[Resistance measurement by the interruption technique of flow].
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Biomedical subjects
Publications and source records attributed to C Gaultier.
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The aim of this study was to assess cardiorespiratory tolerance to exercise in children with non-operated, paucisymptomatic and untreated froms of Ebstein's anomaly. The authors undertook a prospective study in 11 children, mean age 9.6 years, who had lung function tests, cardiorespiratory exercise stress tests (bicycle ergometry N = 8, treadmill N = 3) and contrast echocardiography. All parameters of spirometry were normal. Contrast echocardiography showed a right-to-left interatrial shunt in 7 children (group 1) whereas the remaining 4 children had no shunt (group 2). The resting oxygen saturation was 97.4 +/- 2%, with no difference between the two groups. On the other hand, oxygen saturation at peak VO2 (VO2 max) was 90 +/- 9.5%, significantly lower in group 1 than in group 2 (85.7 +/- 2.2% vs 98.2 +/- 1.2%; p = 0.03). In group 1, the VO2 max was correlated to oxygen saturation (r = 0.98; p < 0.001, N = 6). The oxygen desaturation was correlated with presence of a right-to-left interatrial shunt (p = 0.01). The reduced exercise tolerance of non-operated, paucisymptomatic children with Ebstein's anomaly is due to a right-to-left interatrial shunt. In patients with poor exercise tolerance, contrast echocardiography is advised for the detection of these atrial shunts.
The aim of this experiment was to determine whether ventilatory measurements in adult restrained mice provide a valid assessment of chemosensitivity. We used whole-body plethysmography to compare breathing patterns in eight restrained and eight unrestrained outbred Swiss mice during air breathing, hypercapnia, and hypoxia. The mice in the restrained group were each placed in a loosely restraining wire-mesh cage. The unrestrained mice could move freely inside the plethysmograph. All the mice received three hypercapnic stimuli (8.5% CO2) and three hypoxic isocapnic stimuli (10% O2, 3.5% CO2). As compared to unrestrained mice, restrained mice had significantly lower breath durations (TT, 445+/-110 ms vs. 323+/-32 ms) and higher ventilation (VE) levels (15.7+/-2.6 microl/(sec x g) vs. 22.2+/-4.5 microl/(sec x g)), whereas no difference was observed for tidal volume (VT). The increases in frequency and ventilation from baseline to hypercapnia were not significantly different in restrained and unrestrained mice. The VE response to hypoxia was marginally higher in restrained mice. We conclude that chemosensitivity to hypercapnia, and to a lesser extent to hypoxia, can be measured in restrained adult mice, but that the baseline breathing pattern cannot.
The authors performed a differential conditioning experiment in 30 rats, using 2 odors as the conditioned stimuli (CS+ and CS-) and hypoxia (8% O2) as the unconditioned stimulus. Vanillin was the CS+ and rose the CS- in half of the rats, and vice versa in the other half. Fifteen paired CS+/hypoxia trials and 15 CS- only trials were performed in random order, followed by 3 CS+ only and 3 CS- only trials to test for conditioning. The increase in ventilation from prestimulus levels averaged 116 +/- 85% in response to CS+ versus 55 +/- 36% in response to CS-. This effect was supported by the significant Pre-Post Stimulus x CS Type interaction for this variable (p < .003). The data confirm the sensitivity of breathing to conditioning processes and also indirectly support the hypothesis that feedforward responses may complement feedback reflex pathways in respiratory homeostasis.
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We conducted a reproducibility study of the alternating breath test (ABT) for assessing peripheral chemoreceptor function in infants. The ABT delivers a rapid hypoxic stimulus to the peripheral chemoreceptors with breath-by-breath alternations of the inspired O2 fraction. The reproducibility of the ABT performed on a single occasion has not been extensively studied in infants. Eight unsedated infants (postnatal age, 22+/-19 d; weight, 3.2+/-0.4 kg) were studied in standardized conditions: morning naps, supine position, room temperature 22-24 degrees C, quiet sleep, and face mask attached to a pneumotachograph connected to a two-way electric valve. Respiratory gases were analyzed by mass spectrometer. Two ABTs were performed. Each included a 2-min control run (CR) alternating between air and air, and a 2-min test run (TR) alternating between air and 0.15 O2. After data preprocessing, on average 13+/-11% of the data were rejected because of sighs, apneas, and cycles with the fraction of inspired oxygen above 0.17. Using the remaining validated breaths, the response to ABT was calculated for the CR, for all breaths in the TR (TR(T)), and for the first 50 breaths of the TR (TR50). During the ABTs oxygen saturation did not fall below 96%, and heart rate was not affected. Inspired and end-tidal CO2 fractions remained unchanged during the ABTs. FetO2 oscillated in TRs at a lower values than in CRs and differed significantly between breaths of air and hypoxic breaths of TRs. All infants responded to ABT with percentage alternation coefficients of TRs significantly greater than those of CRs for all respiratory variables. The values of the coefficients were not significantly different between both ABT, and between TR50 and TR(T). The greatest values of the coefficients were for timing variables compared with flows and volume. We conclude that the ABT is a reproducible test of peripheral chemoreceptor function under standardized conditions.
