Purpose: These studies were intended to resolve the conflict between t
he reasonable inference from the scientific literature that atropine m
ight alter neuromuscular fade and the expectation from informal clinic
al experience that it does not. Methods: We examined the effect of a h
igh concentration of atropine (20 mu M) on moderate neuromuscular bloc
k and fade produced by d-tubocurarine (dTC). Isometric twitch tension
was measured in the mouse phrenic nerve-diaphragm preparation. In one
set of experiments, the phrenic nerve was stimulated with trains of 5
pulses at 10 Hz every second. Block and fade were measured in two grou
ps, control and with atropine (n = 6 each). In another set of experime
nts, the phrenic nerve was stimulated with standard train-of-four stim
ulation (TOF, 4 pulses at 2 Hz every 11.5 seconds). Block and fade wer
e measured first in a control period and then in a treatment period wi
th either saline (n = 4) or atropine (n = 4). Results: During 10 Hz tr
ain stimulation, atropine had no significant effect on either the bloc
k of the first twitch (control. 62 +/- 17; atropine: 75 +/- 4) or fade
(control: 55 +/- 12: atropine; 57 +/- 14) produced by dTC. Similarly,
atropine did not differ significantly from saline in altering dTC-ind
uced block of first twitch (saline: 99.5 +/- 14; atropine 92.5 +/- 9.6
% control) or fade (saline 119 +/- 50; atropine 102 +/- 30% control) d
uring TOF stimulation. Conclusions: While atropine may alter ACh relea
se under some conditions, its action is not great enough to alter eith
er block or fade.