17-hydroxyprogesterone caproate reverses induced vasoconstriction of the fetoplacental arteries by the thromboxane mimetic U46619

Damian J. Paonessa, Andrea D. Shields, Bobby Howard, Jennifer L. Gotkin, Shad H. Deering, Nathan J. Hoeldtke, Peter G. Napolitano

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Objective: This study was undertaken to determine whether 17-hydroxyprogesterone caproate (17P) has a vasoactive effect on fetoplacental vasculature. Study design: Two cotyledons were obtained from each of 5 placentas. Baseline perfusion was established with Hanks-based solution. One cotyledon from each pair was then infused with perfusate to which U46619 a thromboxane sympathomimetic had been added. After 30 minutes, a dose of 17P was then administered to each cotyledon. Finally, a vasoconstricting dose of angiotensin II was administered to each cotyledon. Perfusion pressures were recorded throughout. Statistical analysis of pressure change for a single cotyledon was performed by using a paired t test. Statistical analysis of mean perfusion pressure difference between U46619 exposed and nonexposed cotyledons was analyzed by using a students t test. Results: 17P did not significantly alter the perfusion pressure of the control cotyledon. (30.6 ± 8.3 mm Hg vs 30.1 ± 7.8 mm Hg P = .48). 17P administration significantly lowered the perfusion pressure of the U46619 preconstricted vessels in comparison with preadministration. (60.1 ± 13 mm Hg vs 27.3 ± 7.1 mm Hg P = .03). Both groups of cotyledons responded with vasoconstriction to angiotension II with no difference in response between groups (38.3 ± 12 mm Hg vs 45.8 ± 8.2 mm Hg P = .63). Conclusion: 17P reverses induced vasoconstriction by U46619 in fetoplacental arteries.

Original languageEnglish (US)
Pages (from-to)1011-1014
Number of pages4
JournalAmerican Journal of Obstetrics and Gynecology
Volume195
Issue number4
DOIs
StatePublished - Oct 1 2006

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17-alpha-Hydroxyprogesterone
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
Cotyledon
Thromboxanes
Vasoconstriction
Arteries
Perfusion
Pressure
Sympathomimetics
17-alpha-hydroxy-progesterone caproate
Angiotensin II
Placenta
Students

All Science Journal Classification (ASJC) codes

  • Obstetrics and Gynecology

Cite this

17-hydroxyprogesterone caproate reverses induced vasoconstriction of the fetoplacental arteries by the thromboxane mimetic U46619. / Paonessa, Damian J.; Shields, Andrea D.; Howard, Bobby; Gotkin, Jennifer L.; Deering, Shad H.; Hoeldtke, Nathan J.; Napolitano, Peter G.

In: American Journal of Obstetrics and Gynecology, Vol. 195, No. 4, 01.10.2006, p. 1011-1014.

Research output: Contribution to journalArticle

Paonessa, Damian J. ; Shields, Andrea D. ; Howard, Bobby ; Gotkin, Jennifer L. ; Deering, Shad H. ; Hoeldtke, Nathan J. ; Napolitano, Peter G. / 17-hydroxyprogesterone caproate reverses induced vasoconstriction of the fetoplacental arteries by the thromboxane mimetic U46619. In: American Journal of Obstetrics and Gynecology. 2006 ; Vol. 195, No. 4. pp. 1011-1014.
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abstract = "Objective: This study was undertaken to determine whether 17-hydroxyprogesterone caproate (17P) has a vasoactive effect on fetoplacental vasculature. Study design: Two cotyledons were obtained from each of 5 placentas. Baseline perfusion was established with Hanks-based solution. One cotyledon from each pair was then infused with perfusate to which U46619 a thromboxane sympathomimetic had been added. After 30 minutes, a dose of 17P was then administered to each cotyledon. Finally, a vasoconstricting dose of angiotensin II was administered to each cotyledon. Perfusion pressures were recorded throughout. Statistical analysis of pressure change for a single cotyledon was performed by using a paired t test. Statistical analysis of mean perfusion pressure difference between U46619 exposed and nonexposed cotyledons was analyzed by using a students t test. Results: 17P did not significantly alter the perfusion pressure of the control cotyledon. (30.6 ± 8.3 mm Hg vs 30.1 ± 7.8 mm Hg P = .48). 17P administration significantly lowered the perfusion pressure of the U46619 preconstricted vessels in comparison with preadministration. (60.1 ± 13 mm Hg vs 27.3 ± 7.1 mm Hg P = .03). Both groups of cotyledons responded with vasoconstriction to angiotension II with no difference in response between groups (38.3 ± 12 mm Hg vs 45.8 ± 8.2 mm Hg P = .63). Conclusion: 17P reverses induced vasoconstriction by U46619 in fetoplacental arteries.",
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AU - Shields, Andrea D.

AU - Howard, Bobby

AU - Gotkin, Jennifer L.

AU - Deering, Shad H.

AU - Hoeldtke, Nathan J.

AU - Napolitano, Peter G.

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AB - Objective: This study was undertaken to determine whether 17-hydroxyprogesterone caproate (17P) has a vasoactive effect on fetoplacental vasculature. Study design: Two cotyledons were obtained from each of 5 placentas. Baseline perfusion was established with Hanks-based solution. One cotyledon from each pair was then infused with perfusate to which U46619 a thromboxane sympathomimetic had been added. After 30 minutes, a dose of 17P was then administered to each cotyledon. Finally, a vasoconstricting dose of angiotensin II was administered to each cotyledon. Perfusion pressures were recorded throughout. Statistical analysis of pressure change for a single cotyledon was performed by using a paired t test. Statistical analysis of mean perfusion pressure difference between U46619 exposed and nonexposed cotyledons was analyzed by using a students t test. Results: 17P did not significantly alter the perfusion pressure of the control cotyledon. (30.6 ± 8.3 mm Hg vs 30.1 ± 7.8 mm Hg P = .48). 17P administration significantly lowered the perfusion pressure of the U46619 preconstricted vessels in comparison with preadministration. (60.1 ± 13 mm Hg vs 27.3 ± 7.1 mm Hg P = .03). Both groups of cotyledons responded with vasoconstriction to angiotension II with no difference in response between groups (38.3 ± 12 mm Hg vs 45.8 ± 8.2 mm Hg P = .63). Conclusion: 17P reverses induced vasoconstriction by U46619 in fetoplacental arteries.

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