[Equipment for microcomputer-controlled measurement in the evaluation of respiratory mechanical parameters in premature and newborn infants].
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Biomedical subjects
Publications and source records attributed to D Gmyrek.
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We observed a sudden respiratory arrest in four term newborn infants after a clinically symptom-free period. There were no cardiac, pulmonary or metabolic changes responsible for these events. Signs of cerebral dysfunction existed (muscular hypotonia, jitterness, seizures). Cranial computerized tomographic scans were performed during the period of respirator treatment within the first week of life. The density of the brain structures was significantly decreased in all cases, three of the patients showed a complete compression of the lateral ventricles. These findings indicated severe brain swelling as a consequence of cerebral hypoxia. There was a history of umbilical cord occlusion in two cases. In the remaining patients we must assume an undetected hypoxic-ischemic episode prior to the onset of labor. We used hyperventilation, corticosteroids, phenobarbital, diuretics and fluid restriction for therapy. Later on the babies received special physiotherapy. Control CT-scans were performed during the fourth or fifth week of life. The findings were normal in one patient. Signs of mild focal brain atrophy developed in two babies. A more severe cortical atrophic lesion of both temporal lobes was found in one patient. He suffered from a slight cerebral palsy. No neurodevelopmental handicaps could be found in all the other patients on long term follow-up. The EEG examination was performed between the fifth and seventh month of life. No pathologic changes were observed. We conclude that severe generalized brain edema in the newborn is not necessarily followed by extensive brain damage. We think it important to develop more sensitive methods for detecting a hypoxic ischemic crisis preceding the birth.
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The aim of this paper is to report on the influence of phenobarbital, the combination of phenobarbital/nikethamide, the racemate and (+) isomer of methylphenobarbital on the activity of bilirubin UDP-glucuronyltransferase and the concentration of intrahepatic Y and Z protein in rats. The activity of bilirubin DP-glucuronyltransferase increased after the treatment in all groups. Pretreatment with phenobarbital/nikethamide resulted in the highest enzyme activity, using wet weight as reference. (+) Methylphenobarbital isomer as well as the racemate showed effects similar to those of phenobarbital. The concentration of hepatic Y acceptor protein increased in all pretreated groups by about 30%. The drugs did not increase the concentration of Z protein. The (+) isomer of methylphenobarbital seems better suited as an inductive drug in the prophylaxis of hyperbilirubinemia and in the treatment of nonconjugated hyperbilirubinemia than phenobarbital or phenobarbital/nikethamide since it has no sedative effect.
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The bilirubin UDP GT-activity of the liver was studied from week 15 of pregnancy in 23 human fetuses and mature and immature dead newborns, respectively. No measurable bilirubin UDP GT-activity was found up to week 26 of pregnancy. The development of enzymatic activity presumably starts only postnatally, irrespective of gestational age of birth weight. Up to the fifth day the bilirubin UDP GT-activity is less than 0.2 mg of conjugated bilirubin/g liver/h, reaching in the second week values that correspond to approximately 20--30% of adult values. This activity is sufficient to prevent a clinically important hyperbilirubinemia because the concentration of unconjugated serum bilirubin was in all children below 12mg/100 ml.
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