Intensive care medicine experimental · 2026
The effect of dexmedetomidine on rocuronium-induced neuromuscular blockade and its reversal by sugammadex.
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Fedor Marianna, Sallai Nikolett, Fülesdi Béla, Fábián Ákos I
Аннотация
BACKGROUND: Dexmedetomidine (DEX) is increasingly used in the intensive care unit for sedation and also serves as an adjuvant in general anesthesia and in procedural sedations. We tested whether dexmedetomidine at different concentrations influences the activity of the neuromuscular junction at the diaphragm and whether DEX has an impact on the action of rocuronium at the diaphragm as well as the reversal of the neuromuscular block by sugammadex.
METHODS: 20 male Wistar rat phrenic nerve-hemidiaphragm system was used for our experiments. The concentration-response characteristics of DEX and rocuronium were quantified as the depression of the force amplitude of single twitches (ST) in response to electrical stimulation of the phrenic nerve. Rocuronium concentration-response curves were obtained with 0, 1, and 2.67 μg/ml DEX concentration. After a single dose of rocuronium, sugammadex doses were given until additional doses of sugammadex were not accompanied by a further increase in ST force amplitude. The concentration-response curve of sugammadex was also measured in the presence of 1 μg/ml DEX concentration.
RESULTS: DEX at different doses negligibly reduces the force of the contractions and the contractility of the diaphragm. The EC50 of rocuronium [7.74 µM (6.99-8.57)] did not change significantly [7.18 µM (6.58-7.84); p = 0.27] with the addition of DEX 1 µg/ml. At 2.67 µg/ml DEX concentration, the ED50 of rocuronium was significantly reduced [6.37 µM (5.69-7.13); p = 0.015]. With 1 µg/ml DEX concentration, the EC50 of the sugammadex [2.04 µM (1.94-2.14)] needed for the reversal of rocuronium-induced neuromuscular blockade was significantly increased [2.45 µM (2.39-2.51); p < 0.01].
CONCLUSIONS: DEX at clinically administered doses does not significantly influence the function of the neuromuscular junction at the diaphragm. Under routine dosing conditions, the action of the neuromuscular blocking agents and their reversal by sugammadex are also not modified by DEX.
METHODS: 20 male Wistar rat phrenic nerve-hemidiaphragm system was used for our experiments. The concentration-response characteristics of DEX and rocuronium were quantified as the depression of the force amplitude of single twitches (ST) in response to electrical stimulation of the phrenic nerve. Rocuronium concentration-response curves were obtained with 0, 1, and 2.67 μg/ml DEX concentration. After a single dose of rocuronium, sugammadex doses were given until additional doses of sugammadex were not accompanied by a further increase in ST force amplitude. The concentration-response curve of sugammadex was also measured in the presence of 1 μg/ml DEX concentration.
RESULTS: DEX at different doses negligibly reduces the force of the contractions and the contractility of the diaphragm. The EC50 of rocuronium [7.74 µM (6.99-8.57)] did not change significantly [7.18 µM (6.58-7.84); p = 0.27] with the addition of DEX 1 µg/ml. At 2.67 µg/ml DEX concentration, the ED50 of rocuronium was significantly reduced [6.37 µM (5.69-7.13); p = 0.015]. With 1 µg/ml DEX concentration, the EC50 of the sugammadex [2.04 µM (1.94-2.14)] needed for the reversal of rocuronium-induced neuromuscular blockade was significantly increased [2.45 µM (2.39-2.51); p < 0.01].
CONCLUSIONS: DEX at clinically administered doses does not significantly influence the function of the neuromuscular junction at the diaphragm. Under routine dosing conditions, the action of the neuromuscular blocking agents and their reversal by sugammadex are also not modified by DEX.