Subjects with Glenn physiology (Group III) have a unique physiology where hepatic venous and lower body venous blood returns to the heart and enters the systemic ventricle and is recirculated to the body after combining with the pulmonary venous blood. There is no direct connection thru the heart for hepatic venous blood to enter the pulmonary arteries. Therefore, it is suspected that these patients will likely have elevated systemic arterial circulating levels of Substance P and VIP due to intracardiac right to left shunting and reduced pulmonary clearance. However, since these patients typically have normal portal venous pressures, they are not thought to have increased production of these vasoactive peptides. In addition, these patients historically are not at risk for developing PLE and PB. Studying these subjects will allow us to determine how systemic venous and systemic arterial levels of Substance P and VIP are altered by the Glenn circulation. By comparing systemic arterial and venous levels of vasoactive peptides among control, Glenn physiology and Fontan physiology groups we hope to measure differences in vasoactive peptide levels that could be responsible for the development of PLE and PB in Fontan physiology patients.