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Published on: July 30, 2016
Peroxide induces vasoconstriction in the human placenta by stimulating thromboxane
1Department of Obstetrics and Gynecology, Medical College of Virginia, Virginia, Commonwealth University, Richmond 23298-0034.
Lipid peroxides in preeclampsia cause placental vasoconstriction by increasing thromboxane production. Aspirin and thromboxane blockers prevent this effect, indicating thromboxane synthesis is the key mechanism.
Area of Science:
- Obstetrics and Gynecology
- Cardiovascular Physiology
- Biochemistry
Background:
- Preeclampsia is associated with elevated placental lipid peroxides and thromboxane.
- Thromboxane is a potent vasoconstrictor impacting placental vasculature.
- Peroxides may stimulate cyclooxygenase, increasing thromboxane and causing placental vasoconstriction.
Purpose of the Study:
- To investigate if peroxides induce vasoconstriction in human placenta via enhanced thromboxane production.
- To test the hypothesis linking peroxide-induced vasoconstriction to thromboxane synthesis.
Main Methods:
- Isolated human placental cotyledons were perfused with t-butyl hydroperoxide.
- Perfusion was conducted with and without low-dose aspirin or a thromboxane receptor blocker (SQ 29,548).
- Vascular resistance, thromboxane B2, and 6-keto-prostaglandin F1 alpha levels were measured.
Main Results:
- Peroxide perfusion significantly increased vascular resistance and thromboxane B2 secretion.
- The thromboxane B2/6-keto-prostaglandin F1 alpha ratio increased threefold on the fetal side.
- Aspirin blocked peroxide-induced vasoconstriction and thromboxane increase; the thromboxane receptor blocker prevented vasoconstriction but not thromboxane increase.
Conclusions:
- Peroxides induce placental vasoconstriction by stimulating thromboxane synthesis.
- Low-dose aspirin inhibits both thromboxane secretion and vasoconstriction.
- Thromboxane receptor antagonists prevent vasoconstriction, confirming thromboxane's role in peroxide-induced placental vascular changes.
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