A further very interesting example of depression produced by oxygen deficiency is furnished by _heat depression_. It has long been known that with increasing temperature the vital manifestations of all poikilothermic organisms at first undergo a heightening of their intensity. If, however, after a maximum is reached, the temperature is still further increased a sudden depression sets in. The increase in the rapidity of the vital process as a result of increased temperature is readily understood when based on the well-known law discovered by _van’t Hoff_. Numerous investigations on the rapidity of the course of special vital manifestations, as, for instance the growth of the eggs of the frog and sea urchin, the assimilation of carbon dioxide in green plant cells, the number of vacuole pulsations in the infusoria cells, the frequency of the heart rate of the frog and of the mammal, etc., have shown that their increase does in fact follow the _van’t Hoff_ law, being doubled or tripled in amount with every increase of ten degrees of temperature. The genesis of depression produced by _heat_, developed in different organisms at various heights of temperature, requires a closer analysis. This depression takes place at temperatures below that in which coagulation of proteins occurs. Therefore, under certain conditions, with which we shall presently become acquainted, it is capable of being recovered from, whereas in higher temperatures, in which albumen coagulates, vital activity is permanently obliterated. Depression produced by heat is, therefore, in itself not a necrobiotic process, which, as such, must necessarily lead to death. But rather like fatigue it must be looked upon as an asphyxiation process. Its relations to oxygen exchange have been chiefly demonstrated by _Winterstein_[202] by his investigations on the central nervous system of frogs and on medusæ. He found that when placed in a heated chamber in a temperature of 32–40° the activity and reflex excitability of the frog are at first augmented. Within the lapse of a short time this increase has become so great that the slightest touch produces tetanic contractions, similar to those characteristic of strychnine poisoning. Very soon, however, this state of high excitation is followed by one of depression, in which no response to stimuli can be obtained. The animal remains entirely motionless in any position in which it is placed, in the same manner as a frog whose nerve centers have been completely exhausted by strenuous activity. On the basis of our knowledge of the rôle played by the deficiency of oxygen in the bringing about of exhaustion the thought arose, if in this heat depression exhaustion might not likewise be the result of oxygen deficiency. This assumption has been most strikingly confirmed by the investigations of _Winterstein_. It has been demonstrated that recovery of the animal in a state of heat depression cannot be obtained by mere