Why the study?
What are the hemodynamic effects of prostaglandin F2 alpha and prostaglandin E2 on the systemic and pulmonary circulation in anesthetized pregnant women?
What are the hemodynamic effects of prostaglandin F2 alpha and prostaglandin E2 on the systemic and pulmonary circulation in anesthetized pregnant women?
PGE2 may be more suitable than PGF2 alpha for induction in pregnant patients with cardiopulmonary diseases due to its lack of effect on pulmonary hemodynamics and slight decrease in systemic blood pressure.
May favor PGE2 for induction in cardiopulmonary disease; leaves open confirmation in randomized trials.
The hemodynamic effect of prostaglandin F2 alpha (PGF2 alpha) and of prostaglandin E2 (PGE2) was studied in 12 healthy volunteers admitted for suction abortion at 10--12 weeks of gestation. They were anesthesized using natrium thiomebumal, pethidine and pancuronium bromide. PGF 2 alpha was given as an intravenous infusion of 100 micrograms/min, the dose being increased by 100 micrograms every 10 min to a maximum of 300 micrograms/min. PGE2 was administered with 5 micrograms/min, the dose being increased by 5 micrograms every 10 min to a maximum of 15 micrograms/min. During infusion of 300 micrograms PGF2 alpha a significant increase iun cardiac output and femoral arterial pressure of 40% and 25% respectively was measured together with an increase in the pulmonary arterial pressure (125%). Pulmonary vascular resistance was doubled, with a concomitant decrease in systemic resistance (11%). These changes were followed by a significant decrease in pH and PaO2, whereas an increase in PaCO2 was found. During infusion of PGE2 a significant, 36% increase in cardiac output was measured during infusion of 15 micrograms/min PGE2, together with a decrease in systemic blood pressure (31%) and resistance (33%). Heart rate rose significantly, while stroke volume showed only a small increase, and pulmonary pressure was unchanged. These changes were followed by an increase in PaO2. PGF2 alpha seems to have a positive inotropic effect on the heart, whereas its response to PGE2 seems to be a result of the peripheral vasodilatation. The slight decrease in systemic blood pressure without change in pulmonary hemodynamics makes PGE2 suitable for induction in patients with cardiopulmonary diseases.
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Secher et al. (1982) studied this question.
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