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Effect of Xylocaine on infant rat brain mitochondria

Local anesthetics are widely used in obstetric practice to facilitate painless delivery. Their usage has been associated with neonatal respiratory depression and, in the case of fetal injection, with neonatal seizures. Because of these observations the effect of Xylocaine on infant rat brain mitochondrial enzymes was investigated.The neurochemlcal development of 5- to 10-day-old infant rats approximates that of the human newborn. Xylocaine was administered intraperitoneally to infant rats at this age in doses calculated to produce blood levels comparable to those in human newborns with toxic signs and symptoms. Two hours after injection there was a 65% decrease in brain D(—)-beta-hydroxybutyrate dehydrogenase (HBDH) activity and a 40% decrease in succinic dehydrogenase (SDH) activity. Brain cytochrome oxidase (CyO) activity was not significantly decreased. Temporal examination of these enzymes after injection suggested that HBDH was the first enzyme inhibited. These observations are in contrast to the lack of inhibition of liver HBDH, SDH, and CyO. The inhibition of oxidative enzymes in infant rat brain mitochondria persists up to 5 hours after injection. This enzyme inhibition is also demonstrable in measurements of respiration of intact brain mitochondria. Oxygen consumption of normal infant rat brain mitochondria is best supported by D(—)-beta-hydroxybutyrate (BOH), but succinate was also effective. BOH dependent respiration of infant rat brain mitochondria was inhibited by Xylocain in vivo and in vitro. The data suggest that further studies of Xylocaine usage and effects in the perinatal period are indicated.