Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because infants of substance-abusing mothers (ISAM) have an increased risk of sudden infant death syndrome and have abnormal sleeping ventilatory patterns, we studied the effects of mild hypoxia during quiet sleep on ventilatory pattern, heart rate, and arousal in 23 healthy ISAM (mean +/- SEM: 9.0 +/- 0.49 weeks of age) and 15 healthy, similarly aged, control infants. Hypercapnic challenges were performed in six ISAM and eight control subjects. Hypoxic arousal responses were elicited by rapidly decreasing inspired oxygen tension to 80 mm Hg for 3 minutes or until arousal occurred. Failure to arouse to hypoxia occurred in the majority of infants in both groups. All infants had a fall in end-tidal carbon dioxide tension during hypoxia, suggesting that each had a hypoxic ventilatory response. However, the fall in end-tidal carbon dioxide tension was significantly less in the ISAM (mean +/- SEM: -4.0 +/- 0.3 vs -8.0 +/- 1.0 mm Hg), suggesting blunted ventilatory responses to hypoxia. Periodic breathing occurred during 9.5% of hypoxic challenges in control infants compared with 37% in ISAM (p = 0.056). Heart rates were significantly higher in the ISAM before, during, and after hypoxic challenges. Hypercapnic challenges (inspired carbon dioxide tension of 60 mm Hg for a maximum of 3 minutes) resulted in arousal in all infants; however, ISAM required a significantly longer exposure to hypercapnia before arousal (mean +/- SEM; 116 +/- 7.8 vs 79 +/- 13.9 seconds; p < 0.02). We conclude that ISAM have an impaired repertoire of protective responses to hypoxia and hypercapnia during sleep, and that this may play a role in their increased risk for sudden infant death syndrome.
 ...
PMID:Responses to hypoxia and hypercapnia in infants of substance-abusing mothers. 143 17

Siblings of sudden infant death syndrome (SIDS) victims have been shown to have abnormal ventilatory patterns and altered responses to respiratory stimuli during infancy. To evaluate whether these abnormalities persist, we studied ventilatory responses in 20 older SIDS siblings (9.8 +/- 0.9 (mean +/- SEM) years of age) and 20 control subjects (10.2 +/- 0.9 years of age). To evaluate hypercapnic ventilatory responses, we had subjects rebreathe 5% carbon dioxide and 95% oxygen until end-tidal carbon dioxide tension reached 65 mm Hg. Instantaneous minute ventilation, mean inspiratory flow, and respiratory rate were calculated breath by breath. Hypercapnic responses did not differ between SIDS siblings (2.08 +/- 0.14 L/min per mm Hg) and control subjects (1.90 +/- 0.10 L/min per mm Hg; not significant). To assess hypoxic ventilatory responses, we asked subjects to rebreathe 13% oxygen and 7% carbon dioxide, with the balance nitrogen, at mixed-venous end-tidal carbon dioxide tension, until arterial oxygen saturation by pulse oximetry fell to 75%. No differences in hypoxic ventilatory responses were found between the SIDS siblings (-1.39 +/- 0.15 L/min/% saturation) and the control subjects (-1.22 +/- 0.17 L/min/% saturation; not significant). The mean inspiratory flow, tidal volume, respiratory rate, and heart rate responses to hypercapnia and hypoxia were also similar in the two groups. We conclude that there is no difference in hypercapnic and hypoxic ventilatory and cardiac responses, as assessed by rebreathing techniques, between school-aged SIDS siblings and control subjects. We speculate that in SIDS siblings the control of breathing is immature during infancy and that they achieve maturity of control and resolution of breathing abnormalities with time.
 ...
PMID:Hypercapnic and hypoxic ventilatory and cardiac responses in school-aged siblings of sudden infant death syndrome victims. 151 13

Failure to arouse in response to hypoxia has been described in infants at increased risk for sudden infant death syndrome (SIDS) and has been suggested as a possible mechanism for SIDS. However, most SIDS victims are not in a high-risk group before death. Thus, if a hypoxic arousal disorder is an important contributor to SIDS, normal infants might fail to arouse from sleep in response to hypoxia. To test this hypothesis, the authors studied hypoxic arousal responses in 18 healthy term infants younger than 7 months of age (age 12.1 +/- 1.7 [SEM] weeks; 56% girls). Hypoxic arousal challenges were performed during quiet sleep by rapidly decreasing inspired oxygen tension (PIO2) to 80 mm Hg for 3 minutes or until arousal (eye opening, agitation, and crying) occurred. Tests were performed in duplicate when possible. Only 8 infants (44%) aroused in response to one or more hypoxic challenges; arousal occurred during 8 (32%) of 25 trials. There were no significant differences in lowest PIO2 or arterial oxygen saturation during hypoxia between those infants who aroused and those who failed to arouse. All 18 infants had a fall in their end-tidal carbon dioxide tension during hypoxia, suggesting that each had a hypoxic ventilatory response despite failure to arouse in the majority. Periodic breathing occurred following hypoxia in only 1 (13%) of the 8 trials that resulted in arousal, compared with 16 (94%) of 17 trials without arousal (P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hypoxic arousal responses in normal infants. 157 95

