1 n systolic blood pressure were unaffected by vecuronium.

2  was observed for pancuronium competing with vecuronium.

3 est physiotherapy session and midazolam plus vecuronium (0.7 mg/kg) before a subsequent session.

4 ity of the nicotinic ACh receptor antagonist vecuronium (1 microM) to depress evoked ACh release at 5

5 ng therapy, p < .05), was not accentuated by vecuronium (30 +/- 4 torr [4.0 +/- 0.5 kPa] to 35 +/- 6

6 otinamide and bulkier organic cations (e.g., vecuronium and decynium-22) inhibited the uptake of 3H-M

7 .5 (0.3-2.9) for cisatracurium, pancuronium, vecuronium, and rocuronium, respectively.

8 ive antagonists: cisatracurium, pancuronium, vecuronium, and rocuronium.

9 ly ventilated and paralyzed by using 1 mg/kg vecuronium bromide followed by 0.1 mg.kg(-1).hr(-1).

10                 All subjects were paralyzed (vecuronium bromide) and ventilated with room air, while

11                        The administration of vecuronium completely suppressed the 50% increases in VO

12                     However, pancuronium and vecuronium each shifted the apparent IC(50) of (+)-tuboc

13               The total cumulative amount of vecuronium for the episode of paralysis was greater in t

14  shift the apparent IC(50) of pancuronium or vecuronium, indicating independent binding of these two

15 l medical patients results in lower doses of vecuronium to maintain a desired depth of paralysis, and

16                               Atracurium and vecuronium were the most commonly used agents.