Nasal mask ventilation in children.
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Child↗
Biomedical subjects
D Gozal
Publications and source records attributed to D Gozal.
Sleep-disordered breathing and school performance in children.
OBJECTIVE: To assess the impact of sleep-associated gas exchange abnormalities (SAGEA) on school academic performance in children. DESIGN: Prospective study. SETTING: Urban public elementary schools. PARTICIPANTS: Two hundred ninety-seven first-grade children whose school performance was in the lowest 10th percentile of their class ranking. METHODS: Children were screened for obstructive sleep apnea syndrome at home using a detailed parental questionnaire and a single night recording of pulse oximetry and transcutaneous partial pressure of carbon dioxide. If SAGEA was diagnosed, parents were encouraged to seek medical intervention for SAGEA. School grades of all participating children for the school year preceding and after the overnight study were obtained. RESULTS: SAGEA was identified in 54 children (18.1%). Of these, 24 underwent surgical tonsillectomy and adenoidectomy (TR), whereas in the remaining 30 children, parents elected not to seek any therapeutic intervention (NT). Overall mean grades during the second grade increased from 2.43 +/- 0.17 (SEM) to 2.87 +/- 0.19 in TR, although no significant changes occurred in NT (2.44 +/- 0.13 to 2.46 +/- 0.15). Similarly, no academic improvements occurred in children without SAGEA. CONCLUSIONS: SAGEA is frequently present in poorly performing first-grade students in whom it adversely affects learning performance. The data suggest that a subset of children with behavioral and learning disabilities could have SAGEA and may benefit from prospective medical evaluation and treatment.
Child↗
Hypoxic ventilatory roll-off is associated with decreases in protein kinase C activation within the nucleus tractus solitarius of the rat.
Protein kinase C (PKC) inhibition attenuates ventilatory responses to acute hypoxia. Hypoxic ventilatory roll-off (VRO) could reflect underlying changes in PKC activity. Immunoblots of NTS lysates harvested at peak ventilation revealed subcellular translocations of particular PKC isoforms which coincided with PKC activity elevations. In contrast, reductions in PKC activity occurred during VRO, concomitant with selective decreases in PKCbeta and -delta translocation. Thus, alterations in PKC activity within the NTS which occur over time during hypoxia are isoform-selective and coincide with changes in ventilation.
Animals↗
Nitric oxide modulates in vitro intrinsic optical signal and neural activity in the nucleus tractus solitarius of the rat.
Nitric oxide (NO) is a novel neurotransmitter with important cardiorespiratory functions. To determine the functional topography of NO in a brainstem preparation, extracellular and intrinsic optical signal recordings were simultaneously acquired from a 300 microm coronal brainstem slice at the level of the obex. During control conditions, spontaneous spike activity in the nucleus tractus solitarius (NTS) was 6.2 +/- 1.4 Hz. When the competitive NOS inhibitor, L-NAME, was applied to the bath (1 mM), spike activity either ceased or was markedly reduced in frequency (1.2 +/- 0.7 Hz; n = 7; P < 0.01). The decrease in activity was reversed when the NOS substrate L-arginine (L-Arg) was added to the bath (9.4 +/- 1.8 Hz; P < 0.04). Concurrent intrinsic optical signal imaging of the slice preparation consistently revealed coincident decreases in activity within the NTS with L-NAME (deltaT/T: -2.4 +/- 0.9%; P < 0.02), and increases with L-Arg (+2.1 +/- 0.8%; P < 0.04). Such changes were absent in other regions such as the hypoglossal nuclei or area postrema. We conclude that in this brainstem region, NO modulation of neuronal activity is primarily circumscribed to the NTS.
Animals↗
Feeding: an alternative to sedation in children.
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Eating↗
Heart rate variability in children with obstructive sleep apnea.
