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Effects of salbutamol and hyperventilation on the rise in serum potassium after succinylcholine administration
Author(s) -
Inaba H.,
Ohwada T.,
Sato J.,
Mizuguchi T.,
Hirasawa H.
Publication year - 1987
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1987.tb02615.x
Subject(s) - hyperventilation , salbutamol , medicine , respiratory alkalosis , endocrinology , potassium , agonist , metabolic alkalosis , pco2 , anesthesia , receptor , metabolic acidosis , asthma , chemistry , organic chemistry
It is known that circulating catecholamines stimulating betas‐receptors and the acid‐base balance play important roles in the regulation of serum potassium (K+). The present study was undertaken to investigate the effect of salbutamol (SB), a highly selective beta 2 agonist, and hyperventilation (HV)‐induced alkalosis on the change in serum K.+ after succinylcholine (SCh) administration in dogs. Pretreatment with SB (0.4 μg · kg ‐1 · min ‐1 for 30 min) produced sustained decreases in serum K+ and mean arterial pressure, and transient increases in cardiac, output and serum insulin concentration. Maintaining repiratory alkalosis with HV (Paco 2 = 2.6–3.3 kPa) produced sustained decreases in serum K+ and cardiac output. Although both pretreatment with SB and HV‐induced alkalosis significantly reduced the absolute increases in serum K+ after SCh, the effect of SB was more remarkable than that of HV. These results suggest that the degree of beta 2 ‐receptor activity can strongly modulate the change in serum K+ after SCh administration.