Changes in blood glucose levels following experimental cerebral hemorrhage

• Published in: Japanese Journal of Stroke Vol. 2; no. 3; pp. 215 - 220
• Main Authors: Nakazawa, Kenichi, Atarashi, Jonosuke, Terashi, Akiro, Iyoda, Kosuke
• Format: Journal Article
• Language: Japanese
• Published: The Japan Stroke Society 1980
• ISSN: 0912-0726; 1883-1923
• DOI: 10.3995/jstroke.2.215

There still remain many unexplained points concerning the incidence mechanism of the disturbance of glucose metabolism recognized in cerebrovascular diseases. The authors have already reported that hyperglycemia in cerebrovascular diseases is related to the level of cortisol and epinephrine in the blood. This time, using the rabbits with experimental cerebral hemorrhage, our studies are concerned with the relationship between the blood glucose and α- and β-effects of epinephrine, the relationship between the blood glucose and glycogen levels, periodic change of glycogen in hepatic cells, and the influence of dexamethasone on these rabbits. Consequently, the blood glucose that gradually rises following the experimental cerebral hemorrhage has been controlled by β-adrenergic blockade (propranolol). The glycogen level was in parallel with blood glucose level. In order to find out the origin of blood glucose, we carefully observed the liver sections in formaline and found out that the glycogen in the liver cells was gradually decreased. Therefore, the blood glucose level is closely related to cortisol, β-effect of epinephrine, and glycogen. Hepatic glycogen is responsible for the blood glucose increase.