Adults with obstructive sleep apnea syndrome (OSAS) display substantial heart rate changes associated with obstructive events, and recent reports suggest similar heart rate changes in children with OSAS. These rate changes could assist screening of young patients for OSAS. Six-hour polysomnographic recordings were obtained from seven children with OSAS (mean age: 4.5 years; apnea index: 19.5 +/- 5.1) and from seven primary snorers without OSAS who served as controls (mean age: 4.7; apnea index: 0). Scatterplots of each cardiac R-R interval against the preceding interval (Poincaré plots) were used to assess beat-to-beat cardiac variability at different heart rates. Beat-to-beat variation at slow rates was significantly increased in children with OSAS relative to controls, while variation at fast and intermediate heart rates was significantly reduced in these children. We conclude that OSAS alters beat-to-beat variation in characteristic fashions in children, that the variability changes occur at all heart rates but are most significant at slow heart rates, and that these heart rate patterns could assist in screening of suspected cases of OSAS.
Body Weight↗
Recurrence of spondylothoracic dysplasia (Jarcho-Levin syndrome) in a family.
We describe a rare occurrence of two consecutive cases of spondylothoracic dysplasia (Jarcho-Levin syndrome) in a nonconsanguineous Hispanic family. Serial measurements of pulmonary function and energy expenditure were useful in one of these infants for assessment of the evolution and severity of restriction of pulmonary function and the determination of timely therapeutic intervention.
Body Height↗
Eldor needle's advantage over the needle-through-needle technique.
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Anesthesia, Epidural↗
Glucose administration before exercise modulates catecholaminergic responses in glycogen-depleted subjects.
In glycogen-depleted subjects (GD) a nonlinear increase in epinephrine (Epi) and norepinephrine (NE) parallels blood lactate (La) during graded exercise. The effect of glucose (Glc) supplementation and route of administration on these relationships was studied in 26 GD athletes who were randomly assigned to receive 1.3 g/kg Glc by slow intravenous infusion (IV; n = 9), oral administration (PO; n = 9), or artificially sweetened placebo in 1 liter of water (Asp; n = 8) in the 2 h preceding a graded maximal exercise. Performance and La were similar among the three groups in normal glycogen (NG) or GD conditions. However, slightly improved performances were observed in GD compared with NG and were associated with a shift to the right in La curves. Blood Glc concentrations were higher in IV and PO before exercise, but they rapidly decreased to lowest levels in IV, gradually decreased over time in PO, and remained stable in Asp or NG. Insulin concentrations were highest in IV and lowest in Asp and NG at onset of exercise, rapidly decreasing in IV and PO although remaining at higher levels than in Asp or NG. In contrast, higher serum levels of free fatty acids were measured during exercise in Asp with no significant differences in glucagon or glycerol among the three groups. Free and sulfated NE increases were smaller in IV than in PO and Asp on exhaustion. In contrast, free and conjugated Epi were most increased in IV, with smallest increases in Asp. Dopamine levels were most increased in IV at exhaustion. We conclude that the changes of Epi and NE concentrations, associated with the activation of glucoregulatory mechanisms, including hyperinsulinemia, display different magnitude and time courses during exercise in GD subjects who receive oral vs. intravenous load of Glc before exercise. We speculate that the magnitude of insulin surge after acutely increased Glc before exercise in GD subjects may exert dissociative effects on adrenal-dependent glycogenolysis and on sympathetic responses.
Adult↗
Effect of supplemental oxygen on supramaximal exercise performance and recovery in cystic fibrosis.
