Increased quantal release of acetylcholine at the neuromuscular junction following scald injury in the rat.
Following severe burns, patients frequently develop a profound resistance to nondepolarizing neuromuscular blockers. Several mechanisms have been proposed to account for this, including upregulation of nicotinic acetylcholine receptors. We investigated the effects of a 30% body surface area (BSA) scald on neuromuscular transmission in slow-twitch soleus (SOL) and fast-twitch extensor digitorum longus (EDL) of rats. Rats were sacrificed 72 h after the injury, a time at which sepsis is unlikely and body weight gain and core temperature have returned to normal. Further groups of rats were sham operated and either pair fed to the scalded rats or freely fed to assess the influence of food restriction. When compared with muscle from pair-fed control rats, scald resulted in an almost 50% increase in miniature endplate potential (mEPP) frequency in both SOL and EDL. However, scald did not increase mean mEPP amplitude in SOL, although it did cause a 10% increase in EDL. Scald injury did produce a significant increase in the size of the evoked endplate potential in SOL (33%) and EDL (37%). These data indicate that a significant increase in the quantal content of evoked transmitter released in SOL (38%) and EDL (30%) occurred by 72 h after scald. Such an increase may contribute to the resistance to nondepolarizing neuromuscular blockers documented in patients following thermal injury.
Edwards
J P
JP
Division of Neuroscience, School of Biological Sciences, 1.124 Stopford Building, University of Manchester, Oxford Road, Manchester M13 9PT, UK.
Hatton
P A
PA
Little
R A
RA
Pennington
R A
RA
Wareham
A C
AC
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001831:Body Temperature / Q000187:drug effects / Q000502:physiology; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D002056:Burns / Q000378:metabolism* / Q000503:physiopathology; D004351:Drug Resistance; D004435:Eating / Q000187:drug effects / Q000502:physiology; D004594:Electrophysiology; D006614:Hindlimb / Q000294:innervation / Q000378:metabolism; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation / Q000378:metabolism; D009469:Neuromuscular Junction / Q000378:metabolism*; D003473:Neuromuscular Nondepolarizing Agents / Q000494:pharmacology; D018377:Neurotransmitter Agents / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar
D003473:Neuromuscular Nondepolarizing Agents; D018377:Neurotransmitter Agents; D000109:Acetylcholine