Splanchnic release of potassium after hemorrhage and succinylcholine in rabbits.
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 After measurement of baseline K+ (from each catheter) and arterial blood gases, approximately 30 mL/kg of blood was withdrawn, and the animal was allowed to become acidotic until pH approximately 7.00-7.10.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 Blood from each catheter was withdrawn for K+ analysis at 1, 3, 5, and 7 min after SCh.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)
Antognini
J F
JF
Department of Anesthesiology, University of California-Davis 95616-8634.
D000818:Animals; D006470:Hemorrhage / Q000503:physiopathology*; D011188:Potassium / Q000378:metabolism*; D011817:Rabbits; D013153:Splanchnic Nerves / Q000187:drug effects / Q000378:metabolism*; D013390:Succinylcholine / Q000494:pharmacology*
D013390:Succinylcholine; D011188:Potassium