| Effects of acute acidemia on the fetal cardiovascular defense to acute hypoxemia. | |
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MedLine Citation:
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PMID: 18922958 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In complicated pregnancy, fetal hypoxemia rarely occurs in isolation but is often accompanied by fetal acidemia. There is growing clinical concern about the combined effects of fetal hypoxemia and fetal acidemia on neonatal outcome. However, the effects on the fetal defense responses to acute hypoxemia during fetal acidemia are not well understood. This study tested the hypothesis that fetal acidemia affects the fetal defense responses to acute hypoxemia. The hypothesis was tested by investigating, in the late-gestation sheep fetus surgically prepared for long-term recording, the in vivo effects of acute fetal acidemia on 1) the fetal cardiovascular responses to acute hypoxemia and 2) the neural and endocrine mechanisms mediating these responses. Under general anesthesia, five sheep fetuses at 0.8 gestation were instrumented with catheters and Transonic flow probes around the femoral and umbilical arteries. After 5 days, animals were subjected to an acute hypoxemia protocol during intravenous infusion of saline or treatment with acidified saline. Treatment with acidified saline reduced fetal basal pH from 7.35 +/- 0.01 to 7.29 +/- 0.01 but did not alter basal cardiovascular variables, blood glucose, or plasma concentrations of catecholamines, ACTH, and cortisol. During hypoxemia, treatment with acidified saline increased the magnitude of the fetal bradycardia and femoral vasoconstriction and concomitantly increased chemoreflex function and enhanced the increments in plasma concentrations of catecholamines, ACTH, and cortisol. Acidemia also reversed the increase in umbilical vascular conductance during hypoxemia to vasoconstriction. In conclusion, the data support our hypothesis and show that acute acidemia markedly alters fetal hemodynamic, metabolic, and endocrine responses to acute hypoxemia. |
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Authors:
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A S Thakor; D A Giussani |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-10-15 |
Journal Detail:
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Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: 296 ISSN: 0363-6119 ISO Abbreviation: Am. J. Physiol. Regul. Integr. Comp. Physiol. Publication Date: 2009 Jan |
Date Detail:
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Created Date: 2008-12-30 Completed Date: 2009-02-06 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: United States |
Other Details:
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Languages: eng Pagination: R90-9 Citation Subset: IM |
Affiliation:
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Dept. of Physiology, Development & Neuroscience, Univ. of Cambridge, Cambridge CB2 3EG, UK. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acidosis
/
blood,
complications,
physiopathology* Acute Disease Adrenocorticotropic Hormone / blood Animals Blood Glucose / metabolism Blood Pressure Bradycardia / etiology, physiopathology Carbon Dioxide / blood Catecholamines / blood Chemoreceptor Cells / metabolism Disease Models, Animal Female Femoral Artery / embryology, physiopathology* Fetal Hypoxia / blood, complications, physiopathology* Gestational Age Heart Rate Hemodynamics* Hydrocortisone / blood Hydrogen-Ion Concentration Oxygen / blood Pregnancy Reflex Regional Blood Flow Sheep Time Factors Umbilical Arteries / physiopathology* Vascular Resistance |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose; 0/Catecholamines; 124-38-9/Carbon Dioxide; 50-23-7/Hydrocortisone; 7782-44-7/Oxygen; 9002-60-2/Adrenocorticotropic Hormone |
| Comments/Corrections | |
Comment In:
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Am J Physiol Regul Integr Comp Physiol. 2009 Jan;296(1):R88-9
[PMID:
19020289
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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