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Canadian Journal of Anesthesia, Vol 23, 58-70, Copyright © 1976 by Canadian Anesthesiologists' Society
1 Department of Anesthesiology, The University of Utah College of Medicine, Salt Lake City, Utah 84132
2 Epidemiology Division, Brooks Air Force Base, San Antonio, Texas 78235
Urine excretion rates of norepinephrine were measured in 15 children with Tetralogy of Fallot and 25 with atrial septal secundum defects anaesthetized with halothane or morphine before, during and for two hours after surgical correction of their cardiac defects. All patients were paralyzed with d-tubocurarine, the tracheae were intubated and respiration was controlled. Urine was obtained for 90 minutes before induction, during induction, before, during and after bypass and postoperatively. Patients with TF had significantly higher pre-operative urine norepinephrine excretion rates than patients with ASD. In TF children anaesthetized with halothane norepinephrine excretion was significantly decreased during induction and during operation but increased post-operatively. Children with ASD and anaesthetized with halothane did not have urine norepinephrine excretion rates that were significantly different from pre-operative values until the postoperative period. ASD children anaesthetized with morphine had marked elevations in norepinephrine excretion during induction and all subsequent study periods. On the other hand, morphine anaesthetized TF children did not have a significant increase in urine norepinephrine excretion until bypass had been established. Increased norepinephrine excretion was maintained in these patients during all subsequent study periods. These data, when combined with our results in patients with acquired heart disease, demonstrate that disease can alter norepinephrine responses to morphine anaesthesia. In addition our results suggest that dosage of morphine and morphine blood levels might also modify norepinephrine excretion.
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