Linked Life Data

17947499

Source:http://linkedlifedata.com/resource/pubmed/id/17947499

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-1-16
pubmed:abstractText
Intermittent hypoxia (IH) resulting from sleep apnea can lead to pulmonary hypertension (PH) and right heart failure, similar to chronic sustained hypoxia (CH). Supplemental CO(2), however, attenuates hypoxic PH. We therefore hypothesized that, similar to CH, IH elicits PH and associated increases in arterial endothelial nitric oxide synthase (eNOS) expression, ionomycin-dependent vasodilation, and receptor-mediated pulmonary vasoconstriction. We further hypothesized that supplemental CO(2) inhibits these responses to IH. To test these hypotheses, we measured eNOS expression by Western blot in intrapulmonary arteries from CH (2 wk, 0.5 atm), hypocapnic IH (H-IH) (3 min cycles of 5% O(2)/air flush, 7 h/day, 2 wk), and eucapnic IH (E-IH) (3 min cycles of 5% O(2), 5% CO(2)/air flush, 7 h/day, 2 wk) rats and their respective controls. Furthermore, vasodilatory responses to the calcium ionophore ionomycin and vasoconstrictor responses to the thromboxane mimetic U-46619 were measured in isolated saline-perfused lungs from each group. Hematocrit, arterial wall thickness, and right ventricle-to-total ventricle weight ratios were additionally assessed as indexes of polycythemia, arterial remodeling, and PH, respectively. Consistent with our hypotheses, E-IH resulted in attenuated polycythemia, arterial remodeling, RV hypertrophy, and eNOS upregulation compared with H-IH. However, in contrast to CH, neither H-IH nor E-IH increased ionomycin-dependent vasodilation. Furthermore, H-IH and E-IH similarly augmented U-46619-induced pulmonary vasoconstriction but to a lesser degree than CH. We conclude that maintenance of eucapnia decreases IH-induced PH and upregulation of arterial eNOS. In contrast, increases in pulmonary vasoconstrictor reactivity following H-IH are unaltered by exposure to supplemental CO(2).
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
104
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
110-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17947499-15-Hydroxy-11 alpha,9..., pubmed-meshheading:17947499-Animals, pubmed-meshheading:17947499-Anoxia, pubmed-meshheading:17947499-Carbon Dioxide, pubmed-meshheading:17947499-Chronic Disease, pubmed-meshheading:17947499-Disease Models, Animal, pubmed-meshheading:17947499-Dose-Response Relationship, Drug, pubmed-meshheading:17947499-Hypertension, Pulmonary, pubmed-meshheading:17947499-Hypertrophy, Right Ventricular, pubmed-meshheading:17947499-Hypocapnia, pubmed-meshheading:17947499-Ionomycin, pubmed-meshheading:17947499-Ionophores, pubmed-meshheading:17947499-Male, pubmed-meshheading:17947499-Nitric Oxide Synthase Type II, pubmed-meshheading:17947499-Nitric Oxide Synthase Type III, pubmed-meshheading:17947499-Oxygen, pubmed-meshheading:17947499-Polycythemia, pubmed-meshheading:17947499-Pulmonary Artery, pubmed-meshheading:17947499-Rats, pubmed-meshheading:17947499-Rats, Sprague-Dawley, pubmed-meshheading:17947499-Vasoconstriction, pubmed-meshheading:17947499-Vasoconstrictor Agents, pubmed-meshheading:17947499-Vasodilation, pubmed-meshheading:17947499-Vasodilator Agents
pubmed:year
2008
pubmed:articleTitle
Differential effects of chronic hypoxia and intermittent hypocapnic and eucapnic hypoxia on pulmonary vasoreactivity.
pubmed:affiliation
Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-0001, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural