Biomedical subjects
Publications and source records attributed to P Vert.
We describe a new case of postaxial acrofacial dysostosis (Miller) syndrome. This syndrome consists of mandibulofacial dysostosis, similar to that seen in Treacher Collins syndrome, and postaxial limb deficiency. The mode of inheritance remains uncertain.
The compliance (Crs), resistance (Rrs) and passive time constant (tau rs) of the respiratory system were determined by the single-breath method (sb) in 24 healthy term and preterm newborns. In 22 of them, Crssb was compared to the slope of the pressure-volume curve determined by the multiple occlusion technique (mo), which is not dependent on the assumption of a linear flow-volume relationship. Crssb and Rrs correlated significantly with body weight (kg): Crssb = 0.56 x kg + 1.22 (r = 0.67); Rrs = -20.1 x kg + 134.6 (r = -0.68). No difference in Crs and Rrs between prone and supine positions was found. tau rs was not significantly different between premature (0.21 +/- 0.06 s) and full-term infants (0.21 +/- 0.05 s). Crssb was significantly higher than Crsmo in premature babies (2.27 +/- 0.41 ml.cm H2O-1 vs. 1.98 +/- 0.47 ml.cm H2O-1. This difference may be explained by a continuous braking of expiratory airflow after release of the occlusion, or more likely, by a difference in the lung volume at which Crssb and Crsmo are measured. However, the difference between Crssb and Crsmo (approximately 15%) is in the same range as the intrasubject variability, and is meaningless compared to the alterations of respiratory mechanics observed during neonatal ventilatory disorders. Therefore, the single-breath method appears to be a suitable and noninvasive method to measure respiratory mechanics in nonintubated prematures.
Betaxolol levels in blood were monitored in the perinatal period in 28 pregnant hypertensive women and in their babies. In the mothers betaxolol concentrations at delivery ranged from less than 1 to 115 ng.ml-1 after doses of 10 to 40 mg.day-1. The apparent blood half-life was 15.6 to 22.1 h mean (19 h). Umbilical cord levels indicated a rapid equilibrium between fetal and maternal units (ratio 0.93) within few hours after dosing. Milk betaxolol concentrations, measured in few cases, exceeded those in blood by a factor of 3. Amniotic fluid concentrations were similar to those observed in maternal venous blood and umbilical cord blood. In neonates, the blood betaxolol half-life ranged from 14.8 to 38.5 h, with a definite trend towards a negative correlation with gestational age. A 11-61% rise in the betaxolol concentration was observed in 64% of the neonates during the first 12 h of extrauterine life. The data indicate that betaxolol kinetics is not altered in pregnant women and they stress the need for careful and prolonged (72-96 h) intensive monitoring of neonates born to hypertensive mothers treated with beta-blocking agents.
The role of the sympathetic nervous system on cerebral blood flow (CBF) autoregulation was evaluated in newborn piglets. Six animals were studied after ablation of the right superior sympathetic ganglion and compared to 6 control animals. Mean arterial blood pressure (MABP) was decreased by successive blood withdrawal and CBF was measured by radioactive microspheres. In denervated animals, MABP and CBF correlated positively according to a parabolic curve showing an absence of autoregulation when MABP is above 50 mm Hg (y = 0.079x2 - 5.9x + 154, p less than 0.01). In control animals, CBF remains stable throughout the experiment (y = 0.28x + 5). These data suggest a shift to the left of the upper limit of the autoregulation range in denervated animals and consequently a poor adaptation to increased MABP.
The incidence of cytomegalovirus (CMV) infection among 107 low birth weight transfused infants (birth weight less than or equal to 1,500 g) admitted to an intensive care nursery over an 18 month period was evaluated. The diagnosis of CMV infection was based on specific serologic tests (presence of IgM, increased IgG by ELISA technic) and identification of the virus in the urine. During the first 8 months, the infants received untested blood and CMV disease occurred in 8 infants out of 44 (18.2%). During the following 10 months, all transfusions performed in 63 infants were supposed to be CMV negative. However, 32 infants received untested blood due to emergency, and 5 of them developed a CMV infection (15.6%). Finally, only 31 infants received CMV negative blood without any case of CMV infection. These data clearly demonstrate that, considering the severity of the CMV disease in the premature infants, transfusions should be performed with CMV negative blood products.
