Hemlock is probably most dangerous to live stock in the spring, when green herbage is least plentiful and the young shoots of hemlock are fresh and short. Chesnut says that the root is nearly harmless in March, April and May, but dangerous later, especially in the first year of growth; but Esser states that it is only poisonous in the spring. The foliage is more poisonous before flowering than after, when the poisonous principle passes to the fruits, which are more poisonous before ripening (three quarters ripe) than afterwards. Pott remarks that after eating hemlock cows give milk with a bad taste. _Toxic Principle._ Early in summer the toxic principle appears to be chiefly contained in the foliage, but later in the fruit, particularly when still green. Among the substances contained in hemlock are the toxic alkaloid _Coniine_ (C_{8}H_{17}N), the poisonous _Coniceine_ (C_{8}H_{15}N), _Conhydrine_ (C_{8}H_{17}NO), the alkaloid _Methylconiine_ (C_{9}H_{19}N), _Pseudoconhydrine_ (C_{8}H_{17}ON). Coniine may be described as an oily, colourless, quite volatile liquid, quickly turning brown on exposure to the air, and giving a mousy odour to the whole plant. The amount of Coniine in the fresh leaves is given (Pammel) as 0·095 per cent., but in the ripe seeds 0·7 per cent. English fruits contain much more of the total alkaloids than imported fruits. Owing to the volatile character of the poisons hemlock largely loses its toxicity when dried in hay, and is therefore the less likely to prove injurious to domestic animals. _Symptoms._ Hemlock is a dangerous narcotic plant. Even the smallest quantities may cause inflammation of the digestive organs, paralysis and death. The general symptoms are salivation, bloating, dilatation of pupils, rolling of eyes; laboured respiration, diminished frequency of breathing, irregular heart action; loss of sensation, convulsions, uncertain gait, falling, and at the end complete paralysis. Death occurs after a few hours. The poison acts on the motor nerve endings, causing paralysis, dyspnœa resulting from paralysis of the pectoral nerves, and acceleration of the heart from that of the inhibitory fibres of the pneumogastric. Small quantities cause in the _horse_ a little prostration, yawning, acceleration of pulse, dilatation of pupils and sometimes muscular spasms of the neck and shoulders. Large quantities cause nausea, unsuccessful attempts to vomit, gritting of teeth, accelerated respiration and dyspnœa, and muscular tremors commencing in posterior members and spreading to anterior members and spine. There is next difficulty of locomotion, sweating (but not continual), falling, paraplegia, then paralysis, loss of feeling, lowering of temperature, rapid pulse, increasingly difficult respiration, and death from stoppage of respiration.