Nitrate poisoning in cattle

Summary In a series of experiments the effect of administering KNO(2) was studied, during parturition, on the capability of oxygen transport of maternal blood and on oxygen transfer to foetal blood. The following blood parameters were analysed, MHb percentage, pO(2), O(2)-saturation, pH, pCO(2), and (NO(2)) in maternal arterial blood (carotid art.) and venous blood (jugular vein) and in foetal arterial blood (umbilical art.) and venous blood (umbilical vein). The relative O(2)-saturation was calculated from the estimated O(2)-saturation by multiplying with the factor Hb (mmol/1) minus MHb (mmol/1), divided by Hb (mmol/1). In addition, blood pressure in the carotid artery, heart rate, and respiration rate in the dam were continuously recorded for some hours. A dosage of 9 to 12 mg of NO(2)/kg body weight intravenously or of 30 mg of NO(2)/kg body weight orally to the dam caused much higher MHb percentages and NO(2) contents in the maternal blood than in the foetal blood. In maternal blood the ratio of NO(2) content td MHb percentage was proportional to that in foetal blood. In the arterial blood, MHb percentages were almost as high as in the venous blood. After administering of nitrite, relative O(2)-saturation dropped simultaneously with the increase in methaemoglobin. Nitrite treatment caused a drop in the maternal blood pressure; heart rate and respiration rate increased. O(2)-saturation in the blood in the umbilical vein was much lower in the animals with nitrite treatment than in those without. These experimental results show clearly that the oxygen capacity of the blood decreases after nitrite treatment. In pregnant cows the oxygen supply to the foetus will be adversely affected after nitrate intake, especially by the lower oxygen transfer via the placenta, though hardly at all by methaemoglobin formation in the foetal blood. When the oxygen transfer to the foetal blood decreases too sharply, intra-uterine death and ultimately abortion may result.