The effects of supplemental O2 on recovery from supramaximal exercise and subsequent performance remain unknown. If recovery from exercise could be enhanced in individuals with chronic lung disease, subsequent supramaximal exercise performance could also be improved. Recovery from supramaximal exercise and subsequent supramaximal exercise performance were assessed after 10 min of breathing 100% O2 or room air (RA) in 17 cystic fibrosis (CF) patients [25 +/- 10 (SD) yr old, 53% men, forced expired volume in 1 s = 62 +/- 21% predicted] and 17 normal subjects (25 +/- 8 yr old, 59% men, forced expired volume in 1 s = 112 +/- 15% predicted). Supramaximal performance was assessed as the work of sustained bicycling at a load of 130% of the maximum load achieved during a graded maximal exercise. Peak minute ventilation (VE) and heart rate (HR) were lower in CF patients at the end of each supramaximal bout than in controls. In CF patients, single-exponential time decay constants indicated faster recovery of HR (tau HR = 86 +/- 8 and 73 +/- 6 s in RA and O2, respectively, P < 0.01). Similarly, fast and slow time constants of two-exponential equations providing the best fit for ventilatory recovery were improved in CF patients during O2 breathing (tau 1VE = 132.1 +/- 10.5 vs. 82.5 +/- 10.4 s; tau 2VE = 880.3 +/- 300.1 vs. 368.6 +/- 107.1 s, P < 0.01). However, no such improvements occurred in controls. Supramaximal performance after O2 improved in CF patients (109 +/- 6% of the 1st bout after O2 vs. 94 +/- 6% in RA, P < 0.01). O2 supplementation had no effect on subsequent performance in controls (97 +/- 3% in O2 vs. 93 +/- 3% in RA). We conclude that supplemental O2 after a short bout of supramaximal exercise accelerates recovery and preserves subsequent supramaximal performance in patients with CF.
Adult↗
Nitric oxide modulates ventilatory responses to hypoxia in the developing rat.
Nitric oxide (NO) is an important excitatory neurotransmitter in the central nervous system. In the adult rat, both selective and nonselective blockers of constitutive nitric oxide synthase (NOS) induce marked ventilatory reductions during sustained hypoxia, thereby enhancing ventilatory roll-off. Since hypoxic ventilatory depression is greater in developing mammals during the late phases of hypoxic exposure, we hypothesized that limited NOS activity may play a role in the late arm of the ventilatory response. To test our hypothesis, 5-d-, 10-d-, and 15-d-old rat pups underwent a 30-min hypoxic challenge (10% O2) before and after administration of 100 mg/kg N-nitro-L-arginine methyl ester (L-NAME), a competitive NOS inhibitor. Minute ventilation (VE) was measured using whole-body plethysmography. In 5-d-old pups, early VE hypoxic responses were enhanced, and late VE were similar after administration of L-NAME. In contrast, in 15-d-old hypoxic pups, L-NAME administration was associated with smaller early VE increments and significantly larger VE reductions when compared with pretreatment conditions. The role of central nervous system NO in the development of these ventilatory changes was further assessed by Western blots of protein equivalents from the nucleus tractus solitarius (NTS), the first central relay for peripheral chemoreceptor afferent input, which revealed increasing neuronal NOS expression with age. Furthermore, NADPH-diaphorase immunohistochemical staining of neurons in the NTS revealed increased positively labeled neuronal populations within subnuclei of this structure with advancing postnatal age. Current findings suggest that NOS activity mediates both excitatory and inhibitory components of the hypoxic ventilatory response. Furthermore, in brainstem respiratory regions, NO may play a role in modulating the prominent second phase of the biphasic response to hypoxia typically seen in early postnatal life.
Aging↗
Nocturnal ventilatory support in patients with cystic fibrosis: comparison with supplemental oxygen.
Progressive deterioration of lung function in cystic fibrosis (CF) patients may lead to significant hypoxaemia and hypercapnia, especially during sleep. The effects of bi-level noninvasive positive pressure nasal mask ventilation (NIPPV) on respiration and sleep were compared to those of low-flow oxygen therapy in six CF patients (mean +/- SD age 22.3 +/- 4.7 yrs, with severe lung disease (forced expiratory volume in one second (FEV1) 29.4 +/- 3.4% predicted). Compared to the control night, NIPPV and oxygen therapy significantly improved overall night-time oxygen saturation during both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep stages. However, significant increases in transcutaneous CO2 tension occurred during oxygen therapy, while NIPPV markedly improved alveolar ventilation during all sleep states. Sleep architecture and arousals remained unchanged during NIPPV and oxygen therapy treatment nights. We conclude that noninvasive positive pressure ventilation improves sleep-related hypoxaemia and hypercapnia in severe cystic fibrosis patients without affecting sleep. The long-term compliance and benefits of noninvasive positive pressure ventilation remain unclear.
