title: Clinical and clinicopathologic changes in cows with endotoxin-induced mastitis treated with small volumes of isotonic or hypertonic sodium chloride administered intravenously.
abstract: We characterized the clinicopathologic manifestations of experimentally induced endotoxin-induced mastitis. Responses to hypertonic fluid therapy also were assessed. Eight cows received 1 mg of endotoxin by intramammary 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 expanded plasma volume, hyponatremia, transient hyperchloremia and hypophosphatemia, increased serum glucose concentration, and decreased serum activities of liver- and muscle-specific enzymes. Calculated plasma volume increased at 6 hours in cows receiving hypertonic NaCl, and at 12, 24, and 48 hours after endotoxin infusion in both groups. Concurrent observations of decreased serum protein concentration, erythrocyte count, and hematocrit supported observations of increased plasma volume. Relative plasma volume was greater in cows receiving hypertonic NaCl (124.3%) than in cows receiving isotonic NaCl (106.6%) at 6 hours after endotoxin infusion. Cattle receiving hypertonic NaCl had increased voluntary water intake after IV fluid administration. Increased water consumption was not accompanied by increased body weight, indicating probable occurrence of offsetting body water loss. Serum sodium concentration 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 interstitial or intracellular spaces. Serum sodium concentration was decreased in cows receiving isotonic NaCl at 12, 24, and 48 hours after endotoxin administration, compared with concentration prior to endotoxin administration, indicating selective loss of sodium.
authors.affiliation: Department of Large Animal Surgery and Medicine, Auburn University, AL 36849-5522.
authors.forename: J W
authors.initials: JW
authors.lastname: Tyler
authors.forename: E G
authors.initials: EG
authors.lastname: Welles
authors.forename: R J
authors.initials: RJ
authors.lastname: Erskine
authors.forename: H C
authors.initials: HC
authors.lastname: Lin
authors.forename: M A
authors.initials: MA
authors.lastname: Williams
authors.forename: J S
authors.initials: JS
authors.lastname: Spano
authors.forename: J T
authors.initials: JT
authors.lastname: Gaslin
authors.forename: K A
authors.initials: KA
authors.lastname: McClure
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D001835:Body Weight; D002417:Cattle; D002712:Chlorides / Q000097:blood; D004327:Drinking Behavior; D004731:Endotoxins / Q000633:toxicity*; D004906:Erythrocyte Count; D005260:Female; D005440:Fluid Therapy; D006339:Heart Rate; D006454:Hemoglobins / Q000032:analysis; D007958:Leukocyte Count; D008414:Mastitis, Bovine / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D010710:Phosphates / Q000097:blood; D010953:Plasma Volume; D012462:Saline Solution, Hypertonic / Q000627:therapeutic use*; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride / Q000627:therapeutic use*
chemical_list: D001786:Blood Glucose; D002712:Chlorides; D004731:Endotoxins; D006454:Hemoglobins; D010710:Phosphates; D012462:Saline Solution, Hypertonic; D012965:Sodium Chloride; D012964:Sodium