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

Abstract

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 &plusmn; 0.032 (<i>P</i> < 0.05), HCO₃ 24.49 &plusmn; 2.13 mmol/l (<i>P</i> < 0.01), BE 1.11 &plusmn; 1.97 mmol/l (<i>P</i> < 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 &plusmn; 0.022 (<i>P</i> < 0.01), HCO₃^- 21.73 &plusmn; 0.75 mmol/l (<i>P</i> < 0.001), BE 96 &plusmn; 0.86 mmol/l (<i>P</i> < 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.