Uterine Artery Dysfunction and Reduced Utero-Placental Perfusion in a Rat Model of Preeclampsia

2.50
Hdl Handle:
http://hdl.handle.net/10755/160477
Type:
Presentation
Title:
Uterine Artery Dysfunction and Reduced Utero-Placental Perfusion in a Rat Model of Preeclampsia
Abstract:
Uterine Artery Dysfunction and Reduced Utero-Placental Perfusion in a Rat Model of Preeclampsia
Conference Sponsor:Midwest Nursing Research Society
Conference Year:2004
Author:Anderson, Cindy , MS, WHNP, IBCLC
Contact Address:Pharmacology and Physiology, Box 9025, CON, Grand Forks, ND, 58202-9025, USA
The origin of pathology in preeclampsia is thought to be reduced placental perfusion, leading to systemic endothelial dysfunction initiated in the early days of pregnancy. The present study was designed to provide characterization of vascular responsiveness in uterine arcuate arteries in a rat model of reduced utero-placental perfusion. Theoretical/Conceptual Framework: Basic science techniques in vascular physiology were utilized. Subjects: Female Sprague-Dawley rats (n=32). Method: The reduced utero-placental perfusion (RUPP) model was utilized to mimic the underlying pathology of preeclampsia. The uterine arteries and abdominal aorta of pregnant Sprague-Dawley rats were surgically constricted on day 14 of gestation. Systolic blood pressure measurements were obtained before and during pregnancy using a tail cuff measuring system. Weight was measured with each blood pressure evaluation. The rats were euthanized at term on gestational day 20. Fetal number, fetal weights and placental weights were measured. The uterus was removed and arcuate arteries were dissected free from surrounding tissue. The arteries were then mounted on a small vessel wire myograph for isometric force measurement. Vessels were challenged with incremental concentrations of phenylephrine, potassium chloride, angiotensin II, acetylcholine, sodium nitroprusside, calcium ionophore or leptin and concentration/effect relationships analyzed. Results: Systolic blood pressure was increased in the RUPP model compared to control (p < 0.001). Fetal weight (p < 0.01), fetal number (p < 0.05) and placental weight (p < 0.01) were all decreased in the RUPP group, consistent with decreased uterine perfusion. Data suggest a hyperresponsiveness of uterine arcuate arteries to vasoconstrictors in the model of preeclampsia. Impaired relaxation of uterine arteries in response to incremental doses of leptin, calcium ionophore and acetylcholine was also evident. Conclusions: Reduced utero-placental perfusion induced alterations in vascular function in the uterine arcuate arteries. The resulting vasoconstrictor hypersensitivity, impaired relaxation and endothelial dysfunction contribute to the hypertension of preeclampsia.
Repository Posting Date:
26-Oct-2011
Date of Publication:
17-Oct-2011
Sponsors:
Midwest Nursing Research Society

Full metadata record

DC FieldValue Language
dc.typePresentationen_GB
dc.titleUterine Artery Dysfunction and Reduced Utero-Placental Perfusion in a Rat Model of Preeclampsiaen_GB
dc.identifier.urihttp://hdl.handle.net/10755/160477-
dc.description.abstract<table><tr><td colspan="2" class="item-title">Uterine Artery Dysfunction and Reduced Utero-Placental Perfusion in a Rat Model of Preeclampsia </td></tr><tr class="item-sponsor"><td class="label">Conference Sponsor:</td><td class="value">Midwest Nursing Research Society</td></tr><tr class="item-year"><td class="label">Conference Year:</td><td class="value">2004</td></tr><tr class="item-author"><td class="label">Author:</td><td class="value">Anderson, Cindy , MS, WHNP, IBCLC</td></tr><tr class="item-address"><td class="label">Contact Address:</td><td class="value">Pharmacology and Physiology, Box 9025, CON, Grand Forks, ND, 58202-9025, USA</td></tr><tr><td colspan="2" class="item-abstract">The origin of pathology in preeclampsia is thought to be reduced placental perfusion, leading to systemic endothelial dysfunction initiated in the early days of pregnancy. The present study was designed to provide characterization of vascular responsiveness in uterine arcuate arteries in a rat model of reduced utero-placental perfusion. Theoretical/Conceptual Framework: Basic science techniques in vascular physiology were utilized. Subjects: Female Sprague-Dawley rats (n=32). Method: The reduced utero-placental perfusion (RUPP) model was utilized to mimic the underlying pathology of preeclampsia. The uterine arteries and abdominal aorta of pregnant Sprague-Dawley rats were surgically constricted on day 14 of gestation. Systolic blood pressure measurements were obtained before and during pregnancy using a tail cuff measuring system. Weight was measured with each blood pressure evaluation. The rats were euthanized at term on gestational day 20. Fetal number, fetal weights and placental weights were measured. The uterus was removed and arcuate arteries were dissected free from surrounding tissue. The arteries were then mounted on a small vessel wire myograph for isometric force measurement. Vessels were challenged with incremental concentrations of phenylephrine, potassium chloride, angiotensin II, acetylcholine, sodium nitroprusside, calcium ionophore or leptin and concentration/effect relationships analyzed. Results: Systolic blood pressure was increased in the RUPP model compared to control (p &lt; 0.001). Fetal weight (p &lt; 0.01), fetal number (p &lt; 0.05) and placental weight (p &lt; 0.01) were all decreased in the RUPP group, consistent with decreased uterine perfusion. Data suggest a hyperresponsiveness of uterine arcuate arteries to vasoconstrictors in the model of preeclampsia. Impaired relaxation of uterine arteries in response to incremental doses of leptin, calcium ionophore and acetylcholine was also evident. Conclusions: Reduced utero-placental perfusion induced alterations in vascular function in the uterine arcuate arteries. The resulting vasoconstrictor hypersensitivity, impaired relaxation and endothelial dysfunction contribute to the hypertension of preeclampsia.</td></tr></table>en_GB
dc.date.available2011-10-26T22:58:49Z-
dc.date.issued2011-10-17en_GB
dc.date.accessioned2011-10-26T22:58:49Z-
dc.description.sponsorshipMidwest Nursing Research Societyen_GB
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