Mild hypothermia preserves contractile function and inhibits prostaglandin E2 release from metabolically stressed skeletal muscle.
An in vitro model of muscle damage was used to investigate the protective effect of mild hypothermia in muscle injury. Rat epitrochlearis muscles were dissected in their entirety and suspended in Krebs-Ringer solution and DNP, a mitochondrial uncoupler, was added. PGE2 and lactate release and the contractile response to stimulation were measured and compared to untreated controls. Experiments were done at 37, 35, 33 and 27 degrees C. At 37 degrees C, DNP stimulated muscle releases large amounts of PGE2 and lactate and is unable to contract. As the temperature is reduced, there is progressive preservation of contractile force, although high lactate levels at the lowest temperatures indicate that the metabolic stress is still present. In contrast, DNP stimulated PGE2 release is completely inhibited at or below 35 degrees C and may be related to a similar protective phenomenon seen in experimental ischemic neuronal death.
Cwik
V A
VA
Division of Neurology, University of Alberta, Edmonton, Canada.
Majumdar
R
R
Brooke
M H
MH
D000818:Animals; D003080:Cold Temperature; D004140:Dinitrophenols / Q000494:pharmacology; D015232:Dinoprostone / Q000378:metabolism*; D004558:Electric Stimulation; D007036:Hypothermia, Induced; D066298:In Vitro Techniques; D007700:Kinetics; D007773:Lactates / Q000378:metabolism; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009132:Muscles / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D004140:Dinitrophenols; D007773:Lactates; D015232:Dinoprostone