Production of nitric oxide during surgery involving cardiopulmonary bypass

Objectives: Surgery involving cardiopulmonary bypass induces an inflammatory response due to the contact of blood with the extracorporeal circuit. In some patients, this inflammatory response leads to multiple organ failure and death. Inflammatory states may increase the production of nitric oxide, either by increasing the activity of constitutive enzyme systems or by inducing of inflammation-specific systems. We hypothesized that surgery involving cardiopulmonary bypass would increase the production of nitric oxide in association with the inflammatory response. Design: Prospective, single center, observational study. Setting: University-affiliated, tertiary referral cardiothoracic center. Patients: Eleven adult patients undergoing routine myocardial revascularization. Interventions: Surgery for myocardial revascularization. Measurements and Main Results: Observations were made after induction of anesthesia, before bypass, after completion of the bypass, and on return to the recovery area. Parameters measured included hemodynamics, exhaled nitric oxide concentrations, plasma nitrate/nitrite concentration, plasma and bronchoalveolar lavage myeloperoxidase concentrations, and protein carbonyl conversion. All patients survived surgery. Oxygenation index fell significantly after bypass. Plasma myeloperoxidase increased significantly during the study period. Plasma carbonyl conversion also increased, although not significantly. Plasma nitrate/nitrite and airway nitric oxide concentrations did not change through the course of the study. Conclusion: Surgery involving cardiopulmonary bypass induced a demonstrable inflammatory response, but this response was not associated with increased nitric oxide production. (Crit Care Med 1998; 26:272-278) Surgery involving the use of cardiopulmonary bypass leads to systemic endotoxemia and the release of inflammatory cytokines, producing a generalized inflammatory state that, on a molecular level, resembles sepsis [1]. In most patients, this is a self-limiting process but a significant minority of patients develop profound organ dysfunction that may lead to multiple organ failure. After bypass, abnormalities of lung function are particularly common and can prolong postoperative recovery. Thus, significant increases in alveolar-arterial oxygen gradient, which may be accompanied by a gas transfer coefficient decrease by