Studies on hyperkalemia as a cause of death in intestinal ischemia shock in rats

Circ Shock. 1986;19(3):329-45.


Intestinal ischemia shock was induced either by temporary occlusion of the three splanchnic arteries for 40 min (SAO-shock) or by temporary occlusion of the portal vein for 35-40 min (PVO-shock). In both types of shock, life can be considerably prolonged (5-8-fold) by treatment with rat plasma plus glucose. Eventually, death is caused by heart failure due to hyperkalemia (plasma K+ concentration greater than 10 mmol/l). The amount of K+ causing this hyperkalemia is estimated at roughly 10% of the total body K+. Acidosis, low blood pressure, reduced kidney function, and disintegration of erythrocytes in the gastrointestinal (GI) tract probably are of no or minor importance in causing this extreme hyperkalemia. No indication was found that the liver, the skeletal muscles, or the erythrocytes release K+. Although the K+ concentration of the contents of the GI tract as well as the K+ transport by the portal vein were increased, the source of the excess K+ remains obscure. Removal of the contents of the stomach and small intestine, followed by flushing of the gastrointestinal tract, may have a favorable effect on the course of plasma K+ (and plasma glucose) concentration, indicating that toxic products from the damaged intestines may be important lethal factors.

MeSH terms

  • Acidosis / blood
  • Animals
  • Blood Pressure
  • Digestive System / metabolism
  • Digestive System Physiological Phenomena
  • Erythrocytes / metabolism
  • Female
  • Hyperkalemia / metabolism
  • Hyperkalemia / physiopathology*
  • In Vitro Techniques
  • Intestines / blood supply*
  • Ischemia / blood*
  • Kidney / physiopathology
  • Kidneys, Artificial
  • Ligation
  • Peritoneal Dialysis
  • Portal Vein / physiology
  • Potassium / metabolism
  • Rats
  • Shock / metabolism
  • Shock / physiopathology*
  • Splanchnic Circulation


  • Potassium