Hyperoxic Test Research Articles

Imaging methods in assessing the surveillance of type 2 diabetes mellitus for cerebrovascular reserve and brain disease in patients with hemodynamically significant carotid stenosis

Introduction. Type 2 diabetes is the most common form of endocrine disease. Diabetes is a well-established risk factor for stroke. Carotid endarterectomy (CEE) is the main method of preventing a serious complication of stroke in patients with carotid stenosis. Consequently, the assess of type 2 diabetes on the results of CEE is an urgent problem of angiosurgery.Aim: To assess effect of type 2 diabetes on cerebrovascular reserve capacity and brain structure in patients with carotid atherosclerosis by ultrasound and magnetic resonance diagnostic.Material and Methods. 44 patients with hemodynamically significant stenosis of the internal carotid arteries (ICA), who underwent ultrasound and magnetic resonance examinations of the carotid arteries at the pre- and postoperative stages were included in this study. Two groups were formed: group I (n =15) – with a verified diagnosis of type 2 diabetes, group II (n = 29) – without diabetes. To assess the cerebrovascular reserve, functional hypercapnic and hyperoxic tests were performed.Results. The analysis of the results showed statistically significant differences in the ICA blood flow in both groups. Intergroup comparison before surgery in the middle cerebral artery on the side of hemodynamically significant stenosis revealed a statistically significant difference in pulsation and peripheral resistance index. In the common carotid arteries on both sides, significant intergroup differences were found in the velocity parameters of blood flow after the CEE operation. The reactivity index in patients with surgical stenosis with type 2 diabetes in the hyperoxic test was statistically significantly different on the side of the stenosis compared to the same indicator in the group without diabetes. There were no statistically significant differences in the hypercapnic test. The value of reactivity index indicates a negative or paradoxical reaction.Conclusion. The use of simple and accessible functional tests to assess cerebrovascular reserve, plaque structure and changes in the brain in patients with type 2 diabetes at the stage of preoperative preparation according to ultrasound and MRI studies allows us to correct the treatment and subsequent protection of the brain at the stage of surgery to prevent possible complications.

Cerebrovascular reactivity depending on rheumatoid factor and anticitrullinated protein antibody positivity in hypertensive patients with rheumatoid arthritis

Objective – to investigate cerebrovascular reactivity (CVR) depending on rheumatoid factor (RF) and anti-citrullinated protein antibody (ACPA) positivity in hypertensive patients with rheumatoid arthritis (RA).Subjects and methods. A single cross-sectional study included 61 patients (mean age 59.8±7.7 years; 6 men and 55 women) with combined RA and grade 1–2 hypertension (HTN). The duration of RA was 11.2±7.4 years. The duration of HTN was 12.1±8.6 years. All patients were treated with methotrexate. RA patients were categorized into RF/ACPA seronegative and RF/ACPA seropositive subgroups. CVR was evaluated by bilateral transcranial Doppler sonography of the middle cerebral arteries (MCA) in a hyperoxic test (O2 CVR) and in a hypercapnic test (CO2 CVR). We measured MCA mean blood flow velocity (Vmn), time average maximal blood flow velocity (TAMX), peak systolic velocity (Vps) at baseline, within 2 minutes of 100% oxygen inhalation and within 3 minutes of recovery phase (hyperoxic test). We calculated the following indicators for assessing CVR: index changes of flow velocity mean (IFVm), speed modification of velocity (SMFVm) and normalized answer of reserve (NAR). Then, according to the same scheme, we performed a hypercapnic test with the inhalation of a 4% mixture of carbon dioxide with air. Values are presented as Me [Q1 ; Q3 ].Results and discussion. Hypertensive patients with RA had a decrease in response power of MCA blood flow to hyperoxia. RF-seropositive RA patients had a more pronounced decrease in the power of the response to hyperoxia compared with RF-seronegative RA patients. The values of IFVm in the hyperoxic test were –13.4 [–19.9; –0.9] versus –16.2 [–22.7; –13.4]% (р=0.0453), respectively. ACPA-seropositive RA patients had not only a more pronounced decrease in the power of the response of MCA blood flow to hyperoxia, but also a more pronounced slowdown in the response velocity of MCA blood flow to hyperoxia compared with ACPA-seronegative RA patients. The values of IFVm in the hyperoxic test were –9.74 [–15.9; 2.84] versus –20.9 [–25.0; –14.7]% (р=0.0062), the values of SMFVm were –0.05 [–0.09; 0.02] versus –0.09 [–0.20; –0.05] sm/s2 (р=0.0488) respectively. Combined RA and HTN patients had a decrease in response power of MCA blood flow to hypercapnia. However, no statistical differences were found in the state of CO2 CVR between patients with seropositive RA and seronegative RA.Conclusion. Hypertensive patients with seropositive RA have a more pronounced O2 CVR disorder in compared to seronegative RA patients.

