title: Hypokalemia during acute metabolic acidosis on hemodilution with succinylated gelatin in rats.
abstract: Extracellular metabolic acidosis of mineral origin is commonly associated with plasma hyperkalemia. Nevertheless, in previous experiments, animals subjected to acute metabolic acidosis induced by normovolemic hemodilution using a colloidal volume replacement solution containing succinylated gelatin (gelafundin), developed a hypokalemic state with concomitant marked increases in diuresis and renal potassium excretion. In the present study, the succinylated gelatin's impact on diuresis and consequently potassium excretion was studied.
  
  
  
  Anesthetized Wistar rats were subjected to acute metabolic acidosis either due to normovolemic hemodilution with gelafundin (group I) or HCl application (groups II and III). Animals of group III received mannitol in addition. Blood gas analyses were performed regularly. Urine was continuously collected, and the excreted volume as well as potassium concentration was measured.
  
  
  
  In all groups, mean base excess value was about -3.0 mEq/L. Plasma potassium concentration decreased from 5.0 mM to 4.5 mM in group I, whereas it was almost constant in groups II and III. The urine volume amounted to 2300 μL in groups I and III and 1000 μL in group II. Excreted total amount of potassium in urine was 340 μmol (group I), 125 μmol (group II), and 230 μmol (group III), respectively.
  
  
  
  The employed volume replacement solution leads to increased diuresis induced by excretion of succinylated gelatin, which also sufficiently accounts for enhanced potassium loss into urine and decreased plasma potassium concentration. Therefore, generalization of the connection between acute metabolic acidosis and plasma hyperkalemia, as often stated in literature, is not justified.
authors.affiliation: University Hospital Essen, Institute of Physiological Chemistry, University of Duisburg-Essen, Essen, North Rhine-Westphalia, Germany. Electronic address: johanna.teloh@uk-essen.de.
authors.forename: Johanna K
authors.initials: JK
authors.lastname: Teloh
authors.affiliation: University Hospital Essen, Institute of Physiological Chemistry, University of Duisburg-Essen, Essen, North Rhine-Westphalia, Germany.
authors.forename: Ricarda
authors.initials: R
authors.lastname: Rohrig
authors.affiliation: University Hospital Essen, Institute of Physiological Chemistry, University of Duisburg-Essen, Essen, North Rhine-Westphalia, Germany.
authors.forename: Indra N
authors.initials: IN
authors.lastname: Waack
authors.affiliation: University Hospital Essen, Institute of Physiological Chemistry, University of Duisburg-Essen, Essen, North Rhine-Westphalia, Germany.
authors.forename: Herbert
authors.initials: H
authors.lastname: de Groot
mesh_terms: D000138:Acidosis / Q000139:chemically induced / Q000378:metabolism; D000818:Animals; D004231:Diuresis / Q000187:drug effects*; D005780:Gelatin / Q000494:pharmacology*; D006438:Hemodilution / Q000009:adverse effects; D008297:Male; D010952:Plasma Substitutes / Q000494:pharmacology*; D011188:Potassium / Q000097:blood / Q000652:urine*; D017208:Rats, Wistar; D013386:Succinates / Q000494:pharmacology*
chemical_list: D010952:Plasma Substitutes; D013386:Succinates; C060085:succinylated gelatin; D005780:Gelatin; D011188:Potassium
keywords: Acid–base homeostasis; Colloid; Diuresis; Gelafundin; Potassium excretion; Urine