title: Acid-base, metabolic, and hemodynamic effects of sodium bicarbonate or tromethamine administration in anesthetized dogs with experimentally induced metabolic acidosis.
abstract: OBJECTIVE
  To evaluate buffering capacity and side effects of equivalent doses of tromethamine (THAM) and sodium bicarbonate (BIC).
  
  
  METHODS
  18 purebred dogs.
  
  
  METHODS
  Acidosis was induced by having dogs breathe a hypoxic gas mixture (FIO2 = 0.10) until arterial base balance < or = -7.5 mEq/L was reached. Dogs then received a 30-minute infusion of 5% BIC (n = 6) or 0.3M THAM (n = 8), and FIO2 increased to 0.30. Drug doses were calculated to correct base balance to zero.
  
  
  RESULTS
  During hypoxia, for BIC- and THAM-treated groups, median (interquartile range [Q1, Q3]) pHa and arterial base balance decreased to 7.16 (7.07, 7.38) and 7.19 (7.11, 7.31), -14 (-16, 9) and -12 (-16, -11) mEq/L, respectively, and mixed venous lactate concentration increased to 7 (2, 15) and 6 (3, 13) mmol/L, respectively. Immediately after each infusion, acid-base and cardiopulmonary variables returned toward baseline. For respective BIC- and THAM-treated groups, pHa increased to 7.37 (7.26, 7.44) and 7.40 (7.33, 7.49) and base balance increased to 0 (-4, 7) and 0 (-4, 2) mEq/L. Lactate concentration decreased only slightly to 5 (2, 6) and 5 (2, 9) mmol/L, but continued to decrease throughout the study. The only significant (P < or = 0.05) difference between groups was hypernatremia after BIC administration that persisted for 60 minutes. The PaCO2 in BIC-treated dogs increased immediately after infusion, compared with values during hypoxia. Standardized ionized calcium values initially decreased in both groups, but returned to baseline by 60 minutes.
  
  
  CONCLUSIONS
  The buffering capacity of THAM is equal to that of BIC, although THAM does not cause the transient hypernatremia or hypercapnia observed after BIC administration. Hypocalcemia may be transient after administration of either solution. Thus, THAM is an acceptable alternative to BIC for treatment of metabolic acidosis in selected anesthetized dogs.
authors.affiliation: Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
authors.forename: P F
authors.initials: PF
authors.lastname: Moon
authors.forename: L
authors.initials: L
authors.lastname: Gabor
authors.forename: R D
authors.initials: RD
authors.lastname: Gleed
authors.forename: H N
authors.initials: HN
authors.lastname: Erb
mesh_terms: D000136:Acid-Base Equilibrium / Q000187:drug effects*; D000138:Acidosis / Q000662:veterinary*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000097:blood; D004285:Dogs / Q000097:blood / Q000378:metabolism* / Q000502:physiology; D004573:Electrolytes / Q000097:blood; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000662:veterinary; D008297:Male; D017693:Sodium Bicarbonate / Q000494:pharmacology*; D014325:Tromethamine / Q000494:pharmacology*; D014563:Urodynamics / Q000187:drug effects
chemical_list: D001786:Blood Glucose; D004573:Electrolytes; D014325:Tromethamine; D002245:Carbon Dioxide; D017693:Sodium Bicarbonate