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J Thorac Cardiovasc Surg 2004;127:44-50
© 2004 The American Association for Thoracic Surgery

Cardiopulmonary support and physiology

Supplemental nitric oxide and its effect on myocardial injury and function in patients undergoing cardiac surgery with extracorporeal circulation

^a CNR Institute of Clinical Physiology, G. Pasquinucci Hospital, Massa, Italy

Received for publication March 26, 2002; revisions received June 3, 2002; accepted for publication August 16, 2002.

^* Address for reprints: Jacopo Gianetti, MD, PhD, G. Pasquinucci Hospital, CNR, Institute of Clinical Physiology, Via Aurelia Sud, 54100 Massa, Italy
gianetti{at}ifc.cnr.it

BACKGROUND: Cardiopulmonary bypass induces a systemic inflammatory response that may contribute to clinical morbidity. Gaseous nitric oxide at relatively low concentrations may elicit peripheral anti-inflammatory effects in addition to a reduction of pulmonary resistances. We examined the effects of 20 ppm of inhaled nitric oxide administered for 8 hours during and after cardiopulmonary bypass.

METHODS AND RESULTS: Twenty-nine consecutive patients undergoing aortic valve replacement combined with aortocoronary bypass were randomly allocated to either 20 ppm of inhaled nitric oxide (n = 14) or no additional inhalatory treatment (n = 15). Blood samples for total creatine kinase, creatine kinase MB fraction, and troponin I measurements were collected at 4, 12, 24, and 48 hours postsurgery. In addition, we collected perioperative blood samples for measurements of circulating nitric oxide by-products and brain natriuretic peptide. Soluble P-selectin was analyzed in blood samples withdrawn from the coronary sinus before and after aortic clamping. The area under the curve of creatine kinase MB fraction (P = .03), total creatine kinase (P = .04), and troponin I (P = .04) levels were significantly decreased in the nitric oxide–treated patients. Moreover, in the same group we observed blunted P-selectin and brain natriuretic peptide release (P = .01 and P = .02, respectively). Nitric oxide inhalation consistently enhanced nitric oxide metabolite levels (P = .01).

CONCLUSIONS: Nitric oxide, when administered as a gas at low concentration, is able to blunt the release of markers of myocardial injury and to antagonize the left ventricular subclinical dysfunction during and immediately after cardiopulmonary bypass. The organ protection could be mediated, at least in part, by its anti-inflammatory properties.

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