A Strategy to Enhance Confidence in Respiratory Chemoreflex Characterization by Modified Rebreathing

Modelling breath‐by‐breath ventilation (V̇E) in response to carbon dioxide rebreathing in hyperoxic and hypoxic conditions (modified rebreathing) is used to characterize the central and peripheral respiratory chemoreflexes in humans. However, breath‐to‐breath variability produces uncertainty in the estimation of model parameters. We explored whether signal‐averaging of repeated rebreathing trials would improve chemoreflex sensitivity parameter estimation and confidence. Seven healthy males (age: 27±5 years) performed 6 repetitions of modified rebreathing tests in isoxic‐hypoxic (end‐tidal PO2 (PETO2)=50 mmHg) and ‐hyperoxic conditions (PETO2=150 mmHg) over the course of 4 days. End‐tidal PCO2 (PETCO2), PETO2 and V̇E were measured breath‐by‐breath by dual gas analyser and pneumotach. The slope of the V̇E vs PETCO2 relationship above the PETCO2 threshold in the hyperoxic test gave the central chemoreflex sensitivity (L∙min‐1∙mmHg‐1) and the difference in hypoxic versus hyperoxic test slopes provided peripheral chemoreflex sensitivity. Chemoreflex slopes modelled from a single trial versus ensemble‐average of 6 trials were compared by paired t‐test and effect size (Cohen’s d). Breath‐by‐breath data from the 6 trials were aligned to the same starting PETCO2, linearly interpolated to 0.1 mmHg of PETCO2, ensemble‐averaged, and averaged into 0.2 mmHg bins. Central chemoreflex sensitivity did not differ (p=0.94) between single (4.10±2.98 L∙min‐1∙mmHg‐1, 95%CI: 3.82–4.39) versus ensemble‐averaged data (4.13±2.14 L∙min‐1∙mmHg‐1, 95%CI: 3.99–4.27) but the 95%CI was reduced (p=0.031) by 0.29 L∙min‐1∙mmHg‐1 (effect size=1.5) with the ensemble‐averaged approach. Similarly, peripheral chemoreflex sensitivity did not differ (p=0.83) between single (1.69±1.14 L∙min‐1∙mmHg‐1, 95%CI: 1.54–1.84) versus ensemble‐averaged data (1.58±1.32 L∙min‐1∙mmHg‐1, 95%CI: 1.5 –1.66); 95%CI of the ensemble‐averaged data was 0.15 L∙min‐1∙mmHg‐1 lower than a single trial but this was not different (p=0.38; effect size=0.5). Signal averaging of multiple modified rebreathing trials reduces the confidence interval of respiratory chemoreflex sensitivity. This strategy could enhance the ability to detect differences in respiratory chemoreflex control in comparative or interventional studies where modified rebreathing is used.

Relevance of differential control of sympathorespiratory response magnitudes in clinical assessments.

Relevance of differential control of sympathorespiratory response magnitudes in clinical assessments.

