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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

^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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