Effect of ethanol on thromboxane and prostacyclin production in the human placenta

Siler-Khodr, Theresa M; Yang, Yiqian; Grayson, Marcia H; Henderson, George I; Lee, Makau; Schenker, Steven

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Volume 21, Issue 2 , Pages 169-180, June 2000

Effect of ethanol on thromboxane and prostacyclin production in the human placenta

Theresa M Siler-Khodr
- Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, Room 416E, 7703 Floyd Curl Drive, San Antonio, TX 78284, USA
- Corresponding author. Tel.: 210-567-5009; fax: 210-567-3013
Yiqian Yang
- Department of Medicine, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78284, USA
Marcia H Grayson
- Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, Room 416E, 7703 Floyd Curl Drive, San Antonio, TX 78284, USA
George I Henderson
- Department of Pharmacology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78284, USA
Makau Lee
- Department of Medicine, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78284, USA
Steven Schenker
- Department of Medicine, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78284, USA

Received 13 December 1999; received in revised form 11 February 2000; accepted 16 February 2000.

Abstract

Fetal alcohol syndrome (FAS) is frequently associated with intrauterine growth retardation (IUGR). One cause of ethanol-induced IUGR is thought to be related to increased pressor activity in the human placenta, resulting in decreased oxygenation and nutrient transport to the fetus. Thus, we have investigated the effect of ethanol on paracrine substances, such as thromboxane and prostacyclin, that act as vasoregulators within the intrauterine tissues.

In these studies we have utilized the perfused single human cotyledon system to study the effect of ethanol on placental prostanoid production. We assessed the effect of longer (240 min) and more acute (60 min) exposure to ethanol on release of thromboxane B₂ (TxB₂) and 6-keto-prostaglandin F_1α (6-keto-PGF_1α) at the maternal and fetal sides of the placenta.

Thromboxane was increased by both longer and shorter ethanol exposure, especially on the fetal side of the placenta. Prostacyclin was essentially unchanged with exposure to ethanol. The thromboxane:prostacyclin ratio also tended to increase with both 60- and 240-min ethanol exposure, but a statistically significant increase was seen only at a few time points. In the 60-min ethanol exposure, an increase in thromboxane was observed both during and following exposure to ethanol.

The increase in the thromboxane milieu observed with ethanol exposure may lead, at least in part, to the IUGR which is frequently associated with FAS. Prevention of this effect of ethanol on thromboxane production might be a beneficial intervention for FAS.

Keywords: Fetus, Placenta, Mother, Alcohol, Thromboxane, Prostacyclin