Delayed neurovascular dysfunction is alleviated by hydrogen in asphyxiated newborn pigs
Background: The neurovascular unit encompasses the functional interactions of cerebrovascular and brain parenchymal cells necessary for the metabolic homeostasis of neurons. Previous studies indicated marked but only transient (1-4 h) reactive oxygen species-dependent neurovascular dysfunction in ne...
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| Dokumentumtípus: | Cikk |
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S. Karger AG
2013
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| Sorozat: | NEONATOLOGY: FETAL AND NEONATAL RESEARCH
104 No. 2 |
| doi: | 10.1159/000348445 |
| mtmt: | 2398779 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/11383 |
| LEADER | 02910nab a2200253 i 4500 | ||
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| 005 | 20200221131311.0 | ||
| 008 | 170525s2013 hu o 0|| zxx d | ||
| 022 | |a 1661-7800 | ||
| 024 | 7 | |a 10.1159/000348445 |2 doi | |
| 024 | 7 | |a 2398779 |2 mtmt | |
| 040 | |a SZTE Publicatio Repozitórium |b hun | ||
| 041 | |a zxx | ||
| 100 | 1 | |a Oláh Orsolya | |
| 245 | 1 | 0 | |a Delayed neurovascular dysfunction is alleviated by hydrogen in asphyxiated newborn pigs |h [elektronikus dokumentum] / |c Oláh Orsolya |
| 260 | |a S. Karger AG |c 2013 | ||
| 300 | |a 79-86 | ||
| 490 | 0 | |a NEONATOLOGY: FETAL AND NEONATAL RESEARCH |v 104 No. 2 | |
| 520 | 3 | |a Background: The neurovascular unit encompasses the functional interactions of cerebrovascular and brain parenchymal cells necessary for the metabolic homeostasis of neurons. Previous studies indicated marked but only transient (1-4 h) reactive oxygen species-dependent neurovascular dysfunction in newborn pigs after severe hypoxic/ischemic (H/I) stress contributing to the neuronal injury after birth asphyxia. Objectives: Our major purpose was to determine if neurovascular dysfunction would also occur later, at 24 h after a milder H/I stress. We also tested if the putative hydroxyl radical scavenger hydrogen (H2) exerted neurovascular protection. Methods: Anesthetized, ventilated piglets were assigned to three groups of 9 animals: time control, asphyxia/reventilation with air, and asphyxia/reventilation with air +2.1% H2 for 4 h. Asphyxia was induced by suspending ventilation for 8 min. Cerebrovascular reactivity (CR) of pial arterioles was determined using closed cranial window/intravital microscopy 24 h after asphyxia to the endothelium-dependent cerebrovascular stimulus hypercapnia, the neuronal function-dependent stimulus N-methyl-D-aspartate (NMDA), norepinephrine, and sodium nitroprusside. The brains were subjected to histopathology. Results: Hemodynamic parameters, blood gases, and core temperature did not differ significantly among the experimental groups. In the early reventilation period, the recovery of electroencephalographic activity was significantly better in H2-treated animals. Asphyxia/reventilation severely attenuated CR to hypercapnia and NMDA; however, reactivity to norepinephrine and sodium nitroprusside were unaltered. H2 fully or partially preserved CR to hypercapnia or NMDA, respectively. Histopathology revealed modest neuroprotection afforded by H2. Conclusions: Severe stimulus-selective delayed neurovascular dysfunction develops and persists even after mild H/I stress. H2 alleviates this delayed neurovascular dysfunction that can contribute to its neuroprotective effect. | |
| 700 | 0 | 2 | |a Tóth-Szűki Valéria |e aut |
| 700 | 0 | 2 | |a Temesvári Péter |e aut |
| 700 | 0 | 2 | |a Bari Ferenc |e aut |
| 700 | 0 | 2 | |a Domoki Ferenc |e aut |
| 856 | 4 | 0 | |u http://publicatio.bibl.u-szeged.hu/11383/1/OlahO_Neonatology_2013.pdf |z Dokumentum-elérés |