Perioperative neuroprotection

The endpoint of all cerebral injuries like stroke, global cerebral ischemia during cardiac arrest, cardiac, vascular, or brain surgery or head trauma is the inadequate supply of the brain with oxygen and glucose, which triggers a characteristic pathophysiologic cascade leading to neuronal death. Many methods and agents have been investigated to produce neuroprotection from cerebral ischemia along this cascade (e.g., hypothermia, anaesthetics, free radical scavengers, excitatory amino acid antagonists, calcium channel blockers, ionic pump modulators, growth factors, heparinization, antineutrophil/platelet factors, steroids, and gene products). However, essentially none of the pharmacological approaches was identified as useful in humans though most agents have been successfully tested in animal models. Expert opinion suggests that neuroprotective approaches have failed in human trials because there are multiple mechanisms of injury from local and cerebral ischemia. Furthermore, adequate timing might essential because of the temporal sequence of cerebral injury. However, because there are multiple mechanisms of injury, there are most likely also multiple mechanisms of neuroprotection. The most important strategy is profound knowledge on cerebral physiology and homeostasis in health and disease. This review discusses essential physiological mechanisms to warrant adequate supply of glucose and oxygen to the brain. In addition, the influence of potential neuroprotective strategies and agents are reviewed in the perioperative setting.