The impact of CO2 exposure on the ruminal epithelium and blood flow

Fermentative by-products, bacteria, and toxin translocation.

Laminitis, immune response, liver abscess, lactic acidosis, and other syndromes have been associated to the ruminal epithelial barrier dysfunction during ruminal acidosis.

Blood flow into the ruminal epithelium affects nutrients absorption (Dobson, 1984; Dobson et al., 1971; Engelhardt & Hales, 1977). The exposure of local tissue to high CO2 increases blood flow (Diji & Greenfield, 1960; Kontos et al., 1967; Richardson et al., 1961) and ruminal dCO2 increases blood flow into the epithelium or “hyperaemia” (Thorlacius, 1972).

Ruminal hyperaemia might be caused by high dCO2 during normal digestion (Dobson, 1984; Thorlacius, 1972). Extended periods under hyperaemia might induce hypoxia and inflammatory response of the GIT (Glover & Colgan, 2017), as seen during SARA and associated to LPS exposure in in vitro (Kent-Dennis & Penner, 2021). In vivo, the presence of ruminal LPS not always lead to SARA signs. Diets with high LPS might not always produce LPS translocation (Khafipour et al., 2009a, 2009b). In fact, high dCO2 induced hyperaemia might disrupt epithelial barrier (Celebi Sozener et al., 2022; Lang et al., 2000) and LPS might, per se, not (McDaniel et al., 2023).

Perhaps, both must be present to induce LPS translocation (Lang et al., 2005), or dCO2 is the culprit, as hypercapnia induces similar cellular immune response than LPS (Liu et al., 2008). The vast ruminal dCO2 amounts during SARA might be by far more dangerous (Laporte Uribe, 2023) than the total LPS translocated, which is only a small fraction of the overall concentrations found during SARA (Khafipour et al., 2009a, 2009b).

Local dCO2 induced hyperaemia might, therefore, explain the translocation of by-products (Lactate, Histamine, LPS) and bacteria associated to ruminal acidosis.

Laminitis: Peripherally, hypercapnia leads to a transient reduction in cardiovascular pressure followed by a peripheral vasoconstriction in extremities, but not in large vessels (Kontos et al., 1967), which might explain SARA induced laminitis (Boosman et al., 1991).

Lactic acidosis: Ruminal lactate translocation might cause lactic acidosis (Huber, 1976), however the ruminal lactate translocated is lower than the lactate renal clearance (Huber, 1969), which suggest that lactic acidosis must have an internal origin, but this is theme for another blog.

LPS toxemia: Bacterial translocation and liver abscess formation might be due to the local dCO2 induced hyperaemia and the effect on epithelial barrier function, LPS solely does not have this effect (McDaniel et al., 2023).

By monitoring ruminal dCO2 levels and implementing appropriate dietary strategies, we can help to prevent the deleterious effects of high CO2 on the ruminal epithelium and reduce the risk of metabolic disorders associated with ruminal acidosis.