Prenatal cocaine (CC) exposure may result in increased fetal loss, growth retardation, altered neurodevelopment, and sudden infant death syndrome (SIDS). We sought to establish an animal model for prenatal cocaine exposure which (1) would allow us to distinguish the direct effects from the indirect and nutritional effects of the drug, and (2) might be used to address questions of cocaine's toxicity, specifically to the developing respiratory control system. The study design included 38 New Zealand White rabbit does among CC, pair-fed (PF), and free-fed (FF) groups. Miniosmotic pumps were implanted in each doe on day 10 of timed gestation providing continuous subcutaneous administration of either 30 mg/kg/day of cocaine HCl in H2O (CC) or sterile H2O alone (PF and FF). Mean (SEM) plasma cocaine concentration was 1.71 +/- 0.21 mumol/l (519.4 +/- 64.4 ng/ml). Pregnancy outcome compared for incidence of stillbirth, maternal death, spontaneous abortion, and gross malformation among 211 pups was significant only for increased stillbirths among CC pups (18%, p less than 0.04) as compared to PF (6%) and FF pups (7%). External and renal malformation and postnatal weight, crown-rump length, and snout-occiput head circumference for pups aged 4 and 5 days of age did not differ among groups. The direct effects of prenatal cocaine evaluated in our model do not reproduce the altered perinatal outcome observed among humans. However, our results do not determine if physiologic function has been altered. Investigation of the physiologic and pathologic abnormalities that are relevant to this human condition, specifically to the developing respiratory control system, should add clarity to the mechanism of action of cocaine during pregnancy.
 ...
PMID:Effects of prenatal cocaine exposure on perinatal morbidity and postnatal growth in the rabbit. 178 40

The cause of sudden infant death syndrome (SIDS) is unknown, although deficits in cardiopulmonary function and central respiratory control have been suggested as possible mechanisms of the disorder. In this study, we tested the hypothesis that SIDS is associated with a delay in the maturation of hematopoiesis. Prolonged elevation in the levels of fetal hemoglobin (hemoglobin F) in infants with SIDS could denote a compromised delivery of oxygen to sensitive tissue sites. Normally, hemoglobin F (alpha 2 gamma 2) is largely replaced by adult hemoglobin, hemoglobin A (alpha 2 beta 2), during the first six months after birth. Using an isoelectric-focusing procedure for measuring stable hemoglobin subunits, we quantitated the levels of hemoglobin F in blood samples from 59 patients with SIDS and 40 controls (32 living and 8 dead) matched for postconceptional age. The level of hemoglobin F in the population with SIDS was significantly higher than that in the controls in the age range tested (39 to 75 weeks); the mean (+/- SEM) proportion of hemoglobin F was 63.2 +/- 3.6 percent in the group with SIDS, as compared with 48.1 +/- 5.0 percent in the controls (P less than 0.025). The difference in hemoglobin F levels was most pronounced 50 weeks after conception: the proportion of hemoglobin F in the 37 patients with SIDS with a postconceptional age of more than 50 weeks was 47.4 +/- 3.6 percent, as compared with 18.8 +/- 3.1 percent in the 19 controls of that age (P less than 0.0005). We conclude that hemoglobin F is a useful postmortem marker for the population with SIDS that we studied and that it may have value as a prospective marker for some infants at risk for SIDS.
 ...
PMID:Elevated fetal hemoglobin levels in sudden infant death syndrome. 243 54

Elaboration of beta-endorphins (beta-ED) is implicated in the modulation of respiratory control in infants. Therefore, beta-ED concentrations were measured in paired samples of CSF and plasma in three groups of infants. Group 1 and group 3 were used as controls. Group 2 infants suffered prolonged apnea of infancy (near-miss sudden infant death syndrome) and were successfully resuscitated. Age and weight (mean +/- SEM) in groups 1, 2 and 3 were 8.5 +/- 3 months and 7.2 +/- 1.4 kg, 3.8 +/- 0.7 months and 5.2 +/- 0.6 kg, and 3.4 +/- 0.9 months and 3.4 +/- 0.7 kg, respectively. CSF beta-ED concentrations were found to be significantly elevated in group 2, 67.8 +/- 4.7 pg/ml, when compared to group 1, 29.8 +/- 3.1 pg/ml, and group 3, 46.5 +/- 7.2 pg/ml (p less than 0.01). No correlation was observed with plasma and CSF concentrations in all three groups. beta-ED may play a role in the pathophysiology of prolonged infant apnea (near-miss sudden infant death syndrome).
 ...
PMID:Cerebrospinal fluid and plasma beta-endorphin concentrations in prolonged infant apnea (near-miss sudden infant death syndrome). 294 29

