Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ventilatory response to acute hypercapnia was studied in 68 parents of victims of sudden infant death syndrome and 56 control subjects. Tidal volume, inspiratory time, and total respiratory cycle time were measured before and immediately after a vital capacity breath of 13% CO2 in oxygen. Instantaneous minute ventilation, mean inspiratory flow (tidal volume/inspiratory time), and respiratory timing (inspiratory time/total respiratory cycle time) were calculated. Both groups of subjects showed a marked increase in tidal volume (48.4% +/- 26.5%), instantaneous minute ventilation (56% +/- 35%), and tidal volume/inspiratory time (56.8% +/- 33.5%) after inhalation of the test gas, with little change in inspiratory time/total respiratory cycle time. There were no significant differences between the two groups for ventilation before or after inhalation of the test gas. The ventilatory response to acute hypercapnia is mediated by the peripheral chemoreceptors. These results suggest that an inherited abnormality of peripheral chemoreceptor function is unlikely to be a factor leading to sudden infant death syndrome.
 ...
PMID:Response to acute hypercapnia in the parents of victims of sudden infant death syndrome. 671 22

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

The ventilatory response to hypoxia and to hypercarbia was assessed in 36 near-miss sudden infant death syndrome (N.M SIDS) and 23 control infants. Base-line measurements during non-REM sleep documented no significant difference in respiratory frequency, alveolar CO2 and O2 partial pressure (PAco2 and PAo2) or tidal volume between the N-M SIDS and control infants. In the N.M SIDS group, mean inspiratory flow and minute ventilation (VI) were significantly lower than in the control group (p less than 0.001 and p less than 0.01, respectively), and the slope of the ventilatory response to hypercarbia ((delta VI/Torr Paco2) was only 21 +/- 1.9 (SE) ml.kg-1 min-1 Torr PAco2 compared with 62 +/- 3.5 in controls (p less than 0.001). For both groups, the increase in ventilation with hypoxia appeared linear within the PAo2 range assessed (65-115 Torr) and was therefore expressed as the slope of the delta VI/PAo2 plot (ml.kg-1 min-1 per Torr PAo2). The slope of the hypoxic ventilatory response was significantly less in the N-M SIDS than in the control group, -8.3 +/- 1.0 VS. -19.9 +/- 1.5, respectively (p less than 0.001). In summary, in comparison to control infants, N-M SIDS infants as a group have a significantly smaller increase in VI in response to hypoxia as well as to hypercarbia.
 ...
PMID:Diminished hypoxic ventilatory responses in near-miss sudden infant death syndrome. 726 94

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

To determine if a familial abnormality in the control of breathing might explain the reasons for the sudden infant death syndrome (SIDS), three groups of parents were studied. The first (N = 8 sets of parents) had one infant die of SIDS (one SIDS), whereas the second (N = 6) had a SIDS victim plus a second child with a "near-miss" occurrence (two SIDS). When compared to the third group (controls), these parents demonstrated no abnormality in the ventilatory response to hypoxia or hypercapnia. Similarly, they had normal respiratory frequency, tidal volume, inspiratory time, and arterial blood gas tensions. We conclude that a familial abnormality in breathing control measured during wakefulness is not the basis for SIDS.
 ...
PMID:Respiratory control in the parents of sudden infant death syndrome victims. Ventilatory control in SIDS parents. 738 52

1. This paper reviews current knowledge regarding interactions between body temperature and the respiratory responses to hypoxia and/or hypercapnia, with special emphasis on how these interactions might predispose towards sudden infant death syndrome (SIDS). 2. Use has been made of an adult rat model in which body core temperature is fixed by means of an intra-abdominal heat exchanger. Initial studies indicated that hyperthermia (Tb approximately 41 degrees C) enhanced the ventilatory response to hypercapnia, whereas hypothermia (Tb approximately 35 degrees C) interacted with hypoxia to depress respiration. 3. Studies involving hypothalamic lesions in urethane-anaesthetized rats have implicated the posterior hypothalamic area in the hypoxia/hypothermia interaction. Further studies are directed towards examining the role played by more caudal areas, including the raphe nuclei. 4. It has been shown that not only does the hypoxia/hypothermia interaction depress breathing but it also reduces, or sometimes eliminates, the ventilatory response to hypercapnia, which under normal circumstances provides one of the most powerful excitatory inputs to the respiratory centres. This implies that an expected reversal of the respiratory depression by build up of CO2 levels may not occur, which in turn has important implications for SIDS. 5. The literature dealing with the effects of hyperthermia on hypoxic and hypercapnic responses is also reviewed. It is concluded that environmental heat stress may only become a significant problem when it accompanies a febrile infection, under which circumstances it may seriously compromise thermoregulatory ability and alter breathing responses to chemical stimuli.
 ...
PMID:Influence of body temperature on responses to hypoxia and hypercapnia: implications for SIDS. 758 8

