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J Thorac Cardiovasc Surg 1999;117:343-351
© 1999 Mosby, Inc.

SURGERY FOR CONGENITAL HEART DISEASE

ROLE OF THE ENDOTHELIUM IN PLACENTAL DYSFUNCTION AFTER FETAL CARDIAC BYPASS

From the Division of Cardiothoracic Surgery^a and Department of Pediatrics,^b University of California–San Francisco, and Department of Pediatrics,^c New York University, New York.

Supported in part by funding from the National Institutes of Health, grant RO1 HL43357.

Read at the Seventy-eighth Annual Meeting of The American Association for Thoracic Surgery, Boston, Mass, May 3-6, 1998.

Received for publication May 8, 1998. Revisions requested June 19, 1998; revisions received Sept 30, 1998. Accepted for publication Oct 7, 1998. Address for reprints: V. Mohan Reddy, MD, Division of Cardiothoracic Surgery, 505 Parnassus Ave, M593 San Francisco, CA 94143-0118.

Background: Fetal cardiac bypass causes placental dysfunction, characterized by increased placental vascular resistance, decreased placental blood flow, hypoxia, and acidosis. Vasoactive factors produced by the vascular endothelium, such as nitric oxide and endothelin 1, are important regulators of placental vascular tone and may contribute to this placental dysfunction.
Methods: To investigate the role of the vascular endothelium in placental dysfunction related to fetal cardiac bypass, we studied 3 groups of fetal sheep. In the first group (n = 7) we determined placental hemodynamic responses before and after bypass to an endothelium-dependent vasodilator (acetylcholine), an endothelium-independent vasodilator (nitroprusside), and endothelin 1. In the second group (n = 8) a nonspecific endothelin receptor blocker (PD 145065) was administered and placental hemodynamic values were measured before and after bypass. In the third group (n = 5) endothelin 1 levels were measured before and after bypass.
Results: Before fetal cardiac bypass exogenous endothelin 1 decreased placental blood flow by 9% and increased placental resistance by 9%. After bypass endothelin 1 decreased placental flow by 47% and increased resistance by 106%. There was also a significant attenuation of the placental vascular relaxation response to acetylcholine after bypass, whereas the response to nitroprusside was not significantly altered. In fetuses that received the PD 145065, placental vascular resistance increased significantly less than in control fetuses (28% versus 62%). Similarly, placental blood flow decreased significantly more (from 6.3 ± 3.1 to 28.3 ± 10.4 pg/mL; P = .01) in control fetuses than in fetuses receiving PD 145065 (33% versus 20%). Umbilical venous endothelin 1 levels increased significantly in fetuses exposed to fetal bypass but did not change in control fetuses.
Conclusions: The basal endothelial regulatory mechanisms of placental vascular tone were deranged after fetal cardiac bypass. Endothelin receptor blockade, which substantially reduced postbypass placental dysfunction, and other interventions aimed at preserving endothelial function may be effective means of optimizing fetal outcome after cardiac bypass.

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