脳血管障害における糖代謝異常に関する研究

Abstract

In order to clarify the incidence mechanism of the disturbance of glucose metabolism recognized during the acute stage of cerebrovascular disease, a study was made by performing an intravenous glucose tolerance test, and the relationship between the clinical symptoms and glucose metabolism disturbance was investigated. Moreover, rabbits were used as experimental animals, and cerebral hemorrhage was produced experimentally by the cold injury method deviced by Klatzo. The levels of the blood glucose (B. G.), insulin, and cortisol were examined periodically. Furthermore, the influence of β-adrenergic blockade (propranolol) on the blood glucose level measured on the rabbits with experimental cerebral hemorrhage was investigated, and the following results were obtained.Through the clinical observations on the cases of cerebrovascular diseases, the disturbance of glucose metabolism was severe in the cases of cerebral hemorrhage, particularly intraventricular hemorrhage, in comparison to that of cerebral infarction. Those with poor prognoses such as severe disturbance of consciousness, high C.S.F. -pressure, and intraventricular hemorrhage revealed severer than all the others. That is, the more intense stress on the brain caused the severer disturbance of glucose metabolism.In the experimental cerebral hemorrhage, the group of severe injury revealed higher B.G. level, that is hyperglycemic response curve. In the same group, the cortisol level in blood was recognized higher. The hyperglycemic response curve was controlled by administering propranolol. Also, the B.G. level of the internal carotid vein on the damaged hemisphere during the earlier stage of the injury was lower than the other. This means that the glucose uptake in the brain was increasing on the damaged hemisphere.The above results explain that the disturbance of glucose metabolism in cerebrovascular disease is due to the higher cortisol level resulted from the active function of pituitary adrenocortical system and also to the β-adrenergic receptors by epinephrine. This hyperglycemia is possibly related to biological reaction to repair cerebral injury and the lowered function of the brain.