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Vascular response to hypoxic preconditioning in the immature brain

Journal article
Authors Malin Gustavsson
Carina Mallard
Susan J. Vannucci
Mary Ann Wilson
Michael. V. Johnston
Henrik Hagberg
Published in J Cereb Blood Flow Metab
Volume 27
Issue 5
Pages 928-38
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Clinical Sciences
Pages 928-38
Language en
Keywords Animals, Brain/*growth & development/pathology, Cerebrovascular Circulation/*physiology, Enzyme Inhibitors/pharmacology, Flow Cytometry, Gene Expression/physiology, Hypoxia, Brain/genetics/pathology/*physiopathology, Microcirculation/physiology, Nitric Oxide/biosynthesis/physiology, Nitric Oxide Synthase Type I/antagonists & inhibitors, Oligonucleotide Array Sequence Analysis, Rats, Rats, Sprague-Dawley, Reverse Transcriptase Polymerase Chain Reaction, von Willebrand Factor/physiology
Subject categories Medical and Health Sciences


We hypothesized that hypoxic preconditioning (PC) modifies the microvasculature in the immature brain and thereby affects the cerebral blood flow (CBF) during a subsequent hypoxic-ischemic (HI) insult. On postnatal day 6 rats were exposed to hypoxia (36 degrees C, 8.0% O2) or normoxia for 3 h. Unilateral HI (unilateral carotid ligation and 8% hypoxia) was induced 24 h later. Cortical CBF was measured with the 14C-iodoantipyrine technique (at the end of HI) or with laser Doppler flowmetry (Perimed PF5001) before and during HI. At 0, 2, 8, and 24 h cerebral cortex was sampled and analyzed with gene arrays (Affymetrix 230 2.0). L-nitroarginine or vehicle was administrated before hypoxic PC or 30 mins before HI followed by CBF measurement (laser Doppler) during subsequent HI. Twenty-four hours after PC animals were perfusion-fixed and brains immunolabeled for von Willebrand factor and vascular density was determined by stereological quantification. The decrease in CBF during HI was attenuated significantly in PC versus control animals (P<0.01), as detected by both techniques. Several vascular genes (Angpt2, Adm, Apln, Vegf, Flt1, Kdr, Pdgfra, Agtrap, Adora2a, Ednra, serpine1, caveolin, Id1, Prrx1, Ero1l, Acvrl1, Egfl7, Nudt6, Angptl4, Anxa2, and NOS3) were upregulated and a few (Csrp2, Adora2b) were downregulated after PC. A significant increase in vascular density (P<0.05) was seen after PC. Nitric oxide synthase inhibition did not affect CBF during HI after PC. In conclusion, hypoxic PC upregulates vascular genes, increases vascular density and attenuates the decrease of CBF during a subsequent HI, which could contribute to tolerance.

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