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Biomedical subjects

J Milerad

Publications and source records attributed to J Milerad.

52 records · Page 3Linked to original sources
PubMed1993

Nicotine exposure and the risk of SIDS.

The effects of parental smoking and nicotine exposure link a number of seemingly independent observations in SIDS research. There is accumulating evidence that fetal development and wellbeing are closely related to the subsequent risk of SIDS in the offspring. Furthermore, it appears that this risk is related, in particular, to alterations in brain development. The risk of dying of SIDS may thus, in reality, be confined to a limited number of infants with developmental changes in CNS function. Our findings of age-specific attenuation of hypoxic defense following nicotine exposure focus the attention on brain catecholamine metabolism as a potential target for adverse fetal and neonatal influences. To clarify the mechanisms of nicotine exposure on postnatal development of the control of respiration and cardiovascular control may thus offer insights into the ultimate mechanism of SIDS.

Animals↗
PubMed1992

Obstructive sleep apnea in Arnold-Chiari malformation treated with acetazolamide.

We studied respiratory patterns and transcutaneous gas pressures in two infants with Arnold-Chiari type II malformation referred to us due to repeated episodes of stridor and cyanosis. During both active and quiet sleep, respiration was irregular and absent or inverse thoracic breathing movements and frequent decreases in oxygen saturation to below 80% were observed. When breathing air with 2% CO2 or when given acetazolamide 10 mg/kg, chest wall movements normalized and oxygenation increased to near normal levels. After three months of treatment with acetazolamide 20 mg/kg/24 h no further episodes of hypoventilation or hypoxemia were observed and further treatment could be discontinued. We conclude that stimulation of respiration by CO2 or by acetazolamide appears to recruit chest wall muscles and promote upper airway patency in Arnold-Chiari malformation. A treatment trial with acetazolamide seems justifiable in these infants when respiratory problems are present.

Acetazolamide↗
PubMed1989

Respiratory and arousal responses to hypoxia in apnoeic infants reinvestigated.

Respiratory and arousal responses to mild hypoxia (15% oxygen in nitrogen) were recorded in 18 healthy infants and 33 infants who had sustained severe sleep related apnoeic events (ALTE). Respiratory movements and transcutaneous gas pressures (tcPO2 and tcPCO2) were continuously monitored during the 10 min test. The changes in tcPCO2 in relation to the decrease in tcPO2 were used as an index of the ventilatory and metabolic responses to hypoxia. We found that the response of apnoeic infants was within the range of the controls although the distribution of the individual response slopes was shifted towards the lower end of the range. Arousal was observed in 33% of apnoeic infants and 32% of the controls. Regular periodic breathing occurred in 42% of apnoeic infants compared to 28% of controls. In contrast to the controls, periodic breathing in apnoeic infants was not associated with a drop in tcPCO2 to below baseline levels. Apnoeic infants also alternated between regular and periodic breathing during the test. These findings are suggestive of a weak feed back control of breathing but do not support former views of a deficient hypoxic response in infants with ALTE.

Arousal↗
PubMed1989

Hypoxia reinforces laryngeal reflex bradycardia in infants.

The laryngeal chemoreflex involves bradycardia, apnea, swallowing and peripheral vasoconstriction. This reflex was studied in twelve infants, aged 5 days-28 weeks, who had sustained an apparent life-threatening event or were siblings of infants who had died of the sudden infant death syndrome. The bradycardic and apneic components of the reflex were found to be significantly, and sometimes powerfully, reinforced when elicited by pharyngeal water instillation during acute, mild hypoxia (transcutaneous PO2 4.6-8.3 kPa). Apnea duration during normoxia was 0.7-15 sec, and during hypoxia 2-30 sec. Heart rate change ranged from +26% to -21% during normoxia, as compared with -4% to -63% during hypoxia. The percentage change in heart rate was found to inversely correlate with the transcutaneous PO2-level prevailing when the reflex was elicited. The conclusion is that there is a significant reinforcement of the cardiorespiratory adjustments when the laryngeal reflex is activated during simultaneous excitation of the peripheral arterial chemoreceptors. One infant, showing a particularly strong increase of the cardiorespiratory response to laryngeal receptor stimulation during hypoxia, later died of sudden infant death syndrome.

