Abstract

1. The effect of veratrine on nerve may be divided into two stages. The first stage shows the typical veratrine effect: a greatly augmented and prolonged after-potential. It is associated with a prolonged supernormal phase and a lowered threshold of excitation of the resting nerve. The second stage is produced by greater intensity or duration of action. The magnitude of the after-potential begins to decrease and other indications of nerve deterioration become manifest, such as decreased conduction-rate, increased relatively refractory period, raised threshold of excitation and fall of the spike height. The absolutely refractory period and the time constants of the axon spike do not change throughout the veratrinization.

2. After a period of rapid stimulation, the after-potential of veratrinized nerve is increased, and its rising-phase prolonged, SO that its maximum falls 30 to 80 sigmas after the shock. Rest brings about a return of the nerve towards its previous state.

3. During a period of asphyxia, the veratrine after-potential is decreased; with the readmission of oxygen, the after-potential is increased above its initial value, and assumes the form seen after rapid stimulation.

4. Cooling decreases the veratrine after-potential; this change is less rapidly reversible on warming than is the change in spikeform.

5. Anesthetics (urethane, ether vapor) may either increase or decrease the amplitude of the veratrine after-potential. They tend to prolong the rising-phase of the after-potential.

6. Protoveratrine and aconitine produce a prolonged after-potential much lower than that caused by veratrine.