THE EFFECT OF PONTINE TRANSECTION ON THE BLOOD‐SUGAR LEVEL OF THE DECEREBRATED FASTING CAT

Mid‐brain decerebration in the fasting cat resulted, an hour later, in an average blood sugar of 220 mg. per cent., tending to rise to about 250 mg. in 3 hours' time, thereafter falling slowly. When decerebration was through the pons, the level was at first some 30 mg. higher, and in 4 hours rose to almost 340 mg. The initial high sugar consequent on mid‐brain decerebration was not maintained in absence of the adrenals (removed just after decerebration). “Bleeding back” behind the tentorium disturbed markedly both respiration and blood‐sugar concentration, preventing the usual fall of the latter. Destruction of the pituitary, immediately after decerebration, did not make the rate of change of blood sugar any different from that in animals where it was left in situ (though cut off from the brain stem). Cutting, at the start of the experiment, all the structures at the liver hilum, save the portal vein, did not alter the usual behaviour of the blood sugar of the decerebrate animal. Cutting at a later stage was followed by a slight rise in blood pressure, and an average rise of 50 mg. in blood sugar, apparent even in the adrenalectomised animal. High concentrations of liver glycogen did occur 3 hours after decerebration but the average value was 1–3 per cent. Decerebrate animals with high liver glycogen at this stage usually had a high initial, slowly falling blood sugar. Pontine transection some time after decerebration was followed by an average rise in blood sugar of 70 mg. A perceptible, though very small, rise in sugar occurred in absence of adrenals or of hepatic nerves (the latter were cut about 3 hours after decerebration). If the nerves had been out immediately after decerebration the rise in sugar following transection was just as great as when both adrenals and nerves were intact. In absence of adrenals and hepatic nerves, transection of the pons did not interrupt the trend of blood sugar evidenced prior to the section. The main cause of the blood‐sugar rise following transection of the pons of the fasting decerebrate animal is certainly liberation of adrenaline from the suprarenals. A considerable rise in blood pressure followed pontine transection even in the adrenalectomised decerebrate animal. Destroying the hepatic nerves by tearing and application of phenol left an appreciably higher liver glycogen content than when all the hilum structures save the portal vein were cut, suggesting that the arterial flow to the liver may be of consequence in this connection. The author acknowledges with thanks his indebtedness to the Medical Research Council for a grant in aid of expenses; to Professor Brocklehurst for facilities in the Department of Physiology, University of Bristol, where part of the investigation was carried out; to the late Professor J. J. R. Macleod, and to Professor A. Hemingway and Dr. J. M. Peterson for their interest and encouragement.