Pediatric research
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The asphyxiated newborn is particularly vulnerable to hypotension, which contributes to hypoxic brain damage by reducing cerebral perfusion. During asphyxia, cerebral blood flow (CBF)( is pressure passive, that is, CBF autoregulation is abolished. It is important to know if the nonasphyxiated fetus and newborn are similarly vulnerable to hypotension. ⋯ After reinfusion, flow to all organs increased to near control levels. We conclude that the normoxic fetal lamb shows evidence of CBF autoregulation, and is able to preserve relative constancy of CBF within a blood pressure range of +/- 20% of normal. However, the evidence presented in this study suggests that autoregulation may be less effective in response to a hypotensive stress, even though CBF is better preserved than flow to most other organs.
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Arousal responses (AR) to hypercarbia and to hypoxia were ascertained in 25 N-M SIDS infants and 21 control infants in whom ventilatory responses to hypercarbia and hypoxia were also measured. Although the frequency of a positive AR to hypercarbia was not significantly less in the N-M SIDS compared to control group, the overall pattern was a generally absent AR in the lowest hypercarbic ventilatory response slope group progressing to a generally positive AR in the highest hypercarbic response slope group. ⋯ Although the PAO2 level at which an AR occurred did not differ in the two groups, a positive hypoxic AR occurred in 76% of the control versus only 29% of the N-M SIDS group (p less than .01). In summary, infants with a clinical N-M SIDS history and diminished ventilatory response slopes have as a group a concomitant abnormality in hypercarbic and/or hypoxic arousal.
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The time spent in REM, quiet, and indeterminate sleep was computed in 13 aborted SIDS infants and compared to that spent in the same sleep states, in 19 normal infants. Aborted sudden infant death syndrome (SIDS) infants were studied within a week of their aborted SIDS episode and subsequently at monthly intervals through the age of 4 months. ⋯ Sleep staging was performed by two independent observers using electroencephalogram, electrooculogram, electromyogram and behavioral criteria. Although there was an increase in the percentage of time spent in quiet sleep with age in both normal and aborted SIDS infants, the significantly greater regression coefficients in normal infants (6.3 versus 2.9; P less than 0.01) indicate that there are differences in the two groups and suggest a maturational abnormality or delay in sleep state distribution in the aborted SIDS infants.
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The effects of parenteral vitamin E treatment on aspects of the pulmonary biochemical and morphologic response to 100% oxygen were studied in newborn rabbits manifesting chemical evidence of vitamin E deficiency. Pups treated with 2 mg/100 g body weight increased serum vitamin E levels from 0.39 to 2.17 mg/dl by 72 hr and lung tissue vitamin E content from 3.52 to 17 mg/mg wet weight of lung. In vitro lipid peroxidation in lung homoginates of animals in 100% oxygen for 72 hr was inhibited by approximately 80% in animals receiving 100% oxygen plus vitamin E. ⋯ Mophometric analysis of lungs of animals in room air for 72 hr showed 81.6% of lung to be normal as compared with 43.3% normal lung in the group maintained in 100% oxygen for 72 hr. In the group treated with oxygen plus vitamin E, the lungs were similar to room air controls (82.6% normal). This study thus provides further evidence for a direct antioxident affect of vitamin E in lung.
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Comparative Study
Comparison of cytosolic and mitochondrial hepatic enzyme alterations in Reye's syndrome.
The activities of nine enzymes in liver specimens obtained from four children who had died from Reye's syndrome were compared to the corresponding activities of a control group of four children who had died from unrelated causes. At the 95% significance level, the alterations could be classified into three groups. Five activities [lactate dehydrogenase, alanine aminotransferase, glucose 6-phosphatase, cytochrome oxidase, and malate dehydrogenase (mitochondrial plus cytosolic)] showed no change. ⋯ Imbalances of the cytosolic:mitochondrial enzyme activities were evaluated in needle biopsy specimens from four other children under conditions where neurologic abnormalities were less severe. Two patients had elevated ratios of both glutamate:lactate dehydrogenase and cytosolic:mitochondrial malate dehydrogenase activities, and a third had only an abnormal malate dehydrogenase ratio. In contrast to these Reye's syndrome patients, a fourth case admitted with a provisional diagnosis of Reye's syndrome showed no abnormality in either ratio in stage IV coma.