The effect of immobilization on subsequent sensitivity of liMD muscles to d-tubocurarine was examined in a guinea pig model. A foreleg was immobilized in a cast for 1–4 weeks. At the end of this period, isolated nerve-luMDrical muscle preparations were set up and sensitivity to d-tubocurarine assayed. Immobilization increased the ED50 of the drug not only in muscles from the liMD in the cast but also those from contralateral foreliMDs and from hindliMDs. The increase in ED50 was not accompanied by atrophy. In a parallel series of experiments measuring the effect of d-tubocurarine on depolarization by carbachol, the apparent d-tubocurarine-receptor dissociation constant was determined. Immobilization produced no change in this parameter. Because immobilization of one extremity produced sensitivity changes in others, the anesthesiologist must be careful not to assume that monitoring from any liMD will yield normal values in a patient with partial immobility.
[1]
G. Gronert.
Disuse atrophy with resistance to pancuronium.
,
1981,
Anesthesiology.
[2]
H. H. Ali,et al.
Increased d-tubocurarine requirement following major thermal injury.
,
1980,
Anesthesiology.
[3]
D. H. Graham.
Monitoring neuromuscular block may be unreliable in patients with upper-motor-neuron lesions.
,
1980,
Anesthesiology.
[4]
W. Snider,et al.
A physiological correlate of disuse-induced sprouting at the neuromuscular junction
,
1979,
Nature.
[5]
G. Fischbach,et al.
Effect of chronic disuse of rat soleus neuromuscular junctions on postsynaptic membrane.
,
1971,
Journal of neurophysiology.
[6]
P. Fatt.
The electromotive action of acetylcholine at the motor end‐plate
,
1950,
The Journal of physiology.