We assessed the effects of a dietary protein restriction (5% vs. 20% casein in diet) initiated at conception and imposed during the first 2 weeks of rat gestation on postnatal brain development. At the end of the malnutrition period, protein-restricted animals exhibited significantly smaller fetal body weight and brain cortical thickness than controls. At birth and thereafter, body weight was normalized in the progeny. Similarly, brain weight and cytoarchitecture were normal in postnatal animals. In contrast, we observed, during the first 2 postnatal weeks, several abnormalities of brain development which affected all the studied areas for most of the studied parameters: (i) delayed astrocytogenesis as shown by a reduced GFAP staining; (ii) delayed production of hyaluronan in the extracellular matrix studied with binding of biotinylated hyaluronectin; (iii) abnormal neuronal differentiation as shown by reduced expression of MAP-5 and increased expression of MAP-1; (iv) abnormal synaptogenesis as shown by the increased expression of synaptophysin in the basal ganglia; (v) decreased programmed cell death. In adult prenatally protein-restricted animals, all the above parameters were normalized excepted MAP-1 labeling which remained high. In addition, we observed slight alterations of the ventilatory response to hypoxia in adult animals. The present study demonstrates that early protein malnutrition during embryonic development induces multiple, transient alterations of brain development. However, the almost complete normalization in adults of brain architecture and differentiation as well as our physiological data strongly suggest a remarkable plasticity of the developing brain following an early aggression.
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Rapid eye movement sleep can be elicited in the rat by microinjection of the cholinergic agonist carbachol into the oral pontine reticular nucleus. Intracerebroventricular administration, during the light period, of vasoactive intestinal peptide enhances rapid eye movement sleep in several species. Since this peptide is co-localized with acetylcholine in many neurons in the central nervous system, it was assumed that the oral pontine tegmentum could also be one target for vasoactive intestinal peptide to induce rapid eye movement sleep. This hypothesis was tested by recording the sleep-wakefulness cycle in freely-moving rats injected with vasoactive intestinal peptide or its fragments (1-12 and 10-28) directly into the oral pontine reticular nucleus. when administered into the posterior part of this nucleus, vasoactive intestinal peptide at 1 and 10 ng (in 0.1 microliter of saline), but not its fragments, induced a 2-fold enhancement of rapid eye movement sleep during 4 h, at the expense of wakefulness. At the dose of 10 ng, a significant increase in rapid eye movement sleep persisted for up to 8 h. Moreover, when the peptide was injected into the centre of the positive zone, rapid eye movement sleep was enhanced during three to eight consecutive days. These data provide the first evidence that rapid eye movement sleep can be elicited at both short- and long-term by a single intracerebral microinjection of vasoactive intestinal peptide. Peptidergic mechanisms, possibly in association with cholinergic mechanisms, within the caudal part of the oral pontine reticular nucleus may play a critical role in the long-term regulation of rapid eye movement sleep in rats.
Newborn infants may have a high oxygen cost of breathing (OCB) at the time of being weaned from mechanical ventilation. We hypothesized that this increase in oxygen consumption (V'O2) could be reduced by using certain weaning ventilatory modes. We designed a study to assess V'O2 during three weaning ventilatory modes: patient triggered ventilation, synchronous intermittent mandatory ventilation (SIMV) and continuous positive airway pressure in 16 newborn infants before being weaned from mechanical ventilation In seven infants whose OCB was high. V'O2 was not significantly different between CV and PTV (8.9+/-0.6 versus 9.5+/-0.8, respectively) whereas it tended to increase to 10.8+/-1.1 mL x min(-1) x kg(-1) during SIMV and increased significantly to 11.9+/-0.8 mL x min(-1) x kg(-1). In the other nine infants whose OCB was normal, no significant variation of V'O2 was observed. Patient triggered ventilation was a weaning ventilatory mode that significantly reduced the increase in oxygen consumption observed in infants with a high oxygen cost of breathing, as compared to synchronous intermittent mandatory ventilation or continuous positive airway pressure. Further investigations in newborn infants with a high oxygen cost of breathing should be performed prior to routine use of patient triggered ventilation.
