Ischemia in the brain: The effects of carotid artery ligation and decapitation on the energy state of the awake and anesthetized rat

The metabolic state of the awake cerebral cortex was evaluated by monitoring the intramitochondrial NADH level using a non-invasive technique (time-sharing fluorometer/reflectometer). The blood supply to the brain was altered by unilateral or bilateral carotid artery occlusion for various intervals of time and the energy state of the brain was tested by exposing the brain to cortical spreading depression (SD). The results show that in the rat even bilateral occlusion induces only partial ischemia due to the existence of the circle of Willis. The metabolic response to SD showed an oxidation cycle before occlusion and a few hours after the occlusion a reduction cycle was recorded. This effect of the occlusion was reversible, and after 7-8 days the response to SD was again an oxidation cycle as before the ligation. The effects of two types of anesthetics (urethane and Nembutal), as well as partial ischemia (carotides occlusion), on the response to decapitation were tested. The disappearance of the electrical activity (ECoG) was significantly faster in the normal awake brain as well as the carotides occuluded awake rat in comparison to the anesthetized one. The rate of NADH increase after the decapitation, which represents the respiration rate of the brain tissue, was also significantly faster in the awake brain in comparison to the anesthetized state. This was determined by measuring the lag period before NADH started to increase and also by measuring the slope of the curve of the NADH. A significant correlation was found between these two parameters, namely, that when the lag period was short, the slope of increase of NADH was sharper.