Cerebrovascular reactivity in patients with rheumatoid arthritis concurrent with and without hypertension

To compare cerebrovascular reactivity (CVR) in patients with rheumatoid arthritis (RA) concurrent with essential hypertension (Group 1) and in those with RA and normal blood pressure (BP) (Group 2). During the study of Groups 1 (n = 37) and 2 (n = 12), the investigators estimated the prevalence of traditional cardiovascular risk factors, performed 24-hour BP monitoring, investigated CVR by transcranial Doppler (TCD) of the middle cerebral arteries (MCA) by hyperoxic and hypercapnic tests, and endothelium-dependent vasodilation (EDV) and endothelium-independent vasodilation of the brachial artery. The groups were matched for gender, age, RA activity and stage, and antirheumatic therapy volume. According to the results of MCA TCD, the hyperoxic test recorded impaired CVR in 34 (92%) and 10 (83%) patients in Group 1 and 2, respectively; the hypercapnic test revealed this condition in 19 (51%) and 6 (50%) patients in these groups, respectively. The hyperoxic test most commonly showed an insufficient decrease in MCA linear blood flow velocities (LBFV) in 31 (84%) and 8 (66%) patients in Groups 1 and 2, respectively; the hypercapnic test did an excessive increase in MCA LBFV in 12 (32%) and 4 (33%) patients, respectively. There was a high rate of impaired EDV in 32 (86%) and 9 (75%) patients in Groups 1 and 2, respectively. According to the results of MCA TCD, there were high and similar rates of impaired CVR in patients with RA concurrent with and without essential hypertension during the hyperoxic and hypercapnic tests.

Oxygen-related chemoreceptor drive to breathe during H2S infusion

This study addresses the following question: Could the acute depression in breathing produced by hyperoxia, a reflection of the tonic drive to breathe from the arterial chemoreceptors, be accounted for by a background level of endogenous H2S? To address this question, we produced a stable but moderate increase in breathing (24±11%) via continuous infusion of low levels of H2S, in 10 spontaneously breathing urethane-sedated rats. We found that acute exposure to 100% O2 (20 tests) decreased minute ventilation (V˙I) from 301±51 to 210±43ml/min within 15s in control conditions, but no additional significant drop in V˙I was observed during H2S induced hyperpnea. In addition, no decrease in the estimated concentrations of gaseous H2S in the arterial blood was observed during the hyperoxic tests. It is concluded that the ventilatory depression induced by high O2 appears to be limited to the tonic background peripheral chemosensory drive to breathe, but has little or no impact on the CB stimulation produced by low levels of H2S.

The effects of prior hyperventilation duration on central chemoreflex responses using the “Duffin” hyperoxic rebreathing test (1092.16)

The effects of prior hyperventilation duration on central chemoreflex responses using the “Duffin” hyperoxic rebreathing test The “Duffin” hyperoxic rebreathing test was developed from the “Read” rebreathing test by the addition of a five‐minute hyperventilation (HV) prior to switching to the rebreathing circuit. This HV eliminates CO2 stores, such that when the subject equilibrates with the rebreathing circuit, brainstem CO2 is below the ventilatory recruitment threshold (VRT) of the central respiratory chemoreceptors. This allows investigators to quantify the VRT prior to eliciting a central chemoreflex to increases in CO2 during rebreathing. An assumption of the test is that a full five minutes of prior HV is required. However, prolonged HV is uncomfortable for the subject, and there is no experimental evidence to validate this assumption. We aimed to test this assumption experimentally by comparing various durations of prior HV. We hypothesized that there would be no difference in central chemoreflex responses between randomized prior hyperventilation durations (HVD) of one, three and five minutes. Following instrumentation with a pneumotachometer and CO2 and O2 gas analyzers, 19 subjects underwent three hyperoxic rebreathing trials, each with randomized prior HV of one‐, three‐ and five‐minute durations, each coached to 18‐20 Torr PCO2. Rebreathing was carried out by switching to a circuit comprised of a 6L bag containing 7% CO2 and 93% O2. For all three trials, we quantified the VRT (PCO2; Torr), and respiratory frequency (min‐1/Torr CO2), inspired tidal volume (L/Torr CO2) and inspired ventilation (L/min/Torr CO2) with linear regression. We found no differences between HVD in any respiratory variable, within‐subject. Our data suggest that when using the “Duffin” rebreathing test, a one‐minute HV is sufficient to drive CO2 stores below the VRT, and the resulting central chemoreflex responses are no different than the standard five‐minute test.Grant Funding Source: NSERC

