AN UNRESOLVED question is whether during seizures lactic acidosis occurs in brain tissue because cerebral oxygen delivery fails to meet the augmented demands of cerebral oxidative metabolism. Several investigators have reported that brain lactate concentrations increase during experimental seizures in mice, cats, dogs, and monkeys.1-6 Also, during induced generalized and focal seizures in man, falls in jugular venous pH have been observed.7 From these findings it has been inferred that cerebral metabolism rises so sharply during seizures that it outstrips the available oxygen supply, which results in a shift to anaerobic glycolysis and increasing lactate formation by brain tissue.6 However, recent studies from this laboratory imply that brain lactate does not necessarily increase during induced cerebral seizures. Using dogs and monkeys that were artificially ventilated and paralyzed, Plum and his associates8 found that, although cerebral oxygen consumption increased substantially during induced seizures, cerebral blood flow increased proportionately even more so that the sagittal venous blood oxygen tension and content also rose. Thus, during cerebral seizures the oxygen supply to the brain met or exceeded the heightened cerebral metabolic demand. During cerebral seizures lactate dif¬ ferences between arterial and sagittal venous blood did not increase and the concentration of lactate in the cerebrospinal fluid (CSF) did not change significantly.The above findings suggested that during seizures brain tissue lactate formation does not rise if adequate arterial oxygénation is maintained. We sought to confirm this hy¬ pothesis by measuring brain lactate concen¬ trations and other parameters in paralyzed animals before and during experimental cere¬ bral seizures. Studies were done in 12 well-oxygenated dogs and in three dogs that were allowed to become hypoxic. It was found that during the seizure discharge in the well-oxygenated animals brain lactate concentrations did not rise significantly, but during seizures in the hypoxic animals brain lactate rose nearly twofold.
MethodsFifteen healthy mongrel dogs were initially anesthetized with thiopental sodium intrave¬ nously, given atropine 1 mg intravenously, and intubated with cuffed endotracheal tubes. Cannulae were placed in both femoral arteries to monitor blood pressure and obtain blood sam¬ ples, and, in one femoral vein, to give fluids and medications. The dogs were placed prone, con¬ nected to a respirator, and paralyzed with gallamine. Anesthesia was maintained with a Changes in brain lactate during seizures. 70%/30% nitrous oxide/oxygen mixture. Bilat¬ eral craniotomies were performed and a wide skull cap was removed exposing both cerebral hemispheres and the sagittal sinus. The dura was left intact until the time of brain biopsy and kept warm and moist with saline packs and the heat from an operating lamp. A cannula was placed in the sagittal sinus to obtain cere¬ bral venous blood samples. Another cannula was placed percutaneously in the cisterna mag¬ na to ...
