-
Something wrong with this record ?
Reactive oxygen species production in the early and later stage of chronic ventilatory hypoxia
D. Hodyc, E. Johnson, A. Skoumalová, J. Tkaczyk, H. Maxová, M. Vízek, J. Herget
Language English Country Czech Republic
Document type Research Support, Non-U.S. Gov't
NLK
Directory of Open Access Journals
from 1991
Free Medical Journals
from 1998
ProQuest Central
from 2005-01-01
Medline Complete (EBSCOhost)
from 2006-01-01
Nursing & Allied Health Database (ProQuest)
from 2005-01-01
Health & Medicine (ProQuest)
from 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
from 1998
- MeSH
- Pulmonary Artery metabolism MeSH
- Hypoxia complications metabolism MeSH
- Rats MeSH
- Peroxynitrous Acid metabolism MeSH
- Nitric Oxide biosynthesis blood MeSH
- Hydrogen Peroxide metabolism MeSH
- Hypertension, Pulmonary etiology MeSH
- Rats, Wistar MeSH
- Reactive Oxygen Species metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
Pulmonary hypertension resulting from chronic hypoxia is at least partly caused by the increased production of reactive oxygen species (ROS). The goal of the presented study was to investigate the dynamics and the site of production of ROS during chronic hypoxia. In our study Wistar rats were kept for 1, 4 and 21 days in an isobaric hypoxic chamber (FiO2=0.1), while controls stayed in normoxia. We compared NO production in expired air, plasma and perfusate drained from isolated rat lungs and measured superoxide concentration in the perfusate. We also detected the presence of superoxide products (hydrogen peroxide and peroxynitrite) and the level of ROS-induced damage expressed as the concentration of lipid peroxydation end products. We found that the production and release of ROS and NO during early phase of chronic hypoxia has specific timing and differs in various compartments, suggesting the crucial role of ROS interaction for development of hypoxic pulmonary hypertension.
References provided by Crossref.org
Literatura
- 000
- 00000naa a2200000 a 4500
- 001
- bmc12018871
- 003
- CZ-PrNML
- 005
- 20200715093722.0
- 007
- ta
- 008
- 120620s2012 xr df f 000 0eng||
- 009
- AR
- 024 7_
- $a 10.33549/physiolres.932206 $2 doi
- 035 __
- $a (PubMed)22292725
- 040 __
- $a ABA008 $d ABA008 $e AACR2 $b cze
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Hodyc, Daniel, $d 1979- $7 xx0074202 $u Department of Physiology, Second Medical School, Charles University in Prague, Prague, Czech Republic
- 245 10
- $a Reactive oxygen species production in the early and later stage of chronic ventilatory hypoxia / $c D. Hodyc, E. Johnson, A. Skoumalová, J. Tkaczyk, H. Maxová, M. Vízek, J. Herget
- 504 __
- $a Literatura $b 33
- 520 9_
- $a Pulmonary hypertension resulting from chronic hypoxia is at least partly caused by the increased production of reactive oxygen species (ROS). The goal of the presented study was to investigate the dynamics and the site of production of ROS during chronic hypoxia. In our study Wistar rats were kept for 1, 4 and 21 days in an isobaric hypoxic chamber (FiO2=0.1), while controls stayed in normoxia. We compared NO production in expired air, plasma and perfusate drained from isolated rat lungs and measured superoxide concentration in the perfusate. We also detected the presence of superoxide products (hydrogen peroxide and peroxynitrite) and the level of ROS-induced damage expressed as the concentration of lipid peroxydation end products. We found that the production and release of ROS and NO during early phase of chronic hypoxia has specific timing and differs in various compartments, suggesting the crucial role of ROS interaction for development of hypoxic pulmonary hypertension.
- 650 02
- $a zvířata $7 D000818
- 650 02
- $a hypoxie $x komplikace $x metabolismus $7 D000860
- 650 02
- $a peroxid vodíku $x metabolismus $7 D006861
- 650 02
- $a plicní hypertenze $x etiologie $7 D006976
- 650 02
- $a mužské pohlaví $7 D008297
- 650 02
- $a oxid dusnatý $x biosyntéza $x krev $7 D009569
- 650 02
- $a kyselina peroxydusitá $x metabolismus $7 D030421
- 650 02
- $a arteria pulmonalis $x metabolismus $7 D011651
- 650 02
- $a krysa rodu Rattus $7 D051381
- 650 02
- $a potkani Wistar $7 D017208
- 650 02
- $a reaktivní formy kyslíku $x metabolismus $7 D017382
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Johnson, E. $7 _AN068187 $u Department of Physiology, Second Medical School, Charles University in Prague, Prague, Czech Republic
- 700 1_
- $a Skoumalová, Alice, $d 1973- $7 xx0037063 $u Department of Medical Chemistry and Biochemistry, Second Medical School, Charles University in Prague, Prague, Czech Republic
- 700 1_
- $a Tkaczyk, Jakub $7 xx0074223 $u Department of Pathological Physiology, Second Medical School, Charles University in Prague, Prague, Czech Republic
- 700 1_
- $a Maxová, Hana, $d 1968- $7 xx0037102 $u Department of Pathological Physiology, Second Medical School, Charles University in Prague, Prague, Czech Republic
- 700 1_
- $a Vízek, Martin, $d 1943- $7 jn20000402660 $u Department of Pathological Physiology, Second Medical School, Charles University in Prague, Prague, Czech Republic
- 700 1_
- $a Herget, Jan, $d 1945-2019 $7 nlk19990073223 $u Department of Physiology, Second Medical School, Charles University in Prague, Prague, Czech Republic
- 773 0_
- $t Physiological research $x 0862-8408 $g Roč. 61, č. 2 (2012), s. 145-151 $w MED00003824
- 856 41
- $u http://www.biomed.cas.cz/physiolres/archive.htm
- 910 __
- $a ABA008 $b A 4120 $c 266 $y 4 $z 0
- 990 __
- $a 20120620071532 $b ABA008
- 991 __
- $a 20200715093719 $b ABA008
- 999 __
- $a ok $b bmc $g 912887 $s 776089
- BAS __
- $a 3
- BMC __
- $a 2012 $b 61 $c 2 $d 145-151 $i 0862-8408 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
- LZP __
- $a 2012-28/vtme