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J Thorac Cardiovasc Surg 2004;128:109-116
© 2004 The American Association for Thoracic Surgery

Cardiopulmonary support and physiology

Inhaled prostacyclin reduces cardiopulmonary bypass–induced pulmonary endothelial dysfunction via increased cyclic adenosine monophosphate levels

S. Fortier, MDa, R.G. DeMaria, MD, PhDa,c, Y. Lamarche, MDa, O. Malo, MSca, A. Denault, MDb, F. Desjardins, BSca, M. Carrier, MDa, L.P. Perrault, MD, PhDa,*

a Research Center and Department of Surgery, Montreal Heart Institute, Montreal, Quebec, Canada
b Department of Anesthesiology, Montreal Heart Institute, Montreal, Quebec, Canada
c Cardiovascular Surgery Unit, Arnaud de Villeneuve Teaching Hospital, Montpellier, France

Received for publication April 1, 2003; revisions received September 25, 2003; accepted for publication September 29, 2003.

* Address for reprints: Louis P. Perrault, MD, PhD, Research Center, Montreal Heart Institute, 5000 Belanger Street East, Montreal, Quebec H1T 1C8, Canada
lpperrau{at}icm.umontreal.ca

OBJECTIVE: Cardiopulmonary bypass triggers a systemic inflammatory response that alters pulmonary endothelial function, which can contribute to pulmonary hypertension. This study was designed to demonstrate that inhaled prostacyclin, a selective pulmonary vasodilator prostaglandin, prevents pulmonary arterial endothelial dysfunction induced by cardiopulmonary bypass.

METHODS: Three groups of Landrace swine were compared: control without cardiopulmonary bypass (control group); 90 minutes of normothermic cardiopulmonary bypass (bypass group); 90 minutes of cardiopulmonary bypass and treated with prostacyclin during cardiopulmonary bypass (continuous nebulization with continuous positive airway pressure until the end of the cardiopulmonary bypass; prostacyclin group). After 60 minutes of reperfusion, swine were put to death and pulmonary arteries harvested. After contraction to phenylephrine, endothelium-dependent relaxation to bradykinin and acetylcholine was studied in standard organ chamber experiments. The pulmonary artery intravascular cyclic adenosine monophosphate content was compared between the 3 groups (post–cardiopulmonary bypass).

RESULTS: There was a statistically significant improvement of the endothelium-dependent relaxation to bradykinin in the prostacyclin group when compared with the bypass group (P < .05). There was no statistically significant difference for endothelium-dependent relaxation to acetylcholine (P > .05) between the prostacyclin and the bypass groups. There was a statistically significant decrease in the cyclic adenosine monophosphate content and a statistically significant increase of the mean pulmonary artery pressure in the bypass group only (P < .05).

CONCLUSION: Prophylactic use of inhaled prostacyclin has a favorable impact on the pulmonary endothelial dysfunction induced by cardiopulmonary bypass associated with preservation of pulmonary intravascular cyclic adenosine monophosphate content and the pulmonary vascular tone.




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