Acute mountain sickness, chemosensitivity, and cardiorespiratory responses in humans exposed to hypobaric and normobaric hypoxia

We examined the control of breathing, cardiorespiratory effects, and the incidence of acute mountain sickness (AMS) in humans exposed to hypobaric hypoxia (HH) and normobaric hypoxia (NH), and under two control conditions [hypobaric normoxia (HN) and normobaric normoxia (NN)]. Exposures were 6 h in duration, and separated by 2 wk between hypoxic exposures and 1 wk between normoxic exposures. Before and after exposures, subjects (n = 11) underwent hyperoxic and hypoxic Duffin CO2 rebreathing tests and a hypoxic ventilatory response test (HVR). Inside the environmental chamber, minute ventilation (V(E)), tidal volume (V(T)), frequency of breathing (fB), blood oxygenation, heart rate, and blood pressure were measured at 5 and 30 min and hourly until exit. Symptoms of AMS were evaluated using the Lake Louise score (LLS). Both the hyperoxic and hypoxic CO2 thresholds were lower after HH and NH, whereas CO2 sensitivity was increased after HH and NH in the hypoxic test and after NH in the hyperoxic test. Values for HVR were similar across the four exposures. No major differences were observed for Ve or any other cardiorespiratory variables between NH and HH. The LLS was greater in AMS-susceptible than in AMS-resistant subjects; however, LLS was alike between HH and NH. In AMS-susceptible subjects, fB correlated positively and Vt negatively with the LLS. We conclude that 6 h of hypoxic exposure is sufficient to lower the peripheral and central CO2 threshold but does not induce differences in cardiorespiratory variables or AMS incidence between HH and NH.

Carotid body tumors are not associated with an increased risk for sleep-disordered breathing

Tumors in the carotid bodies may interfere with their function as peripheral chemoreceptors. An altered control of ventilation may predispose to sleep-disordered breathing. This study aimed to assess whether patients with unilateral or bilateral carotid body tumors (uCBT or bCBT, respectively) or bilateral CBT resection (bCBR) display sleep-disordered breathing and to evaluate the global contribution of the peripheral chemoreceptor to the hypercapnic ventilatory response. Eight uCBT, eight bCBT, and nine bCBR patients and matched controls underwent polysomnography. The peripheral chemoreflex drive was assessed using euoxic and hyperoxic CO2 rebreathing tests. Daytime sleepiness and fatigue were assessed with the Epworth Sleepiness Scale and the Multidimensional Fatigue Index. All patient groups reported significant fatigue-related complaints, but no differences in excessive daytime sleepiness (EDS) were found. The apnea/hypopnea index (AHI) did not differ significantly between patient groups and controls. Only in bCBT patients, a trend towards a higher AHI was observed, but this did not reach significance (p=0.06). No differences in the peripheral chemoreflex drive were found between patients and controls. Patients with (resection of) CBTs have more complaints of fatigue but are not at risk for EDS. The presence or resection of CBTs is neither associated with an altered peripheral chemoreflex drive nor with sleep-disordered breathing.

In Utero Exposure to Smoking and Peripheral Chemoreceptor Function in Preterm Neonates

We aimed to assess the involvement of peripheral chemoreceptor tonic activity in the ventilatory pattern during sleep in preterm neonates exposed in utero to maternal smoking. Peripheral chemoreceptor activity was measured at thermoneutrality in neonates (postmenstrual age: 36.1 +/- 1.2 weeks) born to nonsmoking (n = 21) or smoking (n = 16) mothers by performing a 30-second hyperoxic test during active and quiet sleep. Blood oxygen saturation, baseline ventilatory parameters, and central apnea were monitored. Prenatal smoking exposure did not modify baseline ventilation. It was interesting to note that prenatal smoking exposure decreased the peripheral chemoreceptor tonic activity during active sleep and increased the response time during quiet sleep. These changes could explain the increase in the time spent in apnea (both with and without blood oxygen desaturation) and in the mean duration of apneic episodes with desaturation found in neonates exposed to smoking in utero. The involvement of a change in the chemoreceptor function is supported by the fact that the peripheral chemoreceptor tonic activity was negatively correlated with the mean duration of apneic episodes with desaturation in the control group only. To our knowledge, this is the first study to reveal that prenatal smoking exposure does not directly modify baseline ventilatory parameters in the neonate but has a negative impact on peripheral chemoreceptor tonic activity. These alterations may increase the risk of sleep respiratory disorders, especially via apnea with desaturation.

