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PubMed1996

Inhibitory effect of an intellectual task on breathing after voluntary hyperventilation.

We investigated the effects of an intellectual task on posthyperventilation (PHV) breathing by using a video game. Eight normal subjects were placed in a supine positions. The game task by itself led to increase ventilation compared with the control tasks via an increase in the average inspiratory flow rate (P < 0.01) and the respiratory frequency (P < 0.001). After hypocapnic voluntary hyperventilation (VHV), the task led to a decrease in the 1-min PHV breathing level compared with the control tasks after VHV [after VHV, first 60 s average minute ventilation while watching television and while playing a video game are 5.54 +/- 2.91 (SD) and 2.05 +/- 1.40 l/min, respectively; P < 0.01]. Only one subject showed PHV apnea for at least 10 s during the control protocol, whereas seven of the same eight subjects showed PHV apnea while performing the task. After isocapnic VHV, the task still led to a decrease in PHV breathing compared with the control tasks. However, this decrease was smaller than in the hypocapnic studies and was only significant during the first 15 s of recovery. These results suggest that increased activity in the higher centers of the central nervous system has an inhibitory effect on PHV breathing at a time when the effects of short-term potentiation after VHV, hypocapnia, and perhaps other mechanisms would be expected to be acting on breathing.

Adult↗
PubMed1999

Airway obstruction during exercise and isocapnic hyperventilation in asthmatic subjects.

We compared pulmonary mechanics measured during long-term exercise (LTX = 20 min) with long-term isocapnic hyperventilation (LTIH = 20 min) in the same asthmatic individuals (n = 6). Peak expiratory flow (PEF) and forced expiratory volume in 1 s (FEV(1)) decreased during LTX (-19.7 and -22.0%, respectively) and during LTIH (-6.66 and 10. 9%, respectively). In contrast, inspiratory pulmonary resistance (RL(I)) was elevated during LTX (57.6%) but not during LTIH (9.62%). As expected, airway function deteriorated post-LTX and post-LTIH (FEV(1) = -30.2 and -21.2%; RL(I) = 111.8 and 86.5%, respectively). We conclude that the degree of airway obstruction observed during LTX is of a greater magnitude than that observed during LTIH. Both modes of hyperpnea induced similar levels of airway obstruction in the posthyperpnea period. However, the greater airway obstruction during LTX suggests that a different process may be responsible for the changes in airway function during and after the two modes of hyperpnea. This finding raises questions about the equivalency of LTIH and LTX in the study of airway function during exercise-induced asthma.

Adult↗
PubMed2006

Excitability of human motor and visual cortex before, during, and after hyperventilation.

In humans, hyperventilation (HV) has various effects on systemic physiology and, in particular, on neuronal excitability and synaptic transmission. However, it is far from clear how the effects of HV are mediated at the cortical level. In this study we investigated the effects of HV-induced hypocapnia on primary motor (M1) and visual cortex (V1) excitability. We used 1) motor threshold (MT) and phosphene threshold (PT) and 2) stimulus-response (S-R) curves (i.e., recruitment curves) as measures of excitability. In the motor cortex, we additionally investigated 3) the intrinsic inhibitory and facilitatory neuronal circuits using a short-interval paired-pulse paradigm. Measurements were performed before, during, and after 10 min of HV (resulting in a minimum end-tidal Pco(2) of 15 Torr). HV significantly increased motor-evoked potential (MEP) amplitudes, particularly at lower transcranial magnetic stimulation (TMS) intensities. Paired-pulse stimulation indicated that HV decreases intracortical inhibition (ICI) without changing intracortical facilitation. The results suggestthat low Pco(2) levels modulate, in particular, the intrinsic neuronal circuits of ICI, which are largely mediated by neurons containing gamma-aminobutyric acid. Modulation of MT probably resulted from alterations of Na(+) channel conductances. A significant decrease of PT, together with higher intensity of phosphenes at low stimulus intensities, furthermore suggested that HV acts on the excitability of M1 and V1 in a comparable fashion. This finding implies that HV also affects other brain structures besides the corticospinal motor system. The further exploration of these physiological mechanisms may contribute to the understanding of the various HV-related clinical phenomenona.

Adult↗
PubMed2007

Effects of hyperventilation on phosphocreatine kinetics and muscle deoxygenation during moderate-intensity plantar flexion exercise.