The effect of phenobarbital and pancuronium on cerebral blood flow (CBF) and CBF autoregulation are studied in newborn piglets after chemically induced seizures with bicuculline. Given 3 or 15 min after the onset of seizures, phenobarbital significantly reduces CBF (59 +/- 11 and 56 +/- 17 vs. 84 +/- 24 ml/min/100 g - p less than 0.01). Moreover, during graded hypotension induced by graded haemorrhage, phenobarbital provides reestablishment of CBF autoregulation altered by seizures. In the same experimental model, pancuronium induces in control animals a rise of CBF (61 +/- 15 vs. 38 +/- 11 ml/min/100 g - p less than 0.001). During graded hypotension pancuronium is associated to a loss of CBF autoregulation (r = 0.76, p less than 0.001). Given as an adjunct treatment, in case of seizures, pancuronium has no significant effect on changes in cerebral haemodynamics. From these data, we conclude that pancuronium jeopardizes the haemodynamic adaptation to the induced hypovolemia and that phenobarbital may present a protective effect on cerebral haemodynamics and the subsequent risk for ischaemia or haemorrhage.
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This study reports the neonatal aspects and prognosis of seizures observed in 71 neonates from 1.3. 1980 to 30.6 1981. Forty-five were full-term, 26 preterm babies. Twenty-one children had status epilepticus (SE), 50 isolated crises (IC). An etiology was found in 68 cases. Acute fetal distress (AFD) was observed in half of the cases. AFD and intracranial hemorrhages represented 62% of the etiologies in term babies, 42% in preterm. Fifteen children died in the neonatal period. The outcome of the 56 survivors was followed until at least two years of age. Forty-one children were neurologically normal; 15 were not: 9 had a cerebral palsy, 12 a mental retardation, 1 was deaf, 4 were epileptic. Sequelae occurred in 24.3% of term, 31.6% of preterm survivors (p less than or equal to 0.01). The outcome was normal in 8 out of 15 living children with SE (53%), in 32 out of 41 (78%) with IC (p less than or equal to 0.01). The prognosis of hypoxic-ischemic seizures was good if crises lasted less than two days. Treatment was discontinued as soon as possible, during the days following the end of the crises and the recovery from the initial disease, without adverse effects. Convulsions following obstetrical abnormalities were less frequent, and the prognosis was better in premature babies than in previous studies.
Over a 4-year period, 63 premature babies presenting with patent ductus arteriosus were treated with indomethacin at two different dosage levels (0.1 and 0.2 mg/kg). For all infants the permanent closure rate was 68% (56% with 0.1 mg/kg and 75% with 0.2 mg/kg - n.s.) and the positive response rate (i.e. permanent and transient closure) 84%. There was no difference between the two dosages in the incidence of side-effects, particularly on diuresis, and in mortality and morbidity rates; the overall mortality rate was 31%. Pharmacokinetic studies performed in 51 cases did not show any difference related to indomethacin dosage. The changes observed after 2 or 3 doses resulted from improvement in haemodynamics. This study confirms the effectiveness of indomethacin in the treatment of patent ductus arteriosus and suggests an advantage for the 0.2 mg/kg dose.
The effects of two doses of tolazoline have been compared in 2 groups of newborns suffering from the persistent fetal circulation syndrome. The effects on PaO2 and AaDO2 were similar in the 2 groups who received either a bolus of 1 or 0.5 mg X kg-1 tolazoline, followed by a continuous infusion of 1 or 0.5 mg X kg-1 X h-1. The observed changes did not differ significantly from those previously observed in babies treated with 2 mg X kg-1. A rise in PaO2 and a reduction in AaDO2 were usually observed shortly after the bolus injection and at plasma levels between 1.5 and 4 micrograms X ml X -1. A progressive rise in plasma level over time occurred after 1 mg X kg-1 (and in the previous study of 2 mg) but not with 0.5 g/kg tolazoline. The elimination half-life of tolazoline in 6 patients was 5 to 13 h. The data suggest that continuous infusion of tolazoline is not necessarily required and that the dose of 0.5 mg/kg is more appropriate and safer than the higher doses usually proposed.