Ventilatory Response to a Hyperoxic Test Is Related to the Frequency of Short Apneic Episodes in Late Preterm Neonates

Chemoreception is frequently involved in the processes underlying apnea in premature infants. Apnea could result from a decrease in carotid body effectiveness. However, increased carotid body activity could also initiate apnea through hypocapnia following hyperventilation when the receptors are stimulated. The aim of this study was to analyze the relationship between carotid body effectiveness and short apneic episodes in older preterm neonates. Carotid body effectiveness was assessed at thermoneutrality in 36 premature neonates (2.07 +/- 0.26 kg) by performing a 30-s hyperoxic test during sleep, the oxygen inhalation involving a ventilation decrease. Blood O(2) saturation (Sp(o2)) and ventilatory parameters were monitored before and during the hyperoxic test. Short episodes of apnea (frequency and mean duration) were recorded during the morning's 3-h interfeeding interval. Pretest Sp(o2) was not related to any of the measured respiratory parameters. A higher frequency of short apneic episodes was linked to a greater ventilation decrease in response to the hyperoxic test (rho = -0.32; p = 0.01). Increased carotid body response is correlated with greater apneic episodes frequency, even in the absence of concomitant oxygen desaturation. Fetal or early postnatal hypoxemia could have increased peripheral chemoreceptor activity, which could initiate a "overshoot/undershoot" situation, which in turn could induce a critical P(o2)/P(co2) combination and apnea.

Inhibitory effects of repeated hyperoxia on breathing in newborn mice

Brief oxygen therapy is commonly used for resuscitation at birth or prevention of hypoxaemia before procedures during the neonatal period. However, O(2) may severely depress breathing, especially when administered repeatedly. The aim of the present study was to test the effects of repeated hyperoxia on breathing control in newborn mice. A total of 97 Swiss mouse pups were assigned to O(2) or air on post-natal day 0, 1 or 2. Each pup in the O(2) group was subjected to four hyperoxic tests (100% O(2) for 3 min followed by 12 min normoxia), whereas pups in the air group were maintained in normoxia. Breathing variables were measured using flow-through barometric plethysmography. O(2) significantly decreased minute ventilation as seen in a decrease in respiratory rate. This decrease became significantly larger with repeated exposure and ranged -17- -26% for all ages combined. Furthermore, hyperoxia increased total apnoea duration, as compared with the baseline value. In newborn mice, repeated hyperoxia increasingly depressed breathing. This finding further supports a need for stringent control of oxygen therapy, most notably repeated oxygen administration in the neonatal period for premature newborn infants and those carried to term.

Ventilatory response to hyperoxia in newborn mice heterozygous for the transcription factorPhox2b

Heterozygous mutations of the transcription factor PHOX2B have been found in most patients with central congenital hypoventilation syndrome, a rare disease characterized by sleep-related hypoventilation and impaired chemosensitivity to sustained hypercapnia and sustained hypoxia. PHOX2B is a master regulator of autonomic reflex pathways, including peripheral chemosensitive pathways. In the present study, we used hyperoxic tests to assess the strength of the peripheral chemoreceptor tonic drive in Phox2b+/-newborn mice. We exposed 69 wild-type and 67 mutant mice to two hyperoxic tests (12-min air followed by 3-min 100% O2) 2 days after birth. Breathing variables were measured noninvasively using whole body flow plethysmography. The initial minute ventilation decrease was larger in mutant pups than in wild-type pups: -37% (SD 13) and -25% (SD 18), respectively, P<0.0001. Furthermore, minute ventilation remained depressed throughout O2 exposure in mutants, possibly because of their previously reported impaired CO2 chemosensitivity, whereas it returned rapidly to the normoxic level in wild-type pups. Hyperoxia considerably increased total apnea duration in mutant compared with wild-type pups (P=0.0001). A complementary experiment established that body temperature was not influenced by hyperoxia in either genotype group and, therefore, did not account for genotype-related differences in the hyperoxic ventilatory response. Thus partial loss of Phox2b function by heterozygosity did not diminish the tonic drive from peripheral chemoreceptors.

