Effects of adenosine receptor agonist on the rocuronium-induced neuromuscular block and sugammadex-induced recovery.
- Author:
Yong Beom KIM
1
;
Sangseok LEE
;
Hey Ran CHOI
;
Junyong IN
;
Young Jin CHANG
;
Ha Jung KIM
;
Young Jin RO
;
Hong Seuk YANG
Author Information
- Publication Type:Original Article
- Keywords: Adenosine A₁-receptor; Neuromuscular junction; Neuromuscular nondepolarizing agents; Rocuronium; Sugammadex
- MeSH: 2-Chloroadenosine; Acetylcholine; Adenosine*; Adult; Data Collection; Depression; Humans; Membranes; Neuromuscular Blockade*; Neuromuscular Junction; Neuromuscular Nondepolarizing Agents; Rats, Sprague-Dawley; Reaction Time; Receptor, Adenosine A1; Receptors, Purinergic P1*
- From:Korean Journal of Anesthesiology 2018;71(6):476-482
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Several types of receptors are found at neuromuscular presynaptic membranes. Presynaptic inhibitory A1 and facilitatory A2A receptors mediate different modulatory functions on acetylcholine release. This study investigated whether adenosine A1 receptor agonist contributes to the first twitch tension (T1) of train-of-four (TOF) stimulation depression and TOF fade during rocuronium-induced neuromuscular blockade, and sugammadex-induced recovery. METHODS: Phrenic nerve-diaphragm tissues were obtained from 30 adult Sprague-Dawley rats. Each tissue specimen was randomly allocated to either control group or 2-chloroadenosine (CADO, 10 μM) group. One hour of reaction time was allowed before initiating main experimental data collection. Loading and boost doses of rocuronium were sequentially administered until > 95% depression of the T1 was achieved. After confirming that there was no T1 twitch tension response, 15 min of resting time was allowed, after which sugammadex was administered. Recovery profiles (T1, TOF ratio [TOFR], and recovery index) were collected for 1 h and compared between groups. RESULTS: There were statistically significant differences on amount of rocuronium (actually used during experiment), TOFR changes during concentration-response of rocuronium (P = 0.04), and recovery profiles (P < 0.01) of CADO group comparing with the control group. However, at the initial phase of this experiment, dose-response of rocuronium in each group demonstrated no statistically significant differences (P = 0.12). CONCLUSIONS: The adenosine A1 receptor agonist (CADO) influenced the TOFR and the recovery profile. After activating adenosine receptor, sugammadex-induced recovery from rocuronium-induced neuromuscular block was delayed.