It is strange that some aspects of infant care have been strongly promoted by modern medicine while others have been neglected. Thus prone sleeping which has been strongly promoted is now related to an increase in SIDS, whereas the promotion of breast feeding in developed countries has been less successful. Unfortunately there has not been sufficient physiological investigation of many infant care practices and some of the proposed mechanisms for SIDS and prone sleeping have not been substantiated. Thus further work is needed on hypercapnia, hypothermia and periodic breathing and respiratory control. Studying infants alone may leave out important physiological mechanisms such as the effect on body warmth when the infant is close to the mother. More investigation is needed of antenatal factors related to SIDS and it is critically important that physiological investigation should not look for single mechanisms but be concerned with the interaction of many physiological factors.
 ...
PMID:Infant care practices and the investigation of physiological mechanisms. 782 Dec 61

Abnormalities in central ventilatory control during sleep and/or impaired arousal have been reported in some infants who subsequently die of SIDS. Hypothetically, these abnormalities may result from dysfunction of the ventral medullary rim, considered to be an integrative site for cardioventilatory control on the basis of research in animals. This paper summarizes comparative neuroanatomic evidence from a previously published study showing that the human medullary arcuate nucleus is homologous to neurons in the cat which participate in chemosensory/autonomic integrative processes of the ventral medullary rim. Next, it summarizes a study of serially or extensively sectioned medullae of 41 SIDS and 27 controls which identified 2 SIDS victims with isolated hypoplasia of the arcuate nucleus confirmed by three-dimensional reconstructions and volume measurements. The volume of the right arcuate nucleus in the SIDS case was 0.7 mm3, compared to a range of 3.4-26.3 mm3 (median 5 mm3) in 3 infant controls. On the basis of pre-cerebellar and other anatomic connections of the arcuate nucleus and of neurons in homologous positions in animals, arcuate hypoplasia may lead to death by dyssynergy between the cerebellum's influence on cardioventilation and the way this influence is integrated with chemosensation and arousal during sleep and hypercarbia during a critical developmental period.
 ...
PMID:Arcuate nucleus hypoplasia in sudden infant death syndrome: a review. 803 76

In postnatal infants, there is similarity between the time course of transient gonadal steroid secretion and the age-related incidence of sudden infant death syndrome (SIDS). The cause of death in SIDS is generally thought to be a ventilatory arrest, but the mechanism responsible for such an event remains unknown. Testosterone has been demonstrated to depress ventilatory drive and increase sleep apnea in adult men. We tested the hypothesis that the gonadal steroid testosterone depresses infant ventilatory drive during sleep. Three newborn male infant primates were gonadectomized after birth. Ventilation was observed and quantified for each animal during completely natural unencumbered sleep by plethysmography for an average of 16 wk. Ventilatory patterns were recorded, and ventilatory drive was challenged with hypercapnia and hypoxia during quiet sleep on the night before and the night after testosterone administration. Hypercapnic ventilatory drive during sleep was significantly depressed by an average of 33.6% on the night after compared with the night before testosterone administration. Depression of the response to hypercapnia after testosterone was not accompanied by any change in resting minute ventilation measured during quiet sleep. Hypoxic ventilatory drive, incidence of apneic events, and length of apnea were not different after testosterone. The effects of injecting a placebo on ventilatory patterns and drive were tested by giving the placebo to all animals on several test weeks. Placebo injections produced no significant change in any measured parameters. These results support the hypothesis that testosterone depresses hypercapnic ventilatory drive during sleep in the infant primate.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Depression of hypercapnic ventilatory drive by testosterone in the sleeping infant primate. 804 60

The interactions between the acid-base variables that contribute to exudate acidosis were studied in the subcutaneous air-pouch after carrageenan injection in rats. We studied the concurrent changes of exudate gases (PCO2 and PO2), main ions ([Na+], [K+], [Ca2+], [Mg2+], [Cl-] and [Lac-]), inorganic phosphate (P(i)) and albumin in acutely inflamed rats (4, 8, 12, 24 and 48 h of inflammation). A notable hypercapnia was found in the exudate after only 8 h (exudate PCO2 = 64.3 +/- 2.9 mm Hg) but this hypercapnia decreased after 48 h (32.9 +/- 12.7 mm Hg), coincident with the greatest increase in exudate cells. With respect to the metabolic acid-base variables, the most important changes found were a parallel decrease in the strong ion difference ([SID]) and exudate pH, as well as increases in the exudate weak acid buffers ([ATOT]) due to albumin and inorganic phosphate (P(i)) increases. However, after 12 h, the exudate acidosis was stable at around pH 7. A similar acid pH was obtained after 24 h of inflammation when the carrageenan solution injected was previously adjusted to a physiological pH (7.4). This pH, analogous to that of the exudate, was the result of compensation by the acid-base independent variables, a fact which suggests that acid pH may be a beneficial condition for cells taking part in inflammatory processes.
 ...
PMID:Factors influencing the acid-base changes in the air-pouch exudate following carrageenan induced inflammation in rats. 887 14


<< Previous 1 2 3 4 5 6 7 8 Next >>