Kirsch J R, Traystman R J, Hurn P D
Department of Anesthesiology, Johns Hopkins University School of Medicine and Hospital, Baltimore, Maryland, USA.
Int Anesthesiol Clin. 1996 Fall;34(4):73-93. doi: 10.1097/00004311-199603440-00007.
A number of anesthetic agents have significant cerebroprotective potential and alter ischemic tolerance in vivo, at least within specific experimental conditions such as focal or incomplete, global cerebral ischemia. As compared to the unanesthetized state, each of these agents has some influence on CBF and metabolism, and many have significant effects on vascular responses to dilator stimuli. Relevant studies that provide clues to the mechanisms of anesthetic action in brain injury have been reviewed, and it is likely that these mechanisms are multifactorial and may overlap from one class of agents to another. Lastly, there is a clear need for further studies that specifically evaluate the neuroprotective mechanism of each agent, determine the effect on outcomes when the anesthetic is administered only as a posttreatment at clinically relevant concentrations, and compare anesthetics with the unanesthetized state when possible.
