Splanchnic release of potassium after hemorrhage and succinylcholine in rabbits.

Abstract

Recent clinical reports document that hyperkalemia may occur after succinylcholine (SCh) administration in hemorrhagic, acidotic humans. Hemorrhagic, acidotic rabbits are a useful model for study of this phenomenon because of profound hyperkalemia after SCh. To determine the etiology of this hyperkalemia, we anesthetized rabbits (n = 5, Group H) with halothane/N2O, and after endotracheal intubation, placed catheters in the femoral artery, femoral vein (FV), and inferior vena cava (IVC), the latter at or above the hepatic veins. After measurement of baseline K+ (from each catheter) and arterial blood gases, approximately 30 mL/kg of blood was withdrawn, and the animal was allowed to become acidotic until pH approximately 7.00-7.10. Plasma K+ was determined again, and SCh 1 mg/kg administered intravenously. Blood from each catheter was withdrawn for K+ analysis at 1, 3, 5, and 7 min after SCh. Control rabbits (Group C, n = 5) were similarly anesthetized and catheterized but were not hemorrhaged. Arterial blood gas and K+ analyses were performed before and after SCh 1 mg/kg, similar to Group H. In Group H, arterial K+ concentration increased after hemorrhage (3.2 +/- 0.3 mmol/L to 6.4 +/- 2.0 mmol/L, P < 0.05). SCh caused a further increase, peaking at 8.3 +/- 1.5 mmol/L at 7 min (P < 0.05). In Group H the IVC-FV K+ difference was 1.6 +/- 1.9 mmol/L, 1.5 +/- 2.1 mmol/L, 0.9 +/- 1.6 mmol/L and 1.6 +/- 1.4 mmol/L, respectively, for the 1-, 3-, 5-, and 7-min periods after SCh.(ABSTRACT TRUNCATED AT 250 WORDS)