Adolescent↗
Maturation of anoxia-induced gasping in the rat: potential role for N-methyl-D-aspartate glutamate receptors.
After anoxia-induced apnea, gasping remains the last operative mechanism for survival. In developing rats, the gasping response to anoxia exhibits triphasic characteristics. Because anoxia is associated with enhanced release of glutamate, we hypothesized that N-methyl-D-aspartate (NMDA) glutamate receptors may underlie components of the gasping response. Rat pups aged 2 d (n = 50), 5 d (n = 43), 10 d (n = 42), and 15 d (n = 45) underwent anoxic challenges with 100% N2 in a whole body plethysmograph, 30 min after intraperitoneal administration of MK801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate; dizocilpine] (3 mg/kg), a noncompetitive NMDA glutamate receptor channel antagonist, or normal saline. In control pups, after primary apnea onset, a triphasic gasping pattern was apparent at all postnatal ages and included two distinct types of gasps (I and II). In 2- and 5-d MK801-treated animals, phase 1 and type I gasps were absent, leading to marked prolongations of the gasp latency and phase 2, the latter displaying type II gasps only. In addition, phase 3 duration was also prolonged with increased type II gasp frequencies. In contrast, in some 10-d-old (40%) and in all 15-d-old MK801-treated pups, although overall gasping duration was prolonged, the triphasic gasping pattern seen in matched controls was also present. We conclude that NMDA glutamate receptors mediate particular phasic components of the gasping response during early postnatal life but not at later stages of development. We speculate that developmental changes occur in both function and expression of NMDA and other neurotransmitters within brainstem regions underlying the neural substrate for gasp generation.
Analysis of Variance↗
Nitric oxide synthase isoforms and peripheral chemoreceptor stimulation in conscious rats.
To test the effect of nitric oxide synthase (NOS) blockade on the ventilatory responses to carotid body chemoreceptor stimulation in freely behaving animals, chronically instrumented adult Sprague-Dawley rats received increasing intravenous doses of sodium cyanide (NaCN; 0-300 micrograms kg-1) before and after i.v. administration of either 100 mg kg-1 N-nitro-L-arginine methyl ester (L-NAME), a non-specific NOS blocker, or 10 mg kg-1 S-methyl-L-thiocitrulline (SMTC), a selective neuronal NOS inhibitor. SMTC did not modify the NaCN dose-response curve. In contrast, L-NAME significantly enhanced the ventilatory responses to NaCN. Western blots of equivalent amounts of protein from carotid body tissue homogenates revealed higher levels of endothelial NOS than of neuronal NOS. We conclude that endothelial NOS provides the major source for NO within the carotid body, and exerts a down-regulatory effect upon peripheral chemoreceptor responsivity.
Animals↗
Functional magnetic resonance imaging reveals brain regions mediating the response to resistive expiratory loads in humans.
Obstructive lung disease is the most common form of respiratory disturbance. However, the location of brain structures underlying the ventilatory response to resistive expiratory loads is unknown in humans. To study this issue, midsagittal magnetic resonance images were acquired in eight healthy volunteers before and after application of a moderate resistive expiratory load (30 cmH2O/liter/s), using functional magnetic resonance imaging (fMRI) strategies (1.5-T magnetic resonance; repetition time: 72 ms; echo time: 45 ms; flip angle: 30 degrees; field of view: 26 cm; slice thickness: 5 mm; 128 x 256 x 1 number of excitations). Digital image subtractions and region of interest analyses revealed significant increases in fMRI signal intensity in discrete areas of the ventral medulla, ventral and dorsal pontomedullary structures, basal forebrain, and cerebellum. Upon load withdrawal, a rapid fMRI signal off-transient occurred in all activated sites. Application of an identical load immediately after recovery from the initial stimulus resulted in smaller signal increases (P < 0.02). Prolongation of load duration was associated with progressive fMRI signal decrease across activated regions. In three additional subjects, the threshold for significant MRI signal increases was established at expiratory loads > or = 15 cmH2O/liter/s and was dose dependent with increasing loads. We conclude that resistive expiratory loads > or = 15 cmH2O/liter/s elicit regional activation of discrete brain locations in humans.
