Document Detail


Chronic hypoxia increases fetoplacental vascular resistance and vasoconstrictor reactivity in the rat.
MedLine Citation:
PMID:  18310520     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
An increase in fetoplacental vascular resistance caused by hypoxia is considered one of the key factors of placental hypoperfusion and fetal undernutrition leading to intrauterine growth restriction (IUGR), one of the serious problems in current neonatology. However, although acute hypoxia has been shown to cause fetoplacental vasoconstriction, the effects of more sustained hypoxic exposure are unknown. This study was designed to test the hypothesis that chronic hypoxia elicits elevations in fetoplacental resistance, that this effect is not completely reversible by acute reoxygenation, and that it is accompanied by increased acute vasoconstrictor reactivity of the fetoplacental vasculature. We measured fetoplacental vascular resistance as well as acute vasoconstrictor reactivity in isolated perfused placentae from rats exposed to hypoxia (10% O(2)) during the last week of a 3-wk pregnancy. We found that chronic hypoxia shifted the relationship between perfusion pressure and flow rate toward higher pressure values (by approximately 20%). This increased vascular resistance was refractory to a high dose of sodium nitroprusside, implying the involvement of other factors than increased vascular tone. Chronic hypoxia also increased vasoconstrictor responses to angiotensin II (by approximately 75%) and to acute hypoxic challenges (by >150%). We conclude that chronic prenatal hypoxia causes a sustained elevation of fetoplacental vascular resistance and vasoconstrictor reactivity that are likely to produce placental hypoperfusion and fetal undernutrition in vivo.
Authors:
Vít Jakoubek; Jana Bíbová; Jan Herget; Václav Hampl
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-02-29
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  294     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-04-02     Completed Date:  2008-05-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1638-44     Citation Subset:  IM    
Affiliation:
Dept. of Physiology, Charles University, Plzenská 130/221, 15000 Prague 5-Motol, Czech Republic.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Angiotensin II / pharmacology
Animals
Anoxia / complications,  physiopathology*
Blood Flow Velocity
Blood Pressure
Chronic Disease
Disease Models, Animal
Dose-Response Relationship, Drug
Female
Fetal Growth Retardation / etiology*,  physiopathology
Gestational Age
Nitroprusside / pharmacology
Placental Circulation* / drug effects
Pregnancy
Rats
Rats, Wistar
Regional Blood Flow
Vascular Resistance* / drug effects
Vasoconstriction* / drug effects
Vasoconstrictor Agents / pharmacology
Vasodilator Agents / pharmacology
Chemical
Reg. No./Substance:
0/Vasoconstrictor Agents; 0/Vasodilator Agents; 11128-99-7/Angiotensin II; 15078-28-1/Nitroprusside

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Estrogen potentiates constrictor prostanoid function in female rat aorta by upregulation of cyclooxy...
Next Document:  Evidence for impaired skeletal muscle contraction-induced rapid vasodilation in aging humans.