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OBJECTIVES: To determine the optimal number of stool specimens needed for the diagnosis of cryptosporidiosis. METHODS: Four hundred thirty-five admissions were reviewed (291 patients) in which stool specimens were examined for Cryptosporidium parvum oocysts (mean of 1.47 specimens per admission), using a modified acid-fast stain. The diagnostic yield of each specimen was determined. RESULTS: Cryptosporidium parvum oocysts were found in 81 of 435 admissions (18.6%). Ninety-six percent of the positive cases were detected on the first stool specimen analysis, and 100% were detected by the second specimen. CONCLUSIONS: Examination of one specimen is generally appropriate for the diagnosis of cryptosporidiosis in a hospitalized patient with AIDS presenting with diarrhea. Examination of a second specimen may be appropriate if the first specimen is negative and there is a high clinical index of suspicion.
Cholinergic regulation of sleep and wakefulness was studied in freely moving rats locally infused with various doses of carbachol into the pontine reticular formation. Induction of REM sleep occurred when carbachol was infused specifically into the posterior oral pontine reticular nucleus (PnO). This effect was observed with 1-10 ng of carbachol, and lasted for at least 6 h. It was antagonized by atropine (100-200 ng) infused into the same site 15 min before carbachol (10 ng), indicating that REM sleep induction resulted from the stimulation of pontine muscarinic receptors. High doses of carbachol (500 ng) did not affect REM sleep but enhanced wakefulness. Cholinergic mechanisms within the PnO may play a critical role in the regulation of REM sleep in the rat.
The cardiorespiratory control system undergoes functional maturation after birth. Until this process is completed, the cardiorespiratory system is unstable, placing infants at risk for cardiorespiratory disturbances, especially during sleep. The profound influence of states of alertness on respiratory and cardiac control has been the focus of intense scrutiny during the last decade. The effects of rapid-eye movement (REM) sleep on various mechanisms involved in cardiorespiratory control are of particular significance during the postnatal period since newborns spend much of their time in this sleep state. In fullterm newborns, REM sleep occupies more than 50% of total sleep time, and this percentage is even greater in preterm newborns. From term to six months of age, the proportion of REM sleep decreases. Since respiratory and cardiac disturbances are known to occur selectively during REM sleep, the predominance of REM sleep may be a risk factor for abnormal sleep-related events during early infancy. Awareness of these developmental changes in sleep patterns is important for clinicians dealing with problems such as apparent life-threatening events (ALTE), sudden infant death syndrome (SIDS), and/or cardiorespiratory responses to respiratory disorders. Our current understanding of respiratory and cardiac control rests mainly on studies conducted during the first months of life. There is a paucity of data on late infancy and early childhood. The present paper will review available data on how sleep affects 1) ventilatory mechanics, in particular of the upper airways and the chest wall; ventilation and apnea; gas exchange; chemoreceptor function; and arousal responses; 2) changes in heart rate and heart rate variability, and the occurrence and mechanisms of bradycardia.
Pulmonary function and exercise tolerance were evaluated in late childhood in two groups of prematurely born children: one group with bronchopulmonary dysplasia (BPD) [n = 15; gestational age at birth (GA): 29.6 +/- 2.8 weeks; birth weight (BW): 1,367 +/- 548 g; age at test: 7.9 +/- 0.6 years], and a second group without significant neonatal lung disease [pre-term (PT)] (n = 9; GA: 30.3 +/- 1.7 weeks; BW: 1,440 +/- 376 g; age at test: 7.8 +/- 0.22 years). The results were compared with a control group of children of similar ages and heights, born at term [term born (TB)]. We observed that total lung resistance (RL) was significantly higher in BPD (11 +/- 3 cmH2O/L/s), and in PT (9 +/- 2) than in TB [5 +/- 1; (P < 0.001 and P < 0.05, respectively)]. In BPD RL was higher than in PT (P < 0.05). Dynamic lung compliance (CLdyn) was decreased in BPD (43 +/- 11 mL/cmH2O) and in PT (56 +/- 17) compared with TB (76 +/- 20) (P < 0.001 and P < 0.05), and also in BPD compared with PT (P < 0.05). Forced expiratory volume in 1 second (FEV1) and FEV1/forced vital capacity (FVC) were lower in BPD (1.07 +/- 0.15 L and 72 +/- 7%) than in PT (1.29 +/- 0.23 L, and 80 +/- 7%) (P < 0.05). Exercise tests were performed in six boys with BPD. The ratio between minute ventilation at maximal workload (VEmax) and the predicted value of maximal voluntary ventilation (MVV) was elevated in the six BPD boys tested, compared with five boys of Group 2 and five TB boys (87 +/- 15% vs. 62 +/- 14% and 65 +/- 13%) (P < 0.05). We conclude that: 1) prematurity and BPD is followed by long-term airway obstruction and a mild degree of exercise intolerance and; 2) premature birth without BPD may be followed by a milder degree of airway obstruction in childhood than in infants who developed BPD during the neonatal period.