To determine the efficacy of theophylline treatment in infants at increased risk for SIDS, we obtained 24-hour cardiorespiratory recordings (pneumograms) in 80 infants given theophylline in whom the initial pneumogram was abnormal. Fifty-three infants had a clinical diagnosis of near-SIDS, and 27 were asymptomatic siblings with a positive family history for SIDS. The initial pneumogram was obtained at a mean age of 6.9 weeks, and the repeat pneumogram 2.3 weeks later, when the mean theophylline blood concentration was 11.2 +/- 0.5 micrograms/ml. Theophylline treatment resulted in comparable and highly significant improvements in both groups. Among all 80 infants, apnea density decreased from 1.6 +/- 0.2% (SEM) to 0.3 +/- 0.1% (P less than 0.001), periodic breathing episodes/100 minutes decreased from 2.7 +/- 0.4 to 0.3 +/- 0.1 (P less than 0.001), and the longest apneic period decreased from 13.5 +/- 0.7 to 10.1 +/- 0.5 seconds (P less than 0.001). Findings on the pneumogram became completely normal with theophylline therapy in 87% of infants with near-SIDS and 81.5% of asymptomatic siblings. Pneumogram normalization was associated with absence of further symptomatic sleep apnea in the near-SIDS group and with continued absence of any clinical symptoms in the asymptomatic family history group. There were no deaths from SIDS.
 ...
PMID:Theophylline improves pneumogram abnormalities in infants at risk for sudden infant death syndrome. 664 38

Ventilatory and heart rate responses to hypercapnia and hypoxia were measured in the following three groups: group I, controls (n equals 15); group II, parents of threatened sudden infant death syndrome (SIDS) infants (n equals 10); and group III, parents of SIDS infants (n equals 17). We found significantly reduced heart rate responses to carbon dioxide and hypoxia in group II (1.4 plus or minus 1.9 percent and 16.0 plus or minus 4.0 percent; mean plus or minus SEM) compared with controls (7.1 plus or minus 1.4 percent and 26 plus or minus 2.4 percent; P less than .025). Ventilatory responses to hypoxia in groups II and III were not significantly different from controls. Two group II mothers had a greatly reduce ventilatory response to carbon dioxide. Four other parents in group II had abnormally low heart rate responses to hypoxia or carbon dioxide. We concluded that parents of threatened SIDS infants had reduced heart rate responses to carbon dioxide and hypoxia and may have reduced ventilatory responses to carbon dioxide.
 ...
PMID:Attenuated responses to CO2 and hypoxia in parents of threatened sudden infant death syndrome infants. 678 12

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. Among the 25 infants having a positive hypercarbic AR, the Mean (+/- SEM) PACO2 at which arousal occurred was 48.5 +/- 1.6 in N-M SIDS versus 42 +/- 1.2 mmHg in control infants (p less than .001). The overall pattern for hypoxic AR was also a generally absent AR in the lowest hypoxic ventilatory response slope group progressing to a generally positive AR in the highest 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.
 ...
PMID:Abnormal hypercarbic and hypoxic sleep arousal responses in Near-Miss SIDS infants. 730 67

Previous reports have demonstrated that premature infants are at greatly increased risk for sudden infant death syndrome (SIDS). Although only 9% of infants are born at less than 36 weeks' gestation, 20% of SIDS victims are former premature infants. The objective of this study was to characterize the time course of SIDS in premature infants and to determine why SIDS occurs at such a high rate in this patient population. A database of all cases of SIDS in Philadelphia from 1987 through 1991 was used to establish the time course for SIDS deaths in term and preterm infants. Gestational age was established by Dubowitz exam. To evaluate distinctly different age groups, infants from 32-36 weeks were excluded from analysis. Age at death and postconceptional age of death were compared for both groups. Data are described in weeks (mean +/- SEM), and analyzed using unpaired t-test and log-rank test to compare survival rate between term and preterm infants. A significant difference (P < 0.01) was noted in age at death of term versus preterm infants. No difference was found in postconceptional age of death. The survival rates were also different (P < 0.001). Preterm infants showed a much wider distribution in age of death from SIDS. The term infants followed the classic SIDS curve. By 32 weeks' postnatal age, 95% of all SIDS had taken place in the term group, but only 75% in the preterm group. The age at death for SIDS differs in the preterm infant.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The timing of SIDS deaths in premature infants in an urban population. 758 6


1 2 Next >>