Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 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.
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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.
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PMID:Hypercapnic and hypoxic ventilatory and cardiac responses in school-aged siblings of sudden infant death syndrome victims. 151 13

To evaluate the effect of respiratory syncytial virus (RSV) infection on reflex apnea elicited by application of water on the laryngeal mucosa, 11 healthy, term lambs were chronically instrumented at 2 wk of age. Six lambs were inoculated with bovine RSV, and five lambs were mock-infected. The lambs were studied awake and unsedated before and 4, 8, 14, and 21 d after infection. RSV infection was associated with slight rhinorrhea and with moderately increased tracheal mucous discharge. There was an average increase of 0.5 degrees C in body temperature. Arterial pH, PO2, and PCO2 remained within the normal range. The ventilatory response to laryngeal chemostimulation measured as the percentage of decrease in ventilation from control was significantly (p less than 0.05) larger among the infected animals when compared with controls on d 4 and 8. There were no differences in indices of respiratory drive (airway occlusion pressure and mean inspiratory flow), ventilatory response to hypoxia (0.10 fraction of inspired O2), or hypercarbia (0.03 fraction of inspired O2). We speculate that RSV infection alters the sensitivity of the laryngeal chemoreceptors so that a prolonged or even fatal apnea may result from stimulation of these receptors. These results may be relevant to the pathogenesis of sudden infant death syndrome associated with RSV infection.
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PMID:Respiratory syncytial virus infection reinforces reflex apnea in young lambs. 157 Feb 5

Repetitive polysomnograms were recorded from a total of 33 infants, 19 healthy preterm infants, and 14 term controls between 40 wk postconceptional age and 6 mo of age. These nighttime recordings lasted 2-4 h, except at 52 wk in preterm infants and at 3 mo of age in term infants when an overnight 12-h recording was performed. Minute by minute values of transcutaneous PO2 (PtCO2) and transcutaneous PCO2 (PtcCO2) levels and variability during the awake state, active sleep, and quiet sleep were obtained through computer analyses of the polygraphic data. The results from preterm infants at corrected postconceptional age could not be differentiated from those of control infants. PtCO2 levels rose between 40 wk and 3 mo, and PtcCO2 levels declined. Sleep states modulated only the variability of PtcO2, not the level; in contrast, state modulation was seen in both variability and level of PtcCO2 throughout the age span studied. During sleep the number of transient declines in PtCO2 greater than 2.03 kPa (15 mm Hg) decreased with advancing age. Hypercapnic PtcCO2 values decreased with age as well, but their prevalence in healthy, young infants suggests the need for reevaluation of criteria for hypercapnia based on transcutaneous measurements. The data demonstrate that ventilatory regulation continues to undergo changes between 1 and 3 mo, the age of highest risk for sudden infant death syndrome.
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PMID:Transcutaneous oxygen and carbon dioxide during the first half year of life in premature and normal term infants. 159 35

Abnormalities in central respiratory control during sleep, arousal and/or cardiac activity have been reported in some infants who subsequently die of the sudden infant death syndrome (SIDS). We postulate that these abnormalities may result from dysfunction of the ventral and ventrolateral medulla, which, based on animal data, is an integrative site for chemosensitivity, ventilation, autonomic function, and arousal. The arcuate nucleus along the ventral surface of the human medulla has been proposed to facilitate chemosensitivity to carbon dioxide and/or hydrogen ion. In this study, we surveyed serially or extensively sectioned medullae of 41 SIDS and 27 controls, and identified two SIDS victims with isolated hypoplasia of the arcuate nucleus. Three-dimensional reconstructions and volume measurements of each hemimedulla of one of these SIDS victims and three controls were performed from serial sections. The volume of the right arcuate nucleus of the SIDS case was 0.7 mm3, compared to a range of 3.4-26.3 mm3 (median 5 mm3) in three infant controls. On the basis of the anatomic connections of the human arcuate nucleus and of neurons in homologous positions in animals, we postulate that arcuate hypoplasia may lead to death by dyssynergy between cerebellar coordination of ventilation and autonomic/chemosensory/arousal integration, especially during sleep, hypercarbia, and in a critical developmental period.
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PMID:Arcuate nucleus hypoplasia in the sudden infant death syndrome. 161 39

