BACKGROUND AND PURPOSE: Vulnerability to cerebral hypoxic-ischemic (H-I) insult and its relation to disruption of the blood-brain barrier were investigated in postnatal rats. METHODS: Pups of postnatal day (P) 7, P14, and P21 underwent ligation of a unilateral carotid artery and were exposed to hypoxic conditions. For the detection of early-phase deterioration, brains were perfusion-fixed 24 hours after H-I insult and examined by argyrophil III method. For the detection of later infarction, animals were fixed at 72 hours after the H-I insult. RESULTS: In either case, tissue damage was detected in the striatum, parietal cortex, and hippocampus. The vulnerability of P7 and P21 rats was remarkable, as compared with P14 rats. Although the developmental status of the vasculature was not significantly different at each age, the permeability of IgG after H-I injury was prominent in P7 rats and to a lesser extent in P14 rats. In P21 rats, however, there was little IgG leakage even 24 hours after the insult. Dexamethasone pretreatment blocked the extravasation of IgG and reduced the damaged tissue in P7 and P14 rats but not in P21 rats. Percentages of reduction in infarcted areas by the dexamethasone became smaller in proportion to ages. CONCLUSIONS: The results suggest that in younger rats vulnerability to H-I insult was in parallel with permeability of the blood-brain barrier, whereas in adults in might be more dependent on cellular vulnerability.
BACKGROUND AND PURPOSE: Vulnerability to cerebral hypoxic-ischemic (H-I) insult and its relation to disruption of the blood-brain barrier were investigated in postnatal rats. METHODS: Pups of postnatal day (P) 7, P14, and P21 underwent ligation of a unilateral carotid artery and were exposed to hypoxic conditions. For the detection of early-phase deterioration, brains were perfusion-fixed 24 hours after H-I insult and examined by argyrophil III method. For the detection of later infarction, animals were fixed at 72 hours after the H-I insult. RESULTS: In either case, tissue damage was detected in the striatum, parietal cortex, and hippocampus. The vulnerability of P7 and P21rats was remarkable, as compared with P14rats. Although the developmental status of the vasculature was not significantly different at each age, the permeability of IgG after H-I injury was prominent in P7 rats and to a lesser extent in P14rats. In P21rats, however, there was little IgG leakage even 24 hours after the insult. Dexamethasone pretreatment blocked the extravasation of IgG and reduced the damaged tissue in P7 and P14rats but not in P21rats. Percentages of reduction in infarcted areas by the dexamethasone became smaller in proportion to ages. CONCLUSIONS: The results suggest that in younger rats vulnerability to H-I insult was in parallel with permeability of the blood-brain barrier, whereas in adults in might be more dependent on cellular vulnerability.
Authors: Haichao Wang; Wei Li; Shu Zhu; Jianhua Li; Jason D'Amore; Mary F Ward; Huan Yang; Rongqian Wu; Willi Jahnen-Dechent; Kevin J Tracey; Ping Wang; Andrew E Sama Journal: J Cereb Blood Flow Metab Date: 2009-12-02 Impact factor: 6.200
Authors: Xiaodi Chen; Grazyna B Sadowska; Jiyong Zhang; Jeong-Eun Kim; Erin E Cummings; Courtney A Bodge; Yow-Pin Lim; Oleksandr Makeyev; Walter G Besio; John Gaitanis; Steven W Threlkeld; William A Banks; Barbara S Stonestreet Journal: Neurobiol Dis Date: 2014-09-26 Impact factor: 5.996
Authors: G Deng; J C Yonchek; N Quillinan; F A Strnad; J Exo; P S Herson; R J Traystman Journal: J Neurosci Methods Date: 2013-11-02 Impact factor: 2.390
Authors: X Chen; S W Threlkeld; E E Cummings; I Juan; O Makeyev; W G Besio; J Gaitanis; W A Banks; G B Sadowska; B S Stonestreet Journal: Neuroscience Date: 2012-09-15 Impact factor: 3.590