Peripheral nerve reconnection: inhibition of early degenerative processes through the use of a novel fluid medium.
Two pharmacologic manipulations were applied to injured nerves in the rat to minimize the secondary damage that accompanies peripheral nerve transection. It is known that calcium influx into the nerve is responsible for some of the processes that have been termed Wallerian degeneration. These disruptive effects of high intracellular calcium were retarded by chlorpromazine, a potent inhibitor of calmodulin. Our results suggested a new method for reducing posttraumatic neural disruption and supported our hypothesis regarding the involvement of calmodulin or some other Ca2+ binding protein in Wallerian degeneration. The second part of this report describes changes observed at the tips of a severed nerve and their prevention through the use of polyvinyl alcohol. Finally, we showed that neither substance produced functional deficits when injected directly into the sciatic nerve of rats and could thus be used in animal experimentation.
D000818:Animals; D001370:Axonal Transport / Q000187:drug effects; D002118:Calcium / Q000502:physiology; D002746:Chlorpromazine / Q000494:pharmacology*; D003470:Culture Media / Q000494:pharmacology; D004338:Drug Combinations; D009410:Nerve Degeneration / Q000187:drug effects*; D011142:Polyvinyl Alcohol / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012584:Sciatic Nerve / Q000502:physiology*; D014855:Wallerian Degeneration / Q000187:drug effects
D003470:Culture Media; D004338:Drug Combinations; D011142:Polyvinyl Alcohol; D002118:Calcium; D002746:Chlorpromazine