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

摘要

Experiments were conducted on calves divided into 3 groups of 6 animals each to determine the influence of the intake of non-acidified and acidified milk replacers 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 litres of the liquid in 2 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 at one, 2, 4 and 6 h after feeding. The samples were analysed for blood pH, actual bicarbonate (HCO3-, mmol/litre), base excess (BE, mmol/litre), 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 compared to that in animals fed non-acidified milk replacer and reached the following levels: pH 7.343+or-0.032 (P<0.05); HCO3 24.49+or-2.13 mmol/litre (P<0.01); and BE 1.11+or-1.97 mmol/litre (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+or-0.022 (P<0.01); HCO3- 21.73+or-0.75 mmol/litre (P<0.001); and BE 96+or-0.86 mmol/litre (P<0.001). In relation to the time after feeding, the group of calves fed non-acidified milk replacer showed an increasing 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/litre) of the albumin type showed metabolic acidosis with subsequent gradual adjustment and compensation by means of metabolic (HCO3-) 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..