that HCl alone or in combination with VFAs at gastric pH < or = 4.0 may be important in the pathogenesis of gastric ulcers in the nonglandular portion of the stomach of horses.

摘要

目的

通过比较盐酸(HCl)或挥发性脂肪酸(VFA)对马非腺胃黏膜的损伤,确定胃溃疡的发病机制。

样本群体

30匹马的胃组织。

方法

使用尤斯灌流小室研究非腺胃黏膜。向正常林格氏液(NRS)中添加HCl和VFA后,测量组织的短路电流(Isc)和电位差,并计算电阻。对组织进行组织学检查。

结果

与暴露于pH 4.0或7.0的NRS中的黏膜Isc相比,暴露于pH 1.5的NRS中的HCl的黏膜Isc显著降低。此外,暴露于60mM乙酸、丙酸和丁酸(pH 4.0或1.5)会导致Isc立即显著降低。仅在暴露于pH 4.0的乙酸的样本中检测到钠转运的恢复。在pH≤4.0暴露于VFA的其他黏膜样本中未观察到钠转运的恢复。

结论及临床意义

乙酸、丁酸和丙酸,以及程度较轻的HCl导致马胃非腺部分的黏膜屏障功能降低。由于它们在pH≤4.0时的脂溶性,未解离的VFA穿透非腺胃黏膜中的细胞,导致细胞内容物酸化、钠转运抑制和细胞肿胀。结果表明,在马胃非腺部分的胃溃疡发病机制中,单独的HCl或与pH≤4.0的VFA联合可能很重要。

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