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Cerebral microcirculatory alterations and the no-reflow phenomenon in vivo after experimental pediatric cardiac arrest

Decreased cerebral blood flow (CBF) after cardiac arrest (CA) contributes to secondary ischemic injury in infants and children. We previously reported cortical hypoperfusion with tissue hypoxia early in a pediatric rat model of asphyxial CA. In order to identify specific alterations as potential the...

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Bibliographic Details
Published in:Journal of cerebral blood flow and metabolism 2019-05, Vol.39 (5), p.913-925
Main Authors: Li, Lingjue, Poloyac, Samuel M, Watkins, Simon C, St. Croix, Claudette M, Alexander, Henry, Gibson, Gregory A, Loughran, Patricia A, Kirisci, Levent, Clark, Robert SB, Kochanek, Patrick M, Vazquez, Alberto L, Manole, Mioara D
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Language:English
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Summary:Decreased cerebral blood flow (CBF) after cardiac arrest (CA) contributes to secondary ischemic injury in infants and children. We previously reported cortical hypoperfusion with tissue hypoxia early in a pediatric rat model of asphyxial CA. In order to identify specific alterations as potential therapeutic targets to improve cortical hypoperfusion post-CA, we characterize the CBF alterations at the cortical microvascular level in vivo using multiphoton microscopy. We hypothesize that microvascular constriction and disturbances of capillary red blood cell (RBC) flow contribute to cortical hypoperfusion post-CA. After resuscitation from 9 min asphyxial CA, transient dilation of capillaries and venules at 5 min was followed by pial arteriolar constriction at 30 and 60 min (19.6 ± 1.3, 19.3 ± 1.2 µm at 30, 60 min vs. 22.0 ± 1.2 µm at baseline, p 
ISSN:0271-678X
1559-7016
1559-7016
DOI:10.1177/0271678X17744717