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.
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.