Rackwitz R, Gäbel G
Institute for Veterinary Physiology, University of Leipzig, Leipzig, Germany.
J Anim Physiol Anim Nutr (Berl). 2018 Feb;102(1):e345-e352. doi: 10.1111/jpn.12752. Epub 2017 Jun 13.
The carbon dioxide released and dissolved in rumen fluid may easily permeate across the epithelial cell membrane. Thus, we hypothesized that CO may act as proton carrier and induce epithelial damage under acidotic conditions. Ovine ruminal epithelia were mounted in Ussing chambers under short-circuit conditions. The serosal buffer solution had a constant pH of 7.4 and was gassed either with 100% oxygen or with carbogen (95% O /5% CO ). The mucosal solution was gassed with either 100% oxygen or 100% carbon dioxide. The mucosal pH was lowered stepwise from 6.6 to 5.0 in the presence or absence of short-chain fatty acids (SCFA). The transepithelial conductance (G ) as an indicator of epithelial integrity and the short-circuit current (I ) as an indicator of active electrogenic ion transfer were continuously monitored. At an initial mucosal pH of 6.6, there was no significant difference in G between the treatment groups. In the absence of both SCFA and CO , G remained constant when the mucosal solution was acidified to pH 5.0. In the presence of SCFA, mucosal acidification induced a significant rise in G when the solutions were gassed with oxygen. A small increase in G was observed in the mucosal presence of CO . However, no difference in final G was observed between SCFA-containing and SCFA-free conditions under carbon dioxide gassing during stepwise mucosal acidification. The SCFA+proton-induced increase in G could also be minimized by serosal gassing with carbogen. Because of the SCFA+proton-induced changes in G and their attenuation by CO , a protective role for mucosally available carbon dioxide may be assumed. We suggest that this effect may be due to the intraepithelial conversion of carbon dioxide to bicarbonate. However, the serosal presence of CO at a physiological concentration may be sufficient to protect the epithelia from SCFA+proton-induced damage for a certain period of time.
瘤胃液中释放并溶解的二氧化碳可轻易透过上皮细胞膜。因此,我们推测在酸中毒条件下,一氧化碳可能作为质子载体并导致上皮损伤。将绵羊瘤胃上皮置于短路条件下的尤斯灌流小室中。浆膜缓冲溶液的pH恒定为7.4,用100%氧气或混合气(95% O₂/5% CO₂)通气。黏膜溶液用100%氧气或100%二氧化碳通气。在存在或不存在短链脂肪酸(SCFA)的情况下,将黏膜pH从6.6逐步降至5.0。连续监测作为上皮完整性指标的跨上皮电导(Gt)和作为主动电生性离子转运指标的短路电流(Isc)。在初始黏膜pH为6.6时,各治疗组之间的Gt无显著差异。在不存在SCFA和CO₂的情况下,当黏膜溶液酸化至pH 5.0时,Gt保持恒定。在存在SCFA的情况下,当溶液用氧气通气时,黏膜酸化导致Gt显著升高。在黏膜存在CO₂的情况下,观察到Gt有小幅增加。然而,在逐步黏膜酸化过程中,二氧化碳通气条件下含SCFA和不含SCFA的条件之间最终的Gt没有差异。SCFA + 质子诱导的Gt增加也可通过用混合气对浆膜通气而最小化。由于SCFA + 质子诱导的Gt变化及其被CO₂减弱,可推测黏膜可利用的二氧化碳具有保护作用。我们认为这种作用可能是由于上皮内二氧化碳转化为碳酸氢盐。然而,生理浓度的浆膜CO₂可能足以在一定时间内保护上皮免受SCFA + 质子诱导的损伤。