The effects of controlled voluntary hyperventilation (Hyp) on phosphocreatine (PCr) kinetics and muscle deoxygenation were examined during moderate-intensity plantar flexion exercise. Male subjects (n = 7) performed trials consisting of 20-min rest, 6-min exercise, and 10-min recovery in control [Con; end-tidal Pco(2) (Pet(CO(2))) approximately 33 mmHg] and Hyp (Pet(CO(2)) approximately 17 mmHg) conditions. Phosphorus-31 magnetic resonance and near-infrared spectroscopy were used simultaneously to monitor intramuscular acid-base status, high-energy phosphates, and muscle oxygenation. Resting intracellular hydrogen ion concentration ([H(+)](i)) was lower (P < 0.05) in Hyp [90 nM (SD 3)] than Con [96 nM (SD 4)]; however, at end exercise, [H(+)](i) was greater (P < 0.05) in Hyp [128 nM (SD 19)] than Con [120 nM (SD 17)]. At rest, [PCr] was not different between Con [36 mM (SD 2)] and Hyp [36 mM (SD 1)]. The time constant (tau) of PCr breakdown during transition from rest to exercise was greater (P < 0.05) in Hyp [39 s (SD 22)] than Con [32 s (SD 22)], and the PCr amplitude was greater (P < 0.05) in Hyp [26% (SD 4)] than Con [22% (SD 6)]. The deoxyhemoglobin and/or deoxymyoglobin (HHb) tau was similar between Hyp [13 s (SD 8)] and Con [10 s (SD 3)]; however, the amplitude was increased (P < 0.05) in Hyp [40 arbitrary units (au) (SD 23)] compared with Con [26 au (SD 17)]. In conclusion, our results indicate that Hyp-induced hypocapnia enhanced substrate-level phosphorylation during moderate-intensity exercise. In addition, the increased amplitude of the HHb response suggests a reduced local muscle perfusion in Hyp compared with Con.

Adult↗
PubMedDate not supplied

Lung function measured by impulse oscillometry and spirometry following eucapnic voluntary hyperventilation.

BACKGROUND: The efficacy of impulse oscillometry (IOS) to measure airway calibre change is not fully established. OBJECTIVES: To evaluate lung function change after eucapnic voluntary hyperventilation (EVH), and to compare IOS indices with spirometric maximal expiratory flow measurements. METHODS: Twenty subjects (10 airway hyperresponsive [AHR+] and 10 normal [AHR--]) underwent IOS and spirometry before and for 15 min after 6 min EVH (inhaling 5% CO2, 21% O2, balance N2) at a target ventilation of 30 times the baseline value of the forced expiratory volume in 1 s (FEV1) at 20 degrees C. AHR+ was defined by a fall in FEV1 of 10% or greater from baseline after a provoking challenge. Airway resistance at 5 Hz (R5), reactance at 5 Hz, resonant frequency (Fres), area of reactance integrated from 5 Hz to Fres (AX), and FEV1 were determined. RESULTS: No baseline spirometry values correlated with falls in FEV1. Baseline R5 and AX values correlated with peak falls in FEV1 (r= -0.51 and -0.46, respectively; P< 0.05). AHR+ subjects demonstrated greater per cent peak falls in FEV1 than did AHR- subjects following EVH (30.6 +/- 14.0% versus 7.5 +/- 2.6%, respectively; P<0.05). Changes in R5, Fres, reactance and AX were greater for AHR+ subjects than for AHR- subjects and correlated with a fall in FEV1 (r= -0.74, -0.70, 0.69 and -0.73, respectively; P<0.05). At a designated specificity of 80%, the per cent change in R5 (50% or greater) and post-EVH AX (12 cm H2O/L or greater) yielded sensitivities to a 10% fall in FEV1 of 90%. CONCLUSION: IOS is an acceptable measure to determine AHR and can supplement spirometry in lung function evaluation.

Adult↗
PubMed2006

Hyperventilation-induced cerebrovascular reactivity among hypertensive and healthy adolescents.

BACKGROUND: It is known that cerebral vasoreactivity is altered in adult arterial hypertension but no information is available about cerebral arteriolar function in hypertensive adolescents. Therefore, the aim of the present work was to assess cerebral vasoreactivity responses in adolescent hypertension. METHODS: 113 hypertensive and 58 normotensive adolescents were assessed with transcranial Doppler sonography by using voluntary hyperventilation (HV) as vasoconstrictory stimulus. Absolute blood flow velocities (systolic, mean and diastolic) and pulsatility indices (PIs) at rest and after HV, as well as percentage change of the blood flow velocities after HV were compared among the groups. RESULTS: Blood flow velocities at rest were significantly higher in hypertensive individuals, while PIs were similar in the two groups. After HV, all blood flow velocity parameters were higher among hypertensive teenagers than in healthy controls, while PIs did not differ between the two groups. Taking the relative changes after HV into account, it was found that HV induced a more pronounced change of the systolic and mean blood flow velocities of the control subjects than in hypertensive adolescents. CONCLUSIONS: Cerebrovascular reactivity to hypocapnia is decreased in hypertensive adolescents as compared to healthy teenagers. Further studies are needed to clarify the clinical significance of altered cerebral microvascular function in adolescent hypertension.

Adolescent↗
PubMed1975

Facilitation through hyperventilation of therapeutic effect of pyrithioxin in cerebral infarct patients.

A method of treatment consisting in administration of a neurodynamic drug, pyrithioxin, combined with a short period of hyperventilation (HV) was applied in cerebral infarct patients with hemiplegia. The combination was superior to pyrithioxin alone for the motor recovery of these patients. In some cases, it induced immediately a partial restoration of motility. The combination constantly brought about an increase in urinary excretion of norepinephrine and vanilmandelic acid, which failed to occur after pyