Cardiac surgery for congenital heart disease often necessitates a period of myocardial ischemia during cardiopulmonary bypass and cardioplegic arrest, followed by reperfusion after aortic cross-clamp removal. In experimental models, myocardial ischemia-reperfusion is associated with significant oxidative stress and ventricular dysfunction. A prospective observational study was conducted in infants (<1 year) who underwent elective surgical repair of a ventricular septal defect (VSD) or tetralogy of Fallot (TOF). Blood samples were drawn following anesthetic induction (baseline) and directly from the coronary sinus at 1, 3, 5, and 10 min following aortic cross-clamp removal. Samples were analyzed for oxidant stress using assays for thiobarbituric acid-reactive substances, protein carbonyl, 8-isoprostane, and total antioxidant capacity. For each subject, raw assay data were normalized to individual baseline samples and expressed as fold-change from baseline. Results were compared using a one-sample t test with Bonferroni correction for multiple comparisons. Sixteen patients (ten with TOF and six with VSD) were enrolled in the study, and there were no major postoperative complications observed. For the entire cohort, there was an immediate, rapid increase in myocardial oxidative stress that was sustained for 10 min following aortic cross-clamp removal in all biomarker assays (all P < 0.01), except total antioxidant capacity. Infant cardiac surgery is associated with a rapid, robust, and time-dependent increase in myocardial oxidant stress as measured from the coronary sinus in vivo. Future studies with larger enrollment are necessary to assess any association between myocardial oxidative stress and early postoperative outcomes.

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To study local regulation of convective O2 delivery, in vivo experiments were conducted using a gas chamber to oscillate the O2 environment at one surface of rat skeletal muscle. Intravital video microscopy enabled quantification of the hemodynamic (RBC velocity, V, and hematocrit, H) and O2 saturation responses in capillaries. To assess how changes in arteriolar diameters lead to the observed blood flow response, a model of the lower three levels of the arteriolar tree was constructed based on published data. Sinusoidal changes in vessel diameter were imposed at the distal end of one terminal arteriole, and the upstream conduction of these diameter changes was simulated. A quasi‐steady model of two‐phase (RBCs and plasma) blood flow was used to calculate time‐dependent hemodynamics in the network. For a range of forcing frequencies, conduction velocities (Vcond), and attenuation lengths, the ability of the system to control RBC supply in a terminal arteriole was studied. Attenuation lengths within the physiological range (2mm to 2cm) did not affect the flow response. Decreases in frequency and increases in Vcond increased the amplitude of the flow response. For a frequency of 0.025 Hz, varying Vcond from 10 μm/sec to 50 μm/sec increased the RBC supply response by 35%. Predicted changes in H and V showed qualitative agreement with experimental results. Supported by NIH HL‐089125, CIHR to CGE and DG, and NSERC to SJMM.