Effects of dissolved carbon dioxide on the integrity of the rumen epithelium: An agent in the development of ruminal acidosis

• Published in: Journal of animal physiology and animal nutrition Vol. 102; no. 1; pp. e345 - e352
• Main Authors: Rackwitz, R., Gäbel, G.
• Format: Journal Article
• Language: English
• Published: Germany Wiley Subscription Services, Inc 01.02.2018
• Subjects: Acidification; Acidosis; Acidosis - physiopathology; Acidosis - veterinary; Animals; Bicarbonates; Buffer solutions; Carbon dioxide; Carbon Dioxide - adverse effects; Carbonates; Conductance; Epithelial cells; Epithelium; Epithelium - drug effects; Fatty acids; Female; Hydrogen ions; Hydrogen-Ion Concentration; Integrity; Mucosa; Oxygen; pH effects; pH regulation; Proton damage; Resistance; Rumen; Rumen - drug effects; Sheep; Short circuits; Short-circuit current; short‐chain fatty acids; Tissue Culture Techniques - veterinary; conductance; pH regulation; short-chain fatty acids; short-circuit current
• ISSN: 0931-2439; 1439-0396
• DOI: 10.1111/jpn.12752

Summary The carbon dioxide released and dissolved in rumen fluid may easily permeate across the epithelial cell membrane. Thus, we hypothesized that CO2 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% O2/5% CO2). 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 (Gt) as an indicator of epithelial integrity and the short‐circuit current (Isc) 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 Gt between the treatment groups. In the absence of both SCFA and CO2, Gt remained constant when the mucosal solution was acidified to pH 5.0. In the presence of SCFA, mucosal acidification induced a significant rise in Gt when the solutions were gassed with oxygen. A small increase in Gt was observed in the mucosal presence of CO2. However, no difference in final Gt was observed between SCFA‐containing and SCFA‐free conditions under carbon dioxide gassing during stepwise mucosal acidification. The SCFA+proton‐induced increase in Gt could also be minimized by serosal gassing with carbogen. Because of the SCFA+proton‐induced changes in Gt and their attenuation by CO2, 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 CO2 at a physiological concentration may be sufficient to protect the epithelia from SCFA+proton‐induced damage for a certain period of time.