BACKGROUND AND METHODS: We hypothesized that beta-adrenergic receptor blockade would result in an increase in serum potassium concentration in hypothermic rats given a potassium load compared to non-beta-blocked, hypothermic, potassium-loaded rats. To test this hypothesis, we investigated the interaction between body temperature and beta-adrenergic receptor blockade on serum potassium concentrations in ureter-ligated rats with and without potassium loading. To achieve this goal, we performed three experiments. In the first experiment, serum potassium concentrations were determined in 16 rats as they were continuously cooled from 37 degrees C to 22 degrees C. In the second experiment, 12 ureter-ligated rats were cooled to 31 degrees C, after which they were rewarmed to 37 degrees C. Serum potassium concentrations were determined before and after cooling and on rewarming. Twelve other ureter-ligated rats were cooled to 31 degrees C, then given a potassium load until their serum potassium concentrations returned to their baseline values, after which they were rewarmed to 37 degrees C. Serum potassium concentrations were determined before and after cooling, during the potassium infusion, and on rewarming. In the third experiment, 14 rats were pretreated with propranolol and 14 rats served as controls. Half of the rats in each of these two groups were kept at 37 degrees C and half were cooled to 25 degrees C. All rats were then given a 690-mumol potassium chloride infusion. Serum potassium concentrations were determined before and after the potassium infusion. RESULTS: The rats developed hypokalemia with cooling, which spontaneously resolved in the rats without supplementation on rewarming to 37 degrees C. The hypothermic hypokalemic rats that had their serum potassium concentrations corrected to normothermic status (2.93 +/- 0.17 mmol/L) had marked increases in serum potassium concentrations (4.22 +/- 0.15 mmol/L) on rewarming. In the normothermic rats, potassium loading after beta-adrenergic receptor blockade resulted in even higher serum potassium concentrations (5.65 +/- 0.36 mmol/L) compared with non-beta-blocked rats given equal potassium loads (4.6 +/- 0.4 mmol/L). However, in hypothermic (25 degrees C) rats given the same potassium load, there was no difference in serum potassium concentrations in beta-blocked (6.5 +/- 0.35 mmol/L) and non-beta-blocked rats (6.63 +/- 0.3 mmol/L). CONCLUSIONS: These results suggest that acute hypothermia causes a decrease in serum potassium, probably secondary to redistribution, which is reversible on rewarming. Supplementation of potassium during hypothermia can cause a significant increase in serum potassium concentration on rewarming. Blocking beta-adrenergic receptors with propranolol did not effect hypothermia-induced hypokalemia, suggesting that the beta-adrenergic mechanism may not be functional in hypothermia.
BACKGROUND AND METHODS: We hypothesized that beta-adrenergic receptor blockade would result in an increase in serum potassium concentration in hypothermic rats given a potassium load compared to non-beta-blocked, hypothermic, potassium-loaded rats. To test this hypothesis, we investigated the interaction between body temperature and beta-adrenergic receptor blockade on serum potassium concentrations in ureter-ligated rats with and without potassium loading. To achieve this goal, we performed three experiments. In the first experiment, serum potassium concentrations were determined in 16 rats as they were continuously cooled from 37 degrees C to 22 degrees C. In the second experiment, 12 ureter-ligated rats were cooled to 31 degrees C, after which they were rewarmed to 37 degrees C. Serum potassium concentrations were determined before and after cooling and on rewarming. Twelve other ureter-ligated rats were cooled to 31 degrees C, then given a potassium load until their serum potassium concentrations returned to their baseline values, after which they were rewarmed to 37 degrees C. Serum potassium concentrations were determined before and after cooling, during the potassium infusion, and on rewarming. In the third experiment, 14 rats were pretreated with propranolol and 14 rats served as controls. Half of the rats in each of these two groups were kept at 37 degrees C and half were cooled to 25 degrees C. All rats were then given a 690-mumol potassium chloride infusion. Serum potassium concentrations were determined before and after the potassium infusion. RESULTS: The rats developed hypokalemia with cooling, which spontaneously resolved in the rats without supplementation on rewarming to 37 degrees C. The hypothermic hypokalemicrats that had their serum potassium concentrations corrected to normothermic status (2.93 +/- 0.17 mmol/L) had marked increases in serum potassium concentrations (4.22 +/- 0.15 mmol/L) on rewarming. In the normothermic rats, potassium loading after beta-adrenergic receptor blockade resulted in even higher serum potassium concentrations (5.65 +/- 0.36 mmol/L) compared with non-beta-blocked rats given equal potassium loads (4.6 +/- 0.4 mmol/L). However, in hypothermic (25 degrees C) rats given the same potassium load, there was no difference in serum potassium concentrations in beta-blocked (6.5 +/- 0.35 mmol/L) and non-beta-blocked rats (6.63 +/- 0.3 mmol/L). CONCLUSIONS: These results suggest that acute hypothermia causes a decrease in serum potassium, probably secondary to redistribution, which is reversible on rewarming. Supplementation of potassium during hypothermia can cause a significant increase in serum potassium concentration on rewarming. Blocking beta-adrenergic receptors with propranolol did not effect hypothermia-induced hypokalemia, suggesting that the beta-adrenergic mechanism may not be functional in hypothermia.
Authors: Aron Kerenyi; Dorottya Kelen; Stuart D Faulkner; Alan Bainbridge; Manigandan Chandrasekaran; Ernest B Cady; Xavier Golay; Nicola J Robertson Journal: Pediatr Res Date: 2012-02-07 Impact factor: 3.756