Adult↗
Ventral medullary surface activity during hypoxia in awake and anesthetized goats.
The rostral ventrolateral medullary surface (VMS) plays a major state-dependent role in the control of breathing; its role during hypoxia remains speculative. We therefore assessed activity within the rostral VMS by measuring reflectance of scattered light in 5 goats during normoxia, hypoxia, and hyperoxia in awake and halothane anesthetic states. Within the first minute of hypoxia, light reflectance began to decrease in the awake state; reflectance reached a stable nadir within 30 min about 10 and 17% below control values (P < 0.01), at 12 and 10% inspired O2, respectively. In the anesthetized state, reflectance decreased (P < 0.01) by 6% at 10% inspired O2. After 30 min in the awake state, reflectance returned (P < 0.01) toward control values, reaching a stable level at 7 and 11% below control at 12 and 10% inspired O2, respectively (P < 0.05). Hyperoxia resulted in a 1% increase (P < 0.05) in reflectance. Changes in reflectance during hypoxia did not consistently parallel changes in breathing, heart rate, or arterial blood pressure. We conclude that, a) decreased reflectance during hypoxia results, in part, from increased neural activity, and b) state exerts a substantial effect on the response of VMS areas to hypoxia.
Anesthesia↗
Ventral medullary neuronal responses to peripheral chemoreceptor stimulation.
Recent findings suggest that carotid chemoreceptor input into the ventral medullary surface intermediate area during hypoxia is inhibitory (Gozal et al., (1994) Neurosci. Lett. 178, 73-76. However, systemic hypoxia is a complex stimulus, and effects of carotid chemoreceptor stimulation per se on intermediate ventral medullary surface neuronal activity are difficult to isolate. Therefore, we studied neural activation of the intermediate ventral medullary surface during peripheral chemoreceptor stimulation by intravenous sodium cyanide using optical procedures in seven pentobarbital-anesthetized cats. Control recordings were also acquired in the suprasylvian cortex of three cats. Images of reflected 660 nm light were collected at l/s with a charge-coupled device camera, triggered by the cardiac R wave, after 0.0, 0.5, 2, 5, 10, 20 and 40 micrograms/kg i.v. sodium cyanide administration before and following carotid sinus denervation. Sodium cyanide doses > 5 micrograms/kg significantly increased ventilation, an effect which was eliminated following carotid sinus denervation. A pronounced, dose-dependent activity decrease within the intermediate ventral medullary surface occurred within seconds of sodium cyanide administration, with subsequent return to baseline. Carotid sinus denervation eliminated rapid-onset neural responses to all sodium cyanide doses. However, at the 40 micrograms/kg dose, a smaller, slower onset (25 s), activity decrease occurred both pre- and postdenervation. In the neocortex, the sodium cyanide-induced fast responses were absent. Intravenous cyanide, acting via a carotid sinus nerve pathway, results in a dose-dependent decrease in neural activity within the intermediate ventral medullary surface of cats. High-dose sodium cyanide also appears to decrease intermediate ventral medullary surface neural activity directly.
Animals↗
Deficient heat shock protein expression: a potential mechanism for the sudden infant death syndrome.
Induction of heat shock proteins follows a metabolic stress and protects from subsequent stresses. Stressors proposed for the sudden infant death syndrome include infection, environmentally-induced hyperthermia and hypoxia. Failure to express heat shock proteins to such stressful conditions may lead to reduced tolerance, and enhance inappropriate physiologic responses and vulnerability which ultimately may lead to infant death.
Fever↗