Metabolic alkalosis mimicking the acute sequestration of HCl in rats: bucking the alkaline tide
Rubin, S.I.; Sonnenberg, B.; Zettle, R.; Halperin, M.L.
Clinical and Investigative Medicine 17(6): 515-521
1994
ISSN/ISBN: 0147-958X PMID: 7895415 Document Number: 431848
Loss or sequestration of HCl induces an acute metabolic alkalosis. The purpose of these experiments was to examine the renal handling of bicarbonate (HCO-3-) in awake, euvolemic rats to determine if a significant degree of bicarbonaturia would develop because, if present, it could lead to large negative balances for sodium (Na+) and/or potassium (K+). Metabolic alkalosis was induced acutely by creating the equivalent of an acute and large loss of HCl; the net effect was to lose Cl- and gain equimolar HCO-3- in rats that were in Na+ and K+ balance. A loop diuretic induced the loss of 1,860 mu-mol Na+, 842 mu-mol K+ and 2,444 mu-mol Cl- over a 4-h period; the loss of Cl- was replaced as its Na+ or K+ salt by infusing equivalent amounts of NaHCO-3 and KHCO-3 (ultimately, a "simple exchange" of 2,444 mu-mol of HCO-3- for Cl-). Metabolic alkalosis was sustained for 4 h (mean plasma (HCO-3-) = 43 mmol/L); there was a parallel fall in the plasma (Cl-). From a renal perspective, the fractional excretion of HCO-3- was only 0.4%. This adaptation could be viewed as potentially life-saving, because excretion of NaHCO-3 would result quickly in a severe reduction in ECF volume and metabolic acidosis and, in addition, in a severe degree of K+-depletion.