Goldhill D R, Martyn J A, Hoaglin D C
Br J Anaesth. 1987 May;59(5):611-6. doi: 10.1093/bja/59.5.611.
A study involving 20 mongrel dogs tested the hypotheses that beta-adrenoceptor blockade or alpha-adrenoceptor stimulation may potentiate and prolong the increase in plasma potassium concentration after suxamethonium administration, and that the beta effect is beta 2-receptor mediated. Propranolol 0.5 mg kg-1 altered the time to peak increase in plasma concentration of potassium after suxamethonium, but did not increase peak concentrations. In controls, the maximum change (0.83 mmol litre-1) occurred at 3 min, while in propranolol-treated dogs the peak change (0.96 mmol litre-1 occurred at 30 min. Similar results were obtained when metoprolol 0.25 mg kg-1 and ICI 118551 0.1 mg kg-1 were used, respectively, as selective beta 1- and beta 2-adrenoceptor blockers. The increases in potassium concentration following suxamethonium in the metoprolol group (0.98 mmol litre-1) and the ICI 118551 group (0.82 mmol litre-1) reached maximum concentrations at 30 min compared with the controls (0.79 mmol litre-1) which achieved a maximum at 3 min. Phenylephrine was infused at 8 micrograms kg-1 min-1 to produce alpha stimulation. The infusion alone altered plasma concentrations of potassium, but the haemodynamic changes were such that conclusions as to the effect of alpha-stimulation on release of potassium after suxamethonium could not be reached.
