Acid-base homeostasis of blood and pH of abomasum in calves fed non-acidified and acidified milk replacer

Experiments were conducted on calves divided into three groups, 6 animals in each, to determine the influence of the intake of non-acidified and acidified milk replacer on the level of acid-base homeostasis in venous blood. The milk replacer was supplied at a dose of 700 g dry matter in 8 l of the liquid in two feedings. The milk replacer was acidified by adding formic acid to ensure the concentration of 0.2% in milk replacer. Venous blood was collected before feeding and 1, 2, 4, and 6 hours after feeding. The samples were analyzed for blood pH, actual bicarbonate HCO3- (mmol/l), base excess BE (mmol/l), partial pressure of carbon dioxide pCO2 (kPa) and partial pressure of oxygen pO2 (kPa). Significant changes were observed in calves fed acidified milk of albumin type. The mean daily values of acid-base parameters in these calves were significantly lower in comparison with animals fed non-acidified milk replacer and reached the following levels: pH 7.343 ± 0.032 (P < 0.05), HCO3 24.49 ± 2.13 mmol/l (P < 0.01), BE 1.11 ± 1.97 mmol/l (P < 0.001). A similar tendency but of a more pronounced decrease in values was recorded in the group of calves fed acidified milk replacer of casein type: pH 7.312 ± 0.022 (P < 0.01), HCO3- 21.73 ± 0.75 mmol/l (P < 0.001), BE 96 ± 0.86 mmol/l (P < 0.001). In relation to the time after feeding the group of calves fed non-acidified milk replacer showed a rising tendency in the level of metabolic components (HCO3-), compensated by respiratory regulating mechanisms (rise in pCO2) conducive to the maintenance of optimum blood pH level. The group of calves fed acidified milk replacer (formic acid 2 ml/l) of the albumin type showed metabolic acidosis with subsequent gradual adjustment and compensation by means of metabolic (HCOHCO3-) rather than respiratory regulation mechanisms. The calves fed acidified casein type milk replacer displayed metabolic acidosis with insufficient metabolic regulation and more intensive respiratory compensation (decrease in pCO2). Concurrent investigations of the abomasum acidity and blood acid-base homeostasis reflected the joint action of both the acidifying effect of formic acid and significantly lower production of bicarbonate (HCO3-) related to the intake of acidified milk and the tendency to the development of metabolic acidosis.