102 Ventilatory response to hyperoxia in newborn mice heterozygous for the transcription factor Phox2b

Introduction The transcription factor Phox2b is a master regulator of the noradrenergic phenotype and of dl neuronal relays of the autonomic medullary reflex pathways including peripheral chemoreceptors and their afferent viscerai pathways. Heterozygous mutations of Phox2b have been found in a high proportion of patients with Central Congenitd Hypoventilation Syndrome (CCHS), a rare autosomal dominant syndrome characterized by hypoventilation during sleep, and impaired ventilatory responses to hypercapnia and hypoxia. We previously showed that Phox2b+/- mutant mice showed a blunted response to CO2 [l], and a large increase in sleep apnea total time [2]. However, the hyperpneic response to hypoxia was normd [l]. The aim of this study was to examine chemosensitivity to 0 2 in Phox2B+/- pups using an hyperoxic test. Methods 136 wild-type and mutant two-day old pups were exposed to two hyperoxic tests (12 min air followed by 3 min 02), followed by 12 min air. Breathing variables and apneas were measured noninvasively using whole body flow plethysmography. We evaluated the ventilatory response to hyperoxia based on the maximal VE decline, i.e., the minima VE value (min VE) over the 3 min of O2 exposure expressed as the percentage of the baseline level. Results . Conclusion Sensitivity to O 2 was not impaired in Phox2B+/- newborn pups, in line with previous results showing their normal hyperpneic response to hypoxia, and in contrast with CCHS. However, hyperoxia caused a sustained ventilatory depression in mutant pups, suggesting that disruption of Phox2B impaired activatory processes of breathing. This latter effect may contibute to sleep-related respiratory disorders in CCHS.

103 Inhibitory effects of repeated hyperoxia on breathing in newborn mice

Brief oxygen therapy is commonly used for resuscitation at birth or for preventing hypoxemia before procedures in critically ill neonates. However, in addition to having various adverse effects, oxygen may severely depress breathing, especially when administered repeatedly. These effects cannot be studied experimentally in humans. In this study, we tested the effects of repeated hyperoxia on breathing control in newborn mice. We randomly assigned 97 Swiss mice to oxygen or air on postnatal day 0, 1, or 2 (P0, PI, and P2). Each pup in the oxygen group was subjected to four hyperoxic tests (100% O 2 for 3 min followed by 12 min normoxia), whereas pups in the air group were continuously maintained in normoxia. Breathing variables were measured noninvasively using whole body flow plethysmography. Oxygen significantly decreased VE at ail ages. This decline increased significantly with repetition (group-by-test interaction, P< 0.0005; age effects were not significant) and ranged from -17% to -26% for ail ages combined. Furthermore, hyperoxia increased total apnea duration, as compared with the prehyperoxia value (group-by-test interaction, P < 0.0296; age effects were not significant). In newborn mice, repeated hyperoxia increasingly depressed breathing, consistent with potentiating effects. This fin-ding further supports a need for stringent control of repeated oxygen therapy in premature newborn infants.

