Food mineral composition and acid–base balance in rabbits

Abstract

Alkali-rich diets are often recommended in human medicine to prevent the pathological consequences of nutritional acid load in conditions of impaired renal function. This study was undertaken in rabbits as common laboratory animals for basic medical research to explore the impact of high versus low dietary alkali intake on systemic acid-base balance and renal control in a typical herbivore. Male rabbits (2.3-4.8 kg) were kept in a metabolism cage. The 24h urine and arterial blood samples were analysed for acid-base data. The metabolic CO2 production was measured to calculate alveolar ventilation. Three randomized groups of animals were fed ad libitum with rabbit chow providing sufficient energy but variable alkali load, assessed by the ashes' cation-anion difference. The average daily nutritional alkali load (+/- SEM) was 67.1 +/- 2.2 mEq x kg(-1) (N = 58) in the group on high, 45.4 +/- 2.5 mEq x kg(-1) (N = 31) in the group on normal and 1.7 +/- 0.5 mEq x kg(-1) (N = 11) in the group on low alkali food. Respective mean arterial base excess values (BE) were 1.4 +/- 0.3 mM, 0.3 +/- 0.4 mM and 0.0 +/- 0.3 mM, being significantly higher on high alkali food (P < 0.05) than in the other groups. Arterial PCO2, alveolar ventilation and metabolic CO2 production were not significantly different between groups. On normal and high-alkali chow, an alkaline urine (pH(u) > 8.0) with 18-20 mmol x kg(-1) bicarbonate/carbonate was excreted daily, typically containing an insoluble precipitate of 35-60% carbonate. On low-alkali diet, the mean pH(u) decreased to 6.26 +/- 0.14, due to a strong reduction of daily excreted soluble bicarbonate and precipitated carbonate to 1.2 +/- 0.6 and 0.7 +/- 0.2 mmol x kg(-1), respectively. Thereby, nearly complete fractional base reabsorption of 97.8 +/- 0.7 % was reached. Herbivore nutritional alkali-load elicited large rates of renal base excretion including precipitates, to which the urinary tract of the rabbits appeared to be adapted. Dietary base variations were more accurately reflected in the urine than by the blood acid-base status. A strongly base-deficient diet exerted maximum impact on renal base saving mechanisms, implying a critical precondition for growing susceptibility to metabolic acidosis also in the rabbit.