D-lactic acidosis (DLA) is a disease associated with D-lactatemia, acidosis and neurological signs. However, these associations are ill-defined. Bacterial fermentation in the intestine causes increasing D-lactic acid concentrations in the body. Therefore, DLA is reported secondary to gastrointestinal diseases, such as short bowel syndrome, gastroenteritis or diarrhea. Despite intestinal origin, sudden D-lactatemia is often a result of impaired D-lactate metabolism in the body.<p> Aims of this work were to determine: 1) Influence of the presence of D-lactate or acidity on neurological disturbances; 2) Effectiveness of parenteral NaHCO3 therapy in correcting cerebrospinal acidity and DLA; 3) Prevalence of DLA in diarrheic lambs and fecal D-lactate thresholds; 4) Effectiveness of malate in preventing DLA.<p> The methodological tools consisted of animal models (calves and lambs): 1) Advanced surgical procedure in calves for long-lasting atlanto-occipital catheterizations; 2) Intravenous infusions of acids to experimentally induce acidosis; 3) Intravenous NaHCO3 therapies; 4) Sampling of cerebrospinal fluid (CSF), blood, urine and feces from experimental / treated calves or diarrheic lambs for blood gas analysis, and D-lactate separation by chromatography.<p> D-lactate entered the central nervous system (> 2 mmol/L) from the circulation following experimentally induced D-lactatemia (> 5 mmol/L) and was responsible for neurological disturbances which correlated (r = 0.9, P < 0.05) with both CSF and serum D-lactate concentrations. A zenith of neurological disturbances, ataxia was evident when D-lactate concentration exceeded 12 mmol/L (CSF) and 26 mmol/L (serum), however, a nadir of acidosis (pH 6.9) caused by HCl infusions produced only mild neurological disturbances (P < 0.05). Therapeutic NaHCO3 infusions did not result paradoxical CSF acidosis, but supportive in correcting (P < 0.05) acidosis (ÄpH + 0.11) and D-lactatemia in calves.<p> In lambs, metabolic acidosis following a range of mild to severe diarrhea was observed with a corresponding range of D-lactate concentrations in both serum (< 0.05−24.0 mmol/L) and feces (< 0.05−31.0 mmol/L). D-lactate was absorbed into the circulation when the fecal D-lactate concentration exceeded 10.2 mmol/L (threshold). In calves, moderate oral use of malate produced a > 50% (P < 0.05) decrease in fecal and serum D-lactate concentrations suggesting prebiotic properties to prevent DLA. <p> This dissertation answers the critical questions about the onset of neurological signs in D-lactic acidosis, and advances the current knowledge on the metabolism of D-lactate, the prevention and treatment of acidosis.