This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Congenital heart disease affects 1% of children worldwide. Many of these heart defects are amenable to surgical correction, with approximately 500,000 children undergoing open heart surgery every year in the USA. One of the major causes of morbidity and mortality associated with open heart surgery in children is the systemic inflammatory response syndrome (SIRS). This syndrome causes end-organ dysfunction following cardiopulmonary bypass (CPB). In children, the lungs are particularly vulnerable to post-CPB dysfunction and this may manifest as acute pulmonary hypertensive crisis and acute lung injury. It is unclear why some children will undergo an exaggerated inflammatory response to CPB and others do not. It is also difficult to predict those children that will develop post-operative pulmonary dysfunction. Possible factors contributing towards the differences in the SIRS and post-CPB lung dysfunction in children include: genetic predisposition, the pre-existing inflammatory state of the child, and the type of cardiac lesion. Children with cyanotic as opposed to acyanotic heart lesions may already have an inflammatory response that is upregulated secondary to chronic hypoxia. While there are numerous markers of the SIRS, none of these are immediately available to the clinician and the links between these markers and actual biological dysfunction are uncertain. One potential early marker of lung dysfunction is exhaled nitric oxide. The purpose of this study is to examine whether exhaled nitric oxide in children undergoing CPB could be an early marker of lung dysfunction for the cardiac anesthesiologist and be used to identify at risk children to potentially prevent further lung damage.
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