Abstract
The present investigations were made on dogs in order to ascer-tain whether or not the heat-tachypnoea of the reflex nature is still causable after removing the centers for the body temperature regulat-ing mechanism, as that of the central nature, such as is elicitable by warming the carotid arteries.
By raising the environmental temperature, the dog, without nar-cotizing, reacted by heat-tachypnoea; at its onset the body tempera-ture was usually normal or a little decreased, or only slightly raised, as well known.
The corpus striatum, the thalamus opticus, and the tuber cine-rum were removed; no narcosis was used, and about one hour was. allowed to elapse before the next warming experiment for recovery from the operative shock.
Afterwards no heat-tachypnoea of the reflex nature was elicited. contrary to that of the central origin. Some acceleration in the re-spiratory rate was always preceded by a material rise of the body temperature; that is, there was no evidence of heat-tachypnoea of the reflex nature occurring.
In the majority of cases where some considerable tachypnoea, such as 90-200 breathing per min., appeared after the brain opera-tion on raising the environmental temperature or on warming the -carotid arteries (S ato and Nemoto), whereby the body temperature was raised, the brain lesion was identical in essential points to that causable by the decerebration of Sherrington. This shows: So far as the midbrain remains nearly intact or even if the anterior col-liculi be excluded, although the brain portions anteriorto it be wholly removed or destroyed, the heat-tachypn oea is capable of being brought about by raising the temperature thereof or the body temperature.
From the above outcome it may be justifiable to conclude:
(1) The central mechanism for regulating the body temperature is indispensable for causing the heat-tachypnoea of the reflex origin.
(2) The heat-tachypnoea of the central origin is induciable if the brain anterior to the midbrain or even the anterior colliculi are excluded.
