PubMed · 10148123
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D J Macrae. 1993. ECMO parallels.. https://doi.org/10.1177/026765919300800112
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BACKGROUND: Rel/NF-kappaB, an oxidative stress-responsive transcription factor, participates transiently in the control of gene expression. The cellular mechanisms that mediate NF-kappaB activation during ischemia (and during reperfusion in the course of treating ischemia) are not known. METHODS AND RESULTS: To investigate the NF-kappaB activation induced during oxidative stress, we examined human cardiac tissue obtained during surgical procedures requiring cardiopulmonary bypass. In vitro, we examined human umbilical vein endothelial cells (HUVECs) exposed to hypoxia, reoxygenation after hypoxia, or a reactive oxygen intermediate (H(2)O(2)). Electrophoretic mobility shift assays performed on right atrial tissue revealed prominent NF-kappaB activation after hearts had been exposed to ischemia and reperfusion. The assays also showed that NF-kappaB activation was observed in hypoxic HUVECs after reoxygenation and in cultures treated with H(2)O(2) (500 micromol/L). Pervanadate (200 micromol/L) also induced marked NF-kappaB activation in HUVECs, indicating that H(2)O(2)-induced NF-kappaB activation is potentiated by the inhibition of tyrosine phosphatases. Western blotting of cytoplasmic IkappaBalpha demonstrated that NF-kappaB activation induced by oxidative stress was not associated with IkappaBalpha degradation. In contrast, tumor necrosis factor-alpha-induced NF-kappaB activation occurred in concert with degradation of IkappaBalpha. Inhibition of IkappaBalpha degradation with a proteasome inhibitor, MG-115, blocked NF-kappaB activation induced by tumor necrosis factor-alpha; however, MG-115 had no effect on NF-kappaB activation during oxidative stress. CONCLUSIONS: This study demonstrated a stimulus-specific mechanism of NF-kappaB activation in endothelial cells that acts independently of IkappaBalpha degradation and may require tyrosine phosphorylation.
OBJECTIVE: Review of our experience with the technically demanding arterial switch operation in transposition of the great arteries in children. METHODS: Twenty-seven children who underwent an arterial switch operation in our clinic were retrospectively reviewed. Except for one child (operated on at eight months), the operation was performed during the neonatal period. The underlying pathology was d-transposition of the great arteries in 25 children and a double outlet right ventricle of transposition type in 2. Five children had an associated ventricular septum defect and 1 aortic isthmus coarctation. The pattern of the coronary arteries was favourable in 18 children, difficult in 7 and dangerous in 3. The operation was performed in cardiopulmonary bypass for repair of the transposition and in a period of deep hypothermic circulatory arrest for repair of the intracardiac defects. RESULTS: One child died perioperatively and 1 postoperatively (operative mortality 7%) from myocardial ischaemia following unsuccessful transfer of a dangerous pattern of coronary arteries. Another child, a low-birth weight baby, died 80 days after the operation from respiratory failure. Postoperative morbidity occurred in 10 patients and medium-term morbidity in 6 patients who presented various degrees of stenosis of a pulmonary artery. During a median follow-up of 18 months no patient required reoperation. The children are asymptomatic and thriving satisfactorily. CONCLUSION: Because it restores the heart physiology, the arterial switch operation is considered the procedure of choice for correction of transposition of the great arteries. The operation involves acceptable mortality and morbidity. Transfer of difficult coronary artery patterns and development of stenosis on the pulmonary arteries remain problematic.
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