Cerebral Metabolic Responses to Electroconvulsive Shock and Their Modification by Hypercapnia

Abstract

Brain glucose metabolism was studied in paralyzed, ventilated rats given electroconvulsive shock (ECS) under normocapnic and hypercapnic conditions. Brains were obtained with a freeze-blowing apparatus. Rates of glucose utilization were determined with [2-14C]glucose and [3H]deoxyglucose as tracers. In normocapnic rats, ECS caused a large increase in the rate of glycolysis to 5--6 mumol/g/min. Brain lactate levels increased three- to fourfold. The stimulation of glucose metabolism was reflected in decreased brain glucose 6-phosphate concentration as early as 2--3 s after ECS. There were significant decreases in brain glucose and glycogen levels at 20 and 30 s after ECS. The decreases in endogenous brain glucose accounted for most of the increases in glucose utilization measured isotopically, implying that influx of glucose from blood into brain did not increase greatly over these time periods. Animals made hypercapnic by respiration with 10% CO2 for 2 min prior to ECS were different in their metabolic responses to ECS in several ways. The increases in glycolytic rate and lactate content of brain were half of those found in normocapnic rats. Brain glycogen and glucose concentrations did not change significantly in the hypercapnic rats during seizure activity. Thus, hypercapnia lessened the stimulation of glycolysis caused by ECS, but increased net influx of glucose from blood to brain. The mechanisms of these effects of hypercapnia are uncertain, but it is postulated that the effect on glycolytic activity is due to the acidosis and that the effect on glucose transport is due to an increase in capillary surface area.

Fueling and Imaging Brain Activation

“…Thus, hexokinase will remain saturated (1 mmol/l glucose is 20 times the K m for glucose, ∼ 0.05 mmol/l) and can operate at V max when disinhibited by downstream consumption of Glc-6-P. These conclusions are consistent with experimental evidence obtained during extreme situations, for example, electroconvulsive or chemically induced seizures that evoke large hyperaemic responses, increased utilization of blood glucose, and consumption of some endogenous glucose and glycogen (King et al, 1967a; King et al, 1967b; Howse et al, 1974; Duffy et al, 1975; Miller et al, 1982). Compensatory responses to huge, abrupt increases in energy demand can maintain adequate brain glucose and ATP levels for intervals ranging from 10 to 30 s to more than several minutes.…”

“…Duration of seizures or CSD (cortical spreading depression) is indicated above the respective data sets. Data are from the following references: (1) (Miller et al, 1982); (2) (Borgstrom et al, 1976); (3) (Cremer et al, 1988); (4) (Van den Berg and Bruntink, 1983); (5) (Ackermann and Lear, 1989); (6) (Adachi et al, 1995). ( C ) Glucose is metabolized in neurons and astrocytes, and autoradiographic studies indicate that a large fraction of the label derived from glucose is not retained in the cell (Figure 4).…”

Anesthetic Considerations for Electroconvulsive Therapy-Especially Hemodynamic and Respiratory Management

“…Increase in middle cerebral artery blood flow velocity is minor under propofol anesthesia compared to thiopental anesthesia [89]. Several authors [90][91][92] have speculated that the reactive hyperemia may be necessary to compensate for the increased oxygen and energy demand after electrical stimulation. Therefore, complete suppression of cerebral hyperemia may be unnecessary, or inappropriate in hemodynamic management during ECT.…”

Anesthesia management for electroconvulsive therapy: hemodynamic and respiratory management

“…An increase in middle cerebral artery blood flow velocity is minor under propofol anesthesia compared to thiopental anesthesia [59]. Several authors [60][61][62] have speculated that the reactive hyperemia may be necessary to compensate for the increased oxygen and energy demand after the electrical stimulation. Therefore, complete suppression of cerebral hyperemia may be unnecessary or inadequate in hemodynamic management during ECT.…”