[Transient augmentation of the evoked spinal cord and peripheral nerve action potentials through ischemia (author's transl)].
An experimental study was carried out on the mechanism of transient augmentation of the evoked spinal cord action potentials, which was reported to be one of the characteristic phenomena of spinal cord ischemia. In twenty curarized cats, four spinal potentials (I, II potentials evoked by epidural stimulation and I', II' by median nerve stimulation) and median nerve evoked potential were measured when the blood supply was cut off completely through a clamping of ascending aorta. Amplitude of I, II and I' potentials as well as that of median nerve evoked potential increased in 2-3 minutes after the interruption of blood flow. Such augmentation showed a close relationship with the strength of stimulation; the weaker the stimulation, the larger the rate of augmentation, suggesting a significant role of subliminal fringe and an increased excitability of nerve fibers under ischemia in this phenomenon. Requisites for such enhancement were 1) ischemia of neural tissue, 2) careful observation on early transient changes, 3) relatively weak stimulation within 2-3 times of threshold. The amplitude of II' potential was reduced rapidly within one minute and disappeared in five minutes after clamping aorta, suggesting that this potential was postsynaptic in nature. Latencies of those spinal cord and median nerve evoked potentials increased gradually through ischemia, which also could be explained by an increased excitability of small fibers in ischemic condition.
D000200:Action Potentials; D000818:Animals; D002415:Cats; D004558:Electric Stimulation; D005071:Evoked Potentials; D007511:Ischemia / Q000503:physiopathology*; D010525:Peripheral Nerves / Q000503:physiopathology*; D013116:Spinal Cord / Q000098:blood supply* / Q000503:physiopathology