CLINICAL AND CLINICOPATHOLOGICAL CHANGES IN COWS WITH ENDOTOXIN-INDUCED MASTITIS TREATED WITH SMALL VOLUMES OF ISOTONIC OR HYPERTONIC SODIUM-CHLORIDE ADMINISTERED INTRAVENOUSLY

We characterized the clinicopathologic manifestations of experimentall y induced endotoxin-induced mastitis. Responses to hypertonic fluid th erapy also were assessed. Eight cows received 1 mg of endotoxin by int ramammary infusion in the left forequarter. Four hours after endotoxin administration, cows received 0.9% NaCl, 5 ml/kg of body weight (n = 4) or 7.5% NaCl, 5 ml/kg (n = 4) IV. Endotoxin-infused cows had expand ed plasma volume, hyponatremia, transient hyperchloremia and hypophosp hatemia, increased serum glucose concentration, and decreased serum ac tivities of liver- and muscle-specific enzymes. Calculated plasma volu me increased at G hours in cows receiving hypertonic NaCl, and at 12, 24, and 48 hours after endotoxin infusion in both groups. Concurrent o bservations of decreased serum protein concentration, erythrocyte coun t, and hematocrit supported observations of increased plasma volume. R elative plasma volume was greater in cows receiving hypertonic NaCl (1 24.3%) than in cows receiving isotonic NaCl (106.6%) at 6 hours after endotoxin infusion. Cattle receiving hypertonic NaCl had increased vol untary water intake after rv fluid administration, Increased water con sumption was not accompanied by increased body weight, indicating prob able occurence of offsetting body water loss. Serum sodium concentrati on in cows receiving hypertonic NaCl was increased 2 hours after fluid administration, but the magnitude of the change was minimal (< 4 mmol /L) and transient, indicating rapid equilibration with either intersti tial or intracellular spaces. Serum sodium concentration was decreased in cows receiving isotonic NaCl at 12, 24, and 48 hours after endotox in administration, compared with concentration prior to endotoxin admi nstration, indicating selective loss of sodium.