Exposure of rainbow trout to environmental hyperoxia (PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (PICO2 approximately 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3- buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl-]i in excess of [Na+]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl-]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.
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PMID:Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout. 175 56

Cot death could be the result of chance coincidence of an adventitious challenge and a baby ill-equipped to meet it. This work was designed to test the hypothesis that there is a subpopulation of babies who lack the appropriate responses to hypoxia and hypercapnia which would enable them to overcome the effects of, for instance, nasal obstruction. The responses of 630 babies to air mixtures which induced significant changes in ventilation in the overwhelming majority, were recorded in a short protocol in which both the addition and withdrawal of hypercapnia and of hypoxia were effected. The results of each test were placed in one of five categories; in 13.6% there was no response to hypoxia, and in 2% the ventilation fell in hypoxia to a significant degree. The study confirms the existence of a subgroup of normal babies with little defence to the respiratory loading of mild upper respiratory tract infections.
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PMID:The prevalence of immature respiratory control in a neonatal population. 233 Jan 68

There is much debate relating to possible abnormalities in respiratory control mechanisms in infants considered at increased risk for sudden infant death syndrome (SIDS). The P0.1 occlusion technique was used to assess the central respiratory response to hyperoxic hypercapnia during quiet sleep in 21 normal infants, 13 siblings of SIDS victims, and 17 infants with apparent life threatening events. The slope of P0.1 plotted against carbon dioxide concentration increased exponentially with age, independent of body weight in each group. Birth weight has a significant effect on slope with a lower weight predisposing to a lower slope. Siblings as a group had a significantly lower slope at any given age than normal infants, whereas the infants who had had apparent life threatening events were not significantly different from the controls. As intragroup variation in both siblings and control groups greatly exceeded the significant intergroup differences observed, the technique cannot identify individual infants as belonging to one or other group.
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PMID:Respiratory control in infants at increased risk for sudden infant death syndrome. 250 88

We measured ventilatory responses to progressive isocapnic hypoxia and to hyperoxic hypercapnia (CO2) using rebreathing techniques in 16 parents of infants with autopsy-confirmed sudden infant death syndrome (SIDS) and 18 control parents matched for age, sex, and body size. Response to ventilatory loading was assessed by repeating the CO2 test with an inspiratory flow-resistive load (16 cm H2O/L/sec). During loaded and unloaded CO2 tests, respiratory effort was also assessed by measuring the pressure generated in the first 0.1 second (P0.1) of the subsequent inspiratory effort after brief manual occlusion of the inspiratory line. Ventilatory responses of the parents of victims of SIDS to chemical and mechanical stimulation were not significantly different from those of control parents. Responses in both groups were similar to previously reported normal values. There was a linear increase in ventilation (VE) in response to hypercapnia and hypoxia and in P0.1 in response to hypercapnia. We found expected increases in P0.1/PCO2 and decreases in VE/PCO2 slopes during loaded breathing in all subjects, but no difference between groups. We conclude that parents of SIDS victims have normal ventilatory chemosensitivity and respiratory drive.
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PMID:Ventilatory chemosensitivity in parents of infants with sudden infant death syndrome. 313 76

Laryngeal airway resistance was measured in anesthetized dogs ranging in age from one day to adult during central and peripheral chemoreceptor stimulation by hypoxia and hypercapnia. Chemoreceptor-mediated regulation of airway resistance was found to be qualitatively similar in all age groups; however, there was a progressive increased sensitivity to both hypoxia and hypercapnia with increasing age. The reduced sensitivity of the laryngeal airway to hypoxic and hypercapnic stimulation in the young animal may predispose the young animal to airway obstruction during periods of hypoxia or hypercapnia. This may bear some relevance to the etiology of certain cases of sudden infant death syndrome.
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PMID:Age-related responses of laryngeal airway resistance to peripheral and central chemoreceptor stimulation. 643 15


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