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Increased thromboxane biosynthesis in normal pregnancy is mainly derived from platelets.
American Journal of Obstetrics and Gynecology
|August 1, 1987
Summary
Thromboxane biosynthesis, a marker of platelet activation, is significantly increased during pregnancy. This elevation is primarily derived from platelets and is effectively reduced by aspirin treatment.
Area of Science:
- Reproductive biology
- Cardiovascular physiology
- Biochemistry
Background:
- Thromboxane B2 is a key product of thromboxane biosynthesis.
- Pregnancy is associated with changes in cardiovascular function and hemostasis.
Purpose of the Study:
- To quantify thromboxane biosynthesis during normal pregnancy.
- To identify the cellular origin of increased thromboxane biosynthesis in pregnancy.
Main Methods:
- Measurement of urinary and plasma metabolites: 2,3-dinor-thromboxane B2 and 11-dehydro-thromboxane B2.
- Selective inhibition of platelet cyclooxygenase using aspirin.
- Assessment of prostacyclin biosynthesis via urinary 2,3-dinor-6-keto-prostaglandin F1 alpha.
Main Results:
- Urinary 2,3-dinor-thromboxane B2 levels were significantly elevated in early pregnancy compared to non-pregnant and postpartum states.
- Plasma and urinary 11-dehydro-thromboxane B2 also increased during pregnancy.
- Aspirin administration resulted in near-complete inhibition of urinary 2,3-dinor-thromboxane B2, indicating a platelet source.
Conclusions:
- Thromboxane biosynthesis is markedly increased in normal pregnancy.
- The primary source of this increased thromboxane biosynthesis is platelets.
- Elevated thromboxane biosynthesis reflects increased platelet activation throughout gestation.