Respiratory Distress in the Term and Near-term Infant

After completing this article, readers should be able to: 1. Differentiate between cardiac and respiratory causes of cyanosis. 2. Describe the primary parenchymal diseases that can cause respiratory distress in the neonate. 3. Describe the primary developmental lung abnormalities that can cause respiratory distress in the neonate. One of the most common reasons for admission of term neonates to a neonatal intensive care unit (NICU) is respiratory distress. (1) The cause may be of pulmonary or nonpulmonary origin. The nonpulmonary causes include cardiac, infectious, metabolic, central nervous system, and miscellaneous conditions. This review focuses on the major pulmonary causes for respiratory distress in term infants, in particular, the first two of the four groups that appear in Table 1. (2) | Parenchymal conditions | || | Developmental abnormalities | | Airway abnormalities | | Mechanical abnormalities | Table 1. Potential Pulmonary Causes for Respiratory Distress in Neonates Differentiating cardiac and respiratory causes of cyanosis is a common clinical problem, particularly in cases in which there is little or no tachypnea or respiratory distress. The major signs of neonatal respiratory distress are tachypnea and cyanosis, in which tachypnea is defined as a respiratory rate consistently greater than 60 breaths/min. A hyperoxia test may assist in differentiating between the two. Pulse oximetry may help to decide whether a formal hyperoxic test is useful. A neonate who exhibits cyanosis without marked respiratory distress and has an O2 saturation of less than 85% in both room air and 100% oxygen likely has an intracardiac shunt. If the O2 saturation increases to more than 85% on 100% oxygen, …

Anxiety sensitivity as a predictor of panic attacks

Anxiety sensitivity (AS) is the fear of physical symptoms of anxiety and related sensations believed to have harmful consequences. AS may play a central role in the nature and etiology of panic disorder (PD) and the genesis of panic attacks. We collected Anxiety Sensitivity Index (ASI) scores from PD patients and controls to determine if AS accurately predicts panic. ASIs were completed prior to panic induction using the modified Read rebreathing test in both hypoxic and hyperoxic conditions. Total scores first-order factors, and individual item ASI scores were correlated with panic presence (Spearman correlation) for each of the hypoxic and hyperoxic rebreathing tests for both study populations. Control subjects' data correlated significantly for items 4, 8, and 11 of the ASI for the hyperoxic ( n=9; r S=0.63, 0.70, and 0.63, respectively) and items 4 and 8 for the hypoxic rebreathing tests ( n=9; r S=0.63 and 0.70, respectively). Panic patients' data correlated significantly for item 1 of the ASI for hyperoxic tests ( n=8; r S=0.76) and item 5 for the hypoxic tests ( n=8; r S=0.95). Total ASI scores or first-order factors (physical, social concerns, and mental incapacitation) scores of either study group did not correlate significantly with panic presence. AS may not be a reliable predictor of panicogenic responses to CO 2-induced panic in either PD or normal control populations. AS may not be an ultimate causal element in eliciting panic attacks.

Reliability of a Rebreathing Procedure to Evaluate Respiratory Chemoreflex Control

0858 PURPOSE: To examine the reliability and reproducibility of a modified rebreathing procedure and assess its utility as a research/diagnostic tool. METHODS: The rebreathing technique used was modified to include 5 minutes of prior hyperventilation and maintenance of iso-oxia at hyperoxic (150 mmHg) or hypoxic (50 mmHg) oxygen tensions during rebreathing (Duffin et al., Respir. Physiol., 2000). Twentyeight healthy subjects (14 men, 14 women) performed both hyperoxic and hypoxic rebreathing experiments in the morning (AM) and evening (PM) of the same day, with 12–13 hours separating AM and PM tests. Reliability was examined using the Pearson product-moment correlation coefficient. A three-way ANOVA was used to evaluate the reproducibility. Within and between-subject coefficients of variation (CVs) were calculated. RESULTS: Mean hyperoxic and hypoxic ventilatory responses to carbon dioxide (CO2) did not differ between the AM and PM. Significant reliability coefficients were observed for hyperoxic (r = 0.45 – 0.75) and hypoxic (r = 0.67 – 0.78) rebreathing responses. Bland-Altman plots confirmed no systematic bias between AM and PM tests. Between-subject CVs for basal (41.0 and 39.1%) and sensitivity (34.3 and 33.7%) responses, for hypoxic and hyperoxic tests were similar, but the CVs for the chemoreflex threshold for CO2 were much less (4.8 and 4.9%) for both hyperoxic and hypoxic tests. Within-subject CVs for basal (23.9 ± 4.1 and 20.7 ± 3.7%), threshold (2.6 ± 0.4 and 2.6 ± 0.4%) and sensitivity (17.5 ± 3.1 and 19.9 ± 2.6%) responses to CO2, for hyperoxic and hypoxic tests, were reasonably low. CONCLUSIONS: The results support the within-day reliability and reproducibility of the modified rebreathing procedure. These data support the use of the modified rebreathing procedure to investigate the effects of interventions/physiological perturbations on the chemoreflex control of breathing. However, its use to diagnose disorders in respiratory chemoreflex control in individual patients is not supported. Supported by the William M. Spear Foundation and Ontario Thoracic Society.

