R J Storella1, T S Ackerman. 1. Department of Anesthesiology, Medical College of Pennsylvania and Hahnemann University, Philadelphia, PA 19102, USA.
Abstract
PURPOSE: These studies were intended to resolve the conflict between the reasonable inference from the scientific literature that atropine might alter neuromuscular fade and the expectation from informal clinical experience that it does not. METHODS: We examined the effect of a high concentration of atropine (20 microM) on moderate neuromuscular block 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 groups, control and with atropine (n = 6 each). In another set of experiments, the phrenic nerve was stimulated with standard train-of-four stimulation (TOF, 4 pulses at 2 Hz every 11.5 seconds). Block and fade were measured first in a control period and then in a treatment period with either saline (n = 4) or atropine (n = 4). RESULTS: During 10 Hz train stimulation, atropine had no significant effect on either the block 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-induced block of first twitch (saline: 92.5 +/- 14; atropine 92.5 +/- 9.6% control) or fade (saline 119 +/- 50; atropine 102 +/- 30% control) during TOF stimulation. CONCLUSIONS: While atropine may alter ACh release under some conditions, its action is not great enough to alter either block or fade.
PURPOSE: These studies were intended to resolve the conflict between the reasonable inference from the scientific literature that atropine might alter neuromuscular fade and the expectation from informal clinical experience that it does not. METHODS: We examined the effect of a high concentration of atropine (20 microM) on moderate neuromuscular block 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 groups, control and with atropine (n = 6 each). In another set of experiments, the phrenic nerve was stimulated with standard train-of-four stimulation (TOF, 4 pulses at 2 Hz every 11.5 seconds). Block and fade were measured first in a control period and then in a treatment period with either saline (n = 4) or atropine (n = 4). RESULTS: During 10 Hz train stimulation, atropine had no significant effect on either the block 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-induced block of first twitch (saline: 92.5 +/- 14; atropine 92.5 +/- 9.6% control) or fade (saline 119 +/- 50; atropine 102 +/- 30% control) during TOF stimulation. CONCLUSIONS: While atropine may alter ACh release under some conditions, its action is not great enough to alter either block or fade.