In patients with intracranial mass lesions, the anesthetics commonly used during surgery may cause large increases in intracranial pressure (ICP) resulting in compromise of cerebral perfusion or herniation of brain, and irreversible brain damage. Hyperventilation has been reported to prevent significant increase of ICP during the first 30 minutes of anesthesia in patients with mass lesions. Based on those results, prolonged hyperventilation has become the standard treatment to prevent anesthetic-induced increase of ICP in patients with mass lesions. However, accommodation to the effects of hyperventilation may occur due to adaptation of cerebral vessels to the constricting effect of hyperventilation, restoration of cerebrospinal fluid volume, or increase of brain tissue volume. Consequently, we do not know whether hyperventilation remains an effective way to prevent anesthetic-induced increase of ICP after the first 30 minutes of anesthesia. The specific aims of the proposed studies are 1) to determine the effect of hyperventilation on ICP over a prolonged time in the presence of anesthetics and a mass lesion; 2) to examine the contribution of changes in cerebral blood volume, cerebrospinal fluid (CSF) volume, and brain tissue volume to changes in ICP during prolonged anesthesia and hyperventilation. The proposed studies will employ anesthetized and mechanically ventilated dogs. Intracranial pressure will be determined via direct cannulation. Cerebral blood volume will be determined by measuring gamma emission from a radioactive tracer. The rates of CSF production and resistance to reabsorption of CSF will be determined by the method of ventriculocisternal perfusion. Brain water content will be determined from the ratio of wet/dry weight of samples of brain tissue. The long-term objectives of these studies are 1) to determine the duration of efficacy of hyperventilation as a means of controlling ICP with commonly used anesthetic agents, and 2) to determine whether one anesthetic agent is superior to others in permitting control of ICP by hyperventilation.
NIH ExPorter
NIH ExPorter