Blood Gas Monitoring, Transcutaneous↗
PubMed1989

The effect of palatoplasty on airway patency and growth in infants with clefts and failure to thrive.

We monitored respiratory patterns, transcutaneous PO2 (tcPO2) and transcutaneous PCO2 (tcPO2) in three infants with clefts and severe failure to thrive. Unexplained dysphagia, muscular weakness and cardiac enlargement were other prominent symptoms. During sleep, repeated obstructive apneas accompanied by significant hypoxemia (tcPO2 less than 6 kPa) were recorded in all infants. Relief of the respiratory obstructions by means of nasopharyngeal intubation led to rapid growth catch-up and disappearance of the cardiac and gastrointestinal symptoms. This improvement in clinical condition was paralleled by an increase in transcutaneous PO2. Palatal closure according to Veau-Wardill-Killner led to a marked decrease in the number of airway obstructions and a significant improvement in blood gas homeostasis. The clinical condition of the infants was equally improved. We suggest that a respiratory investigation should be performed in infants with clefts and poor growth in spite of adequate caloric intake. Early closure of the palate should be considered in infants with signs of a respiratory failure.

Airway Obstruction↗
PubMed1987

The epidemiology of sudden infant death syndrome and attacks of lifelessness in Sweden.

Infants who died showing the syndrome of sudden infant death (SIDS) and infants who survived attacks of lifelessness (AL) were examined in a prospective epidemiological multicentre study over 24 months covering close to 40% of all births in Sweden. Seventy SIDS cases and 34 cases of AL were observed, giving an incidence for SIDS of 0.94/1000 and for AL of 0.46/1000. This SIDS incidence is higher than that observed during the seventies. The boy/girl ratio was 1.4:1 for SIDS and 1.6:1 for AL. The age distribution for AL resembled that for SIDS. Similarities were also seen with regard to place of occurrence. Sixty per cent of the SIDS cases occurred during the daytime/evening. Twenty-nine per cent of the infants with AL had more than one apneic spell during the three-day-period around the attack, indicating a period of respiratory instability, but only 12% had such spells later on. None of the infants who had had AL died from SIDS. The possible relationship between AL and SIDS is discussed.

Age Factors↗
PubMed1987

Effects of theophylline on ventilatory response to hypoxic challenge.

The respiratory and arousal responses to mild hypoxia during quiet sleep were studied using inductive plethysmography and transcutaneous gas electrodes in 11 apnoeic infants before and after the administration of oral theophylline (3 mg/kg). Theophylline changed the ventilatory response to a more biphasic pattern--that is, ventilation decreased after an initial increase. The relative ventilatory slope (defined as the decrease in transcutaneous carbon dioxide tension (PCO2) in relation to the fall in transcutaneous oxygen tension (PO2)) decreased significantly after theophylline. Four infants were roused during hypoxia before theophylline administration compared with none after treatment. Theophylline abolished the periodic breathing induced by hypoxia in one of six infants. These findings suggest that methylxanthines may not, as previously thought, enhance the respiratory drive during hypoxia.

Arousal↗
PubMed1987

Ventilatory and metabolic responses to acute hypoxia in infants assessed by transcutaneous gas monitoring.