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To assess the effects of intravenous tolazoline on hemodynamics and regional blood flow distribution, 12 anesthetized newborn piglets were studied. Six piglets received saline and served as controls, the other 6 received two bolus doses of tolazoline (1 and 2 mg/kg). Mean arterial blood pressure decreased from control levels of 69.4 +/- 5.6 to 54.6 +/- 7.0 and 47.0 +/- 5.6 mm Hg, respectively, after 1 and 2 mg/kg of tolazoline, and heart rate increased from 220 +/- 9 to 270 +/- 13 and 282 +/- 8 beats/min, respectively. Cardiac output and regional blood flows were measured 15 min after tolazoline by the radioactive microsphere technique. Cardiac index did not change significantly. There was a redistribution of cardiac output toward the coronary circulation, with an increase in coronary blood flow from a control value of 249.3 +/- 39.9 to 361.0 +/- 56.4 ml/min/100 g of tissue after 1 mg/kg of tolazoline. Bronchial blood flow was also significantly increased. After a dose of 2 but not 1 mg/kg, the renal blood flow was markedly decreased from 139.8 +/- 17.8 to 104.4 +/- 24.5 ml/min/100 g. The other regional blood flows were not significantly modified. We conclude that tolazoline is a potent coronary vasodilator during the neonatal period. In addition we speculate that the decrease in renal blood flow might play a role in the renal toxicity of tolazoline.
The physiologic factors that predispose premature infants to apnea are reviewed in this article. Management and treatment of "idiopathic apnea" are discussed. "Symptomatic apnea" should be treated according to its primary cause.
After presentation of the actual knowledge concerning the pathophysiology of bronchopulmonary dysplasia, the prevention and the management of the disease are discussed. Techniques of ventilation, weaning procedures and prescription of drugs are also analyzed. The importance of a slow reduction of oxygen supply and the possibility of discharge with oxygen therapy is emphasized.
The quantitative 2-[14C]deoxyglucose autoradiographic method was used to compare the effects of acute and chronic administration of caffeine on rat brain energy metabolism. The acute intravenous administration of caffeine (10 mg/kg) to naive rats induced widespread increases in glucose utilization in 20 of 62 structures, mainly in striatal and related areas as well as in the 2 raphe nuclei and the locus coeruleus. After 2 weeks' chronic intraperitoneal injection of caffeine (10 mg/kg), increases in glucose utilization were seen in 6 of 62 structures: the substantia nigra, pars compacta, dorsal raphe, locus coeruleus and the 3 parts of the caudate nucleus. An acute caffeine injection (10 mg/kg) to these chronically caffeine-treated rats induced a further increase in glucose utilization in 9 additional structures but there was no significant difference in the effects of an acute administration of caffeine whether the rats had been chronically pretreated with caffeine or saline. The results of the present study show that brain energy metabolism seems to be subject to only partial tolerance to central stimulation by caffeine.
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Eighteen newborns (gestational age 28 to 42 weeks and post-natal age 0.5 to 44 days) suffering from convulsions not controlled by phenobarbital were treated with clonazepam 0.1 mg/kg (8 cases) or 0.2 mg/kg (10 cases) administered by slow intravenous infusion. The plasma half-lives in these "phenobarbital pretreated neonates' were of the same order of magnitude as those reported in adults (20-43 h). Post-natal age did affect clearance, which was 50-70% less than in adults and older children. At the end of the infusion period, plasma clonazepam ranged from 28 to 117 ng/ml in the 0.1 mg/kg group and from 99 to 380 ng/ml in the 0.2 mg/kg group. In the former an immediate therapeutic response was observed in 7 out of 8 cases, and in the latter a significant and somehow delayed effect on convulsion was present only in 6 cases. The data suggest that optimal therapeutic response might already have been achieved with the 0.1 mg/kg dose. Higher doses and toxic concentrations of clonazepam may be detrimental to complete control of seizures and may expose the newborn to an unnecessary risk of adverse events.
The concentrations of acebutolol and of its main active metabolite diacetolol in milk and plasma were studied in 7 hypertensive mothers treated with acebutolol, a cardioselective beta-adrenoceptor blocking agent. Clinical monitoring on their newborn babies was also done, as well as measurement of plasma level of the drug in them. The ratio between milk and plasma concentrations ranged from 1.9 to 9.2 for acebutolol and from 2.3 to 24.7 for diacetolol, and in any given milk sample, the diacetolol concentration was always higher than that of acebutolol. In a newborn infant, plasma concentrations of the two transplacentally acquired substances was raised when breast feeding started and remained high. Clinical signs of pharmacological beta-blockade were observed. Evaluation of the iatrogenic risk shows that pharmacologically active amounts of acebutolol might be received by a neonate if the daily maternal dosage exceeds 400 mg/day and/or renal function in the mother is impaired.