The Impact of CO₂ Exposure on Ruminal Epithelium and Blood Flow
Fermentative By-products, Bacterial, and Toxin Translocation
Epithelial Barrier Dysfunction
Laminitis, immune activation, liver abscesses, lactic acidosis, and other syndromes have long been associated with ruminal epithelial barrier dysfunction during ruminal acidosis.
Blood flow into the ruminal epithelium directly influences nutrient absorption (Dobson, 1984; Dobson et al., 1971; Engelhardt & Hales, 1977). Exposure of local tissues to high CO₂ increases blood flow (Diji & Greenfield, 1960; Kontos et al., 1967; Richardson et al., 1961). Similarly, high ruminal dCO₂ induces epithelial hyperaemia (Thorlacius, 1972), a response also observed during normal digestion (Dobson, 1984; Thorlacius, 1972).
Hyperaemia and Inflammation
While transient hyperaemia supports nutrient transport, extended periods of high dCO₂ may induce tissue hypoxia and activate inflammatory pathways in the gastrointestinal tract (Glover & Colgan, 2017), as seen in subacute ruminal acidosis (SARA). In vitro, SARA is associated with lipopolysaccharide (LPS) exposure (Kent-Dennis & Penner, 2021). However, in vivo evidence is inconsistent: diets rich in LPS do not always trigger LPS translocation (Khafipour et al., 2009a, 2009b).
Instead, high dCO₂–induced hyperaemia itself may weaken the epithelial barrier (Celebi Sozener et al., 2022; Lang et al., 2000). LPS alone may not produce this effect (McDaniel et al., 2023). Possibly, both high dCO₂ and LPS act together to drive barrier dysfunction (Lang et al., 2005) — or dCO₂ may be the primary culprit, since hypercapnia induces immune responses similar to LPS exposure (Liu et al., 2008). Importantly, the massive dCO₂ accumulation observed during SARA (Laporte-Uribe, 2024) is likely more dangerous than the relatively small fraction of LPS translocated into circulation (Khafipour et al., 2009a, 2009b).
By-product and Bacterial Translocation
Local dCO₂-induced hyperaemia may therefore explain the translocation of fermentation by-products (e.g., lactate, histamine), LPS, and bacteria typically linked to ruminal acidosis.
Laminitis: Hypercapnia causes a transient fall in cardiovascular pressure, followed by vasoconstriction in peripheral tissues but not in large vessels (Kontos et al., 1967). This mechanism may underlie SARA-induced laminitis (Boosman et al., 1991).
Lactic acidosis: Ruminal lactate translocation has been suggested as a cause (Huber, 1976), but the amount translocated is below renal clearance thresholds (Huber, 1969). This implies lactic acidosis has an endogenous origin, a topic warranting further exploration.
LPS toxemia: Bacterial translocation and liver abscess formation are likely linked to dCO₂-induced hyperaemia and epithelial disruption. LPS exposure alone does not replicate these effects (McDaniel et al., 2023).
Conclusion
Monitoring ruminal dCO₂ and implementing dietary strategies to prevent CO₂ holdup may safeguard the epithelial barrier, reduce by-product and bacterial translocation, and lower the risk of metabolic disorders associated with ruminal acidosis.