Reliability of a Rebreathing Procedure to Evaluate Respiratory Chemoreflex Control

0858 PURPOSE: To examine the reliability and reproducibility of a modified rebreathing procedure and assess its utility as a research/diagnostic tool. METHODS: The rebreathing technique used was modified to include 5 minutes of prior hyperventilation and maintenance of iso-oxia at hyperoxic (150 mmHg) or hypoxic (50 mmHg) oxygen tensions during rebreathing (Duffin et al., Respir. Physiol., 2000). Twentyeight healthy subjects (14 men, 14 women) performed both hyperoxic and hypoxic rebreathing experiments in the morning (AM) and evening (PM) of the same day, with 12–13 hours separating AM and PM tests. Reliability was examined using the Pearson product-moment correlation coefficient. A three-way ANOVA was used to evaluate the reproducibility. Within and between-subject coefficients of variation (CVs) were calculated. RESULTS: Mean hyperoxic and hypoxic ventilatory responses to carbon dioxide (CO2) did not differ between the AM and PM. Significant reliability coefficients were observed for hyperoxic (r = 0.45 – 0.75) and hypoxic (r = 0.67 – 0.78) rebreathing responses. Bland-Altman plots confirmed no systematic bias between AM and PM tests. Between-subject CVs for basal (41.0 and 39.1%) and sensitivity (34.3 and 33.7%) responses, for hypoxic and hyperoxic tests were similar, but the CVs for the chemoreflex threshold for CO2 were much less (4.8 and 4.9%) for both hyperoxic and hypoxic tests. Within-subject CVs for basal (23.9 ± 4.1 and 20.7 ± 3.7%), threshold (2.6 ± 0.4 and 2.6 ± 0.4%) and sensitivity (17.5 ± 3.1 and 19.9 ± 2.6%) responses to CO2, for hyperoxic and hypoxic tests, were reasonably low. CONCLUSIONS: The results support the within-day reliability and reproducibility of the modified rebreathing procedure. These data support the use of the modified rebreathing procedure to investigate the effects of interventions/physiological perturbations on the chemoreflex control of breathing. However, its use to diagnose disorders in respiratory chemoreflex control in individual patients is not supported. Supported by the William M. Spear Foundation and Ontario Thoracic Society.

Peripheral chemoreceptor activity in sleeping neonates exposed to warm environments

In neonates, it is often assumed that ventilatory control and heat stress interact. Thus the two factors have been implicated in various pathologies (apnoea, sudden infant death syndrome). However, little is known about the mechanisms of this interaction, and the influence of sleep is still debated. This study aimed at determining the influence of warm exposure on the decrease in ventilation V ̇ E during a hyperoxic test (HT), which is considered to be a measure of peripheral chemoreceptor activity. The test was performed in active (AS) and quiet sleep (QS) in 12 neonates exposed to thermoneutral or warm environments. The HT consisted of 30 s of inspired, 100% O 2. The ventilatory response was assessed in terms of a response time, defined as the time elapsing between HT onset and the first significant change in V ̇ E . Our results show that, in both thermal conditions, the fall in V ̇ E was higher in AS than in QS. Warm exposure significantly enhanced the ventilatory response in AS (–27.5 ± 8.7% vs. –38.3 ± 8.8%, P < 0.01) but not in QS. A thermometabolic drive or inputs from thermoreceptors could be involved in the reinforcement of peripheral chemoreceptor activity in AS in warmer environments, which could contribute to an increasing risk of apnoea in neonates with altered chemoreceptor function. Since hypothalamic structures are involved in thermoregulatory, sleep processes and (probably) in respiratory control, it could well be the principal site where this interaction occurs.