Paradoxical preservation of neural conduction by lidocaine.
The interaction of glucose lack and local anesthetic on impulse conduction was investigated in rabbit vagus nerve. Glucose lack depressed the compound action potential 50 per cent in 47 +/- 7 min (+/- SD, n = 5) and extinguished it in 69 +/- 7 min. Lidocaine hydrochloride, 0.1 mmol/1 (0.0027 g/dl), delayed the onset of inexcitability caused by glucose lack: 50 per cent depression required 85 +/- 9 min, extinction required 131 +/- 20 min (P less than 0.001). The delay decreased with lower and higher lidocaine concentrations. Lidocaine also significantly decreased the potassium loss and sodium gain occasioned by 2.5 h of glucose deprivation. Thus, delayed extinction of excitability by local anesthetic in very low concentration may be due to decrease in permeability of the axonal plasma membrane not only to sodium but also to potassium ions.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001369:Axons / Q000187:drug effects*; D005947:Glucose / Q000502:physiology*; D066298:In Vitro Techniques; D008012:Lidocaine / Q000494:pharmacology*; D009431:Neural Conduction / Q000187:drug effects*; D011188:Potassium / Q000378:metabolism; D011817:Rabbits; D012964:Sodium / Q000378:metabolism; D014630:Vagus Nerve / Q000187:drug effects / Q000378:metabolism
D008012:Lidocaine; D012964:Sodium; D005947:Glucose; D011188:Potassium