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Michael F. Stiefel, Gregory G. Heuer, John M. Abrahams, Stephanie Bloom, Michelle J. Smith, Eileen Maloney-Wilensky, M. Sean Grady, and Peter D. Leroux

, 52 Similarly, in an experimental model of SAH nimodipine led to a brief initial decrease in CBF. 10 Not long ago, the administration of nimodipine for traumatic SAH was described as a rare cause of systemic hypoxemia 6 and was associated with significant changes in fibrinolytic activity. 46 Thus, the relationship between calcium-channel blocking agents, vasospasm, CBF or adequacy of CBF, and SAH is complex and not fully understood. Recently, it has become possible to measure brain tissue PO 2 and other aspects of cerebral metabolism. This monitoring of

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Michael F. Stiefel, Gregory G. Heuer, Michelle J. Smith, Stephanie Bloom, Eileen Maloney-Wilensky, Vincente H. Gracias, M. Sean Grady, and Peter D. Leroux

increased, decreased, or normal CBF. 34, 35, 72 Other studies demonstrate that cerebral infarction can occur despite normal ICP and CPP and that not all episodes of cerebral ischemia are associated with increased ICP. 36, 70, 72 It can be inferred from these various studies that an understanding of ICP alone may be inadequate in the treatment of some patients and that additional measures of cerebral metabolism, CBF, or the adequacy of CBF may be necessary for effective patient care. Recently, continuous direct measurement of O 2 in brain tissue has become possible in