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Thomas H. Jones, Richard B. Morawetz, Robert M. Crowell, Frank W. Marcoux, Stuart J. FitzGibbon, Umberto DeGirolami and Robert G. Ojemann

recording sites. The method eliminates the ischemia-modifying effects of anesthesia; neurological function can be correlated with local CBF and neuropathology. Preliminary experience with this model suggested a CBF threshold for infarction. 20 The present study is an expanded assessment of the brain's tolerance to focal ischemia. Ischemic insults of varied severity and duration were produced. Neurological function, local CBF, and pathology were correlated. We found that local CBF defines ischemia thresholds for function and structure: when local flow falls below a

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Peter T. Kan, Kenneth V. Snyder, Parham Yashar, Adnan H. Siddiqui, L. Nelson Hopkins and Elad I. Levy

angiogram to assess the extra- and intracranial vasculature in conjunction with the interpretation of the delay maps to help distinguish these chronic disease states from acute ischemia. Thresholds for Penumbra and Infarcts Currently, no consensus exists on the thresholds of CBF, CBV, and TTP used to define core infarcts and ischemic penumbra. According to Konstas et al., 11 a < 50% reduction of CBF on CT perfusion imaging suggests salvageable penumbra, whereas tissue with a > 66% reduction of CBF would likely progress to infarction. Wintermark et al. 24 , 25

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Takatoshi Sorimachi, Hiroshi Abe, Shigekazu Takeuchi and Ryuichi Tanaka

= occlusion period + repolarization latency − depolarization latency. An additional 63 animals were subjected to two periods of ischemia (“double ischemia” experiment). The double-ischemia experiments were designed to identify the depolarization threshold of the first ischemic episode such that there was no accumulation of ischemic damage resulting from a second ischemic episode lasting a period equal to the single-ischemia threshold. The experiment was conducted as follows. During the first phase, each animal was subjected to a set period of ischemia to obtain a range of

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Joseph M. Darby, Howard Yonas, Elizabeth C. Marks, Susan Durham, Robert W. Snyder and Edwin M. Nemoto

observations raise serious concerns about the potential for causing ischemia when dopamine is employed empirically. An important consideration in the interpretation of our study is the flow threshold at which we chose to define ischemia. Thresholds for neuronal function and viability exist and are well described in animal models of ischemia. 29, 30 Although such flow thresholds have been identified experimentally, similar thresholds have been difficult to define in man. Interpretation of the available data in this regard is limited in that there may be regional selective

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Cerebral blood flow and metabolism in severely head-injured children

Part 1: Relationship with GCS score, outcome, ICP, and PVI

J. Paul Muizelaar, Anthony Marmarou, Antonio A. F. DeSalles, John D. Ward, Richard S. Zimmerman, Zhongchao Li, Sung C. Choi and Harold F. Young

defective) ↓ ↓ ↑ 15, 25, 28, 29 blood viscosity (autoregulation intact) = ↓ = 25, 29, 30 blood viscosity (autoregulation defective) ↑ = ↓ 25, 29 PaCO 2 (acutely) ↓ ↓ ↑ 27, 31 PaCO 2 (chronically) = = = 27 conductance vessel diameter (vasospasm above ischemia threshold) ↓ ↑ ↑ 14 * CBF = cerebral blood flow; CBV = cerebral blood volume; AVDO 2 = arteriovenous difference in oxygen; CMRO 2 = cerebral metabolic rate of oxygen; CPP = cerebral perfusion pressure. ↑: increase