ABSTRACT
BACKGROUND: Aminophylline is an inhibitor of phosphodiesterase; it increase the cAMP and, in turn, the level of acetylcholine at the neuromuscular junction. In doing so, it has an antifatigue action. It antagonizes nondepolarizing neuromuscular blockade in animals, and has been anecdotally noted to do so in humans, as well. We investigated the interaction of aminophylline and vecuronium on the dose response curve in vitro. METHODS: Institutional approval was obtained. Thirty seven male Spague Dawley rats (150~200 g) were divided into four groups (control, aminophylline 2.5, 5.0 and 7.5 microgram/ml). The animal were anesthetized with 40 mg/kg phentobarbital. The left hemidiaphragm with phrenic nerve was dissected and mounted within 5 minutes in bath containing 100 ml Krebs solution at 32oC. The phrenic nerve was stimulated at supramaximal intensity by a Grass S88 stimulator through an SIU5 isolation unit. The twitch height was measured by precalibrated Grass FT03 force displacement transducer and recorded. After stabilization of twitch response, vecuronium was added to the solution to obtained an initial concentration 1.0 microgram/ml with aminophylline 0, 2.5, 5.0, or 7.5 microgram/ml. When a stable 3~5 twitch was obtained after first dose, additional vecuronium was added to the Krebs solution in increments of 0.5 microgram/ml to achieve a more than 90% neuromuscular block. The data were analyzed by repeated measures of ANOVA and kappa2 test. RESULTS: There was a significant increase in the effective dose of vecuronium needed to depress the twitch response in aminophylline 5.0 and 7.5 microgram/ml added groups compared with control group and aminophylline 2.5 microgram/ml group. CONCLUSIONS: We conclude that aminophylline shows decreased sensitivity to vecuronium in the phrenic nerve diaphragm preparation of rats.