Clinical Translation of Cerebral Preconditioning
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COMMENTARY
Clinical Translation of Cerebral Preconditioning Guohua Xi
Published online: 23 February 2010 # Springer Science+Business Media, LLC 2010
Cerebral preconditioning (PC) refers to a phenomenon whereby prior treatment with a variety of stimuli can induce protection against later brain injury [1, 2]. It is well known that PC is one of the most powerful methods of reducing stroke-induced brain injury in animal models. Preconditioning has been used for heart and brain surgery and is now a clinical reality [3, 4]. In the brain, ischemic PC has been used during clipping of cerebral aneurysm and attenuates tissue hypoxia during aneurysm clipping [5]. A preconditioning workshop was held at the University of Michigan in Ann Arbor on July 24 to 25, 2009. The workshop brought together 20 experts from the United States who discussed the mechanisms of PC-induced neuroprotection and how to translate those results to the clinic. Neuroprotection is a major issue in neurosurgery since neurosurgical procedures may result in trauma, hemorrhage, and/or ischemia. Cognitive dysfunction and ischemic brain damage can also occur in patients after heart bypass surgery and carotid endarterectomy. Dr. Michael Wang (University of Michigan) reviewed clinical targets of PC and suggested that brain injury after neurosurgery, carotid endarterectomy and coronary artery bypass graft surgery, and vasospasm following subarachnoid hemorrhage are major potential clinical targets for cerebral PC [6]. Mechanisms of PC were updated during the workshop. Dr. John Hallenbeck (National Institute of Neurological Disorders and Stroke) presented natural tolerance in hibernation torpor as a guide to target selection for stroke and his recent findings indicate that SUMOylation has an G. Xi (*) Department of Neurosurgery, University of Michigan, Ann Arbor, MI 48109-2200, USA e-mail: [email protected]
important role in ischemic tolerance [7]. Whether or not cerebral blood flow has a role in PC-induced neuroprotection was presented by Dr. Thaddeus Nowak (University of Tennessee). Dr. Anne Stetler (University of Pittsburgh) reviewed molecular mechanisms of PC [8]. Although results from animal studies are promising, most PC studies have been done in young and healthy animals. Whether or not aged, hypertensive, or diabetic animals should be included in future preconditioning experiments was also discussed. In addition, data showing that inducible nitrous oxide synthase promoter polymorphism affords protection against cognitive dysfunction after carotid endarterectomy was reported by Dr. Raqeeb Haque (Columbia University) [9], and the results suggest that cognitive dysfunction could be an endpoint to measure success in future potential preconditioning trials. To develop safe and noninvasive PC approaches is critical for clinical translation of cerebral PC. Recently, many noninvasive PC methods are available to induce brain tolerance [2]. Dr. Jeffrey Gidday (Washington University) summarized pharmacologic PC. There are many promising approaches, such as PC with
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