Transcutaneous PO2, transcutaneous PCO2 and respiratory pattern were monitored during acute mild hypoxia (15% O2) in quiet sleep. Eighteen healthy infants were studied sequentially at 1-5 days, 4-8 weeks and 10-14 weeks of age. The transcutaneous PCO2 changes (delta PCO2) related to the transcutaneous PO2 fall, were used as an index of the total ventilatory and metabolic response during the test. This calculated index was related to the occurrence of arousal and periodic breathing. Transcutaneous PCO2 increased above control levels in infants 1-5 days old, decreased markedly in infants 4-8 weeks of age, and decreased slightly or remained unchanged in the 10-14 weeks old infants. The changes in response pattern were significant (P less than 0.006). These differences in response were not reflected in the lowest values of transcutaneous PO2 attained during the test. The lowest transcutaneous PO2 levels did not differ significantly between the age groups, indicating that the mechanisms maintaining PO2 during hypoxia may change during development. Periodic breathing was always associated with a decrease in transcutaneous PCO2 and in 8 out of 10 tests where it occurred it commenced at the lowest transcutaneous PCO2 level recorded. These results do not support the concept that periodic breathing is a sign of hypoventilation. Arousal was observed in less than half of the infants and was not related to the degree of hypoxaemia. We conclude that hypoxic arousal in infants may not be the important escape mechanism as suggested previously.

Arousal↗
PubMed1985

Alveolar hypoventilation treated with medroxyprogesterone.

Two children aged 1 and 20 months developed alveolar hypoventilation syndrome. They suffered severe apnoeic episodes and periodically required assisted ventilation. Their ventilatory response to carbon dioxide was lower than that of normal children and the transcutaneous oxygen tension during sleep was well below the normal range. Treatment with medroxyprogesterone acetate resulted in an improved response to carbon dioxide, and assisted ventilation was no longer needed. Oxygen and carbon dioxide tensions improved but were still slightly abnormal during sleep. There were no clinical side effects of treatment but one infant had slight pituitary suppression.

Carbon Dioxide↗
PubMed1980

Ventilatory studies in two older infants with prolonged apnea.

Two infants, both born before term, were found apneic, cyanotic and limp at home when they were 9 weeks and 2 weeks old, respectively. Their respiration was monitored in the hospital and found to be remarkably periodic during sleep, and was in one case accompanied by pronounced bradycardia. The periodic breathing and apnea seemed to be caused by a decreased oxygen tension which can induce an instability of the central respiratory control mechanisms.

Apnea↗
PubMedDate not supplied

Plasma levels of somatostatin and gastrin in sick infants and small for gestational age infants.

Sick neonates often have a disturbed gastrointestinal motility. As somatostatin inhibits various gastrointestinal functions, we investigated whether or not somatostatin levels are high in sick infants. Somatostatin and gastrin levels were measured in plasma samples collected from sick and healthy neonates. Somatostatin levels were found to be significantly elevated in sick infants when compared to healthy ones, both term (91 versus 5 pM) and preterm (35 versus 5 pM). We suggest that the gastrointestinal symptoms seen in infants during illness may be related to an enhanced secretion of gastric somatostatin.

Gastrins↗
PubMedDate not supplied

Smoking and the sudden infant death syndrome.

The aims of this review are (a) to critically examine the epidemiologic evidence for a possible association between smoking and the sudden infant death syndrome (SIDS), (b) to review the pathology and postulated physiological mechanism(s) by which smoking might be causally related to SIDS, and (c) to provide recommendations for SIDS prevention in relation to tobacco smoking. Over 60 studies have examined the relation between maternal smoking during pregnancy and risk of SIDS. With regard to prone-sleep-position intervention programs, the pooled relative risk associated with maternal smoking was RR = 2.86 (95% CI = 2.77, 2.95) before and RR = 3.93 (95% CI = 3.78, 4.08) after. Epidemiologically, to distinguish the effect of active maternal smoking during pregnancy from involuntary tobacco smoking by the infants of smoking mothers is difficult. Clear evidence for environmental tobacco smoke exposure can be obtained by examining the risk of SIDS from paternal smoking when the mother is a non-smoker. Seven such studies have been carried out. The pooled unadjusted RR was 1.49 (95% CI = 1.25, 1.77). Consideration of the pathological and physiological effects of tobacco suggests that the predominant effect from maternal smoking comes from the in utero exposure of the fetus to tobacco smoke. Assuming a causal association between smoking and SIDS, about one-third of SIDS deaths might have been prevented if all fetuses had not been exposed to maternal smoking in utero.

Female↗