Under the technique described above, 20 to 50 c.c. of blood from animals in pancreatic diabetes and showing the typical diabetic polyphagia were transfused into normal animals. The results were practically identical with those from the blood of starving animals, that is, a temporary stimulation of the gastric hunger mechanism.
From 20 to 50 c.c. of blood from normal dogs or from dogs whose digestion was at its height were transfused into dogs while their gastric tonus and hunger contractions were being registered. In the majority of these experiments the transfusion had no effect at all on the motor condition of the empty stomach. In a few cases it acted as a very slight and transient stimulus, but in no instance did the blood from normal animals produce the marked effects obtained from the blood of starving and of diabetic animals. Hence we conclude that the latter results are due to something in the blood of starving and of diabetic animals not present, or present in less concentration, in the blood of normal animals. It is evidently not due to the transfusion of the above-named quantities of defibrinated blood as such, although defibrinated blood contains a substance which induces contraction in vascular and intestinal muscle. The intravenous injections of 20 to 50 c.c. of 0.9 per cent NaCl is also without effect on the hunger mechanism.
It is well known that intravenous injections of considerable quantities of fresh defibrinated blood may cause temporary vasomotor and cardiac disturbances. Lowering of the arterial blood pressure is usually a feature of these disturbances. Is vasodilation a factor in the marked results produced by blood from starving and diabetic animals? The following control tests were made: A mixture of 1 per cent peptone in 0.9 per cent NaCl was injected intravenously, and amyl nitrite was administered by inhalation. If sufficient peptone or amyl nitrite is given to affect the gastric tonus and hunger contractions, this effect is always in the direction of inhibition and paralysis. It is not clear, however, that this inhibition is due solely to the vasodilation, but the experiments show that a moderate general vasodilation does not necessarily lead to stimulation of the gastric hunger apparatus.
As a preliminary step in the analysis of the stimulation of the gastric hunger mechanism by starved and diabetic blood, we have tested the action of acetone and oxybutyric acid on the gastric hunger contractions. It is well known that prolonged starvation as well as diabetes leads to acidosis, although there is practically no acidosis in pancreatic diabetes in dogs (Mariott). It seemed possible that the acetone bodies might be the stimulating factors in the starvation and the diabetic blood. The action of the acetone bodies dissolved in Ringer's solution was tested on a number of animals with uniformly negative results. That is to say, the acetone bodies in concentrations that affect the gastric hunger apparatus at all cause inhibition and depression. No indication of any primary or secondary stimulation by the acetone bodies could be secured. It is therefore clear that the stimulating action of starvation and diabetic blood on the hunger mechanism is not due, at least not directly, to the acetone bodies.