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Effect of cell‐free hemoglobin transfusion and 20‐HETE synthesis inhibition on pial arteriolar diameter during middle cerebral artery occlusion
Author(s) -
Cao Suyi,
Kwansa Herman,
Roman Richard J,
Koehler Raymond C
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1274-d
Subject(s) - medicine , dilation (metric space) , vasodilation , hemoglobin , anesthesia , exchange transfusion , albumin , occlusion , middle cerebral artery , cardiology , ischemia , mathematics , combinatorics
Transfusion of cell‐free hemoglobin polymers (Hb) during middle cerebral artery occlusion (MCAO) can decrease infarct volume. Without MCAO, Hb transfusion produces pial arteriolar constriction that is blocked by the 20‐HETE synthesis inhibitor HET0016. We tested whether superfusion of 1 uM HET0016 in a cranial window would augment pial arteriolar dilation after Hb exchange transfusion during MCAO. In anesthetized rats MCAO initially produced 36±10% dilation which subsided to 19±6% dilation at 30 min of MCAO in the MCA border region. Subsequent exchange transfusion with 5% albumin solution resulted in no further change in diameter (22±16% of preischemia at 2h MCAO). In a group with initial dilation of 37±17%, HET0016 superfusion did not attenuate the loss of dilation at 30 min (25±12%) or the level of dilation after albumin transfusion (26±23%). Exchange transfusion of Hb resulted in a greater loss of dilation (4±19% of preischemia at 2h MCAO). Prior superfusion of HET0016 failed to block this loss of dilation (1±13%). Therefore, blunted vasodilation after Hb transfusion may limit efficacy of this O 2 carrier during MCAO. Blunted vasodilation is not dependent on 20‐HETE synthesis. (Supported by NS38684)