Diuretics
In patients undergoing renal transplantation, the intensity and
duration of dTc neuromuscular blockade is increased after a dose of furosemide (1
mg/kg intravenously).[542]
Furosemide reduced the
concentration of dTc required to achieve 50% depression of twitch tension in the
indirectly stimulated rat diaphragm and intensified the neuromuscular blockade produced
by dTc and succinylcholine.[543]
Furosemide appears
to inhibit the production of cyclic adenosine monophosphate. Breakdown of adenosine
triphosphate is inhibited and results in reduced output of acetylcholine. Acetazolamide
has been found to antagonize the effects of anticholinesterases in the rat
phrenic-diaphragm preparation.[544]
However, in
one report, 1 mg/kg furosemide facilitated recovery of the evoked twitch response
after pancuronium.[545]
Chronic furosemide treatment
had no effect on either dTc- or pancuronium-induced neuromuscular blockade.[546]
By contrast, mannitol appears to have no effect on nondepolarizing
neuromuscular blockade. Furthermore, increasing urine output by the administration
of mannitol or other osmotic or tubular diuretics has no effect on the rate at which
dTc and presumably other neuromuscular blockers are eliminated in urine.[230]
However, this lack of effect on excretion of dTc should not be surprising. Urinary
excretion of all neuromuscular blockers that are long acting depends primarily on
glomerular filtration. Mannitol is an osmotic diuretic that exerts its effects by
altering the osmotic gradient within the proximal tubules so that water is retained
within the tubules. An increase in urine volume in patients with adequate glomerular
filtration therefore would not be expected to increase the excretion of neuromuscular
blockers.
