In man, ordinary medicinal doses do not affect respiration, but 10 to 20 min. may render it irregular and labored. Under small doses, the breathing-rate of animals either remains unaltered at first, or is markedly lowered; it is never increased. With larger doses and concentrated solutions, the course of poisoning is so rapid that respirations can scarcely be counted; convulsive movements also interfere with observation, but we can say that in this stage the rate is lowered, and continues so. As the animal passes into a comatose condition, a slight rise may occur, which increases if recovery is proceeding, but which soon gives place to a marked slowing and then complete cessation of breathing. The heart may continue to beat for some little time after this, and if so, even if in other respects the animal seems dead, artificial respiration will restore it to life.

The general character of the respiratory changes resembles (according to Preyer), not that occurring in apnoea, but that which occurs when the vagi are divided and the cut end of the central branch is stimulated, or irritated, by electricity. At the beginning of the poisoning the inspirations are deeper than normal, then follows a pause, and then short shallow expirations. In many instances during the convulsive stage there occurs on inspiration a tetanic spasm of the diaphragm, such as Traube found after direct vagus irritation.

1 The glistening condition of the eye usually described, and the evacuation of the bladder and bowel, are not, I think, so constant as commonly supposed: in four cases within my experience, the former symptom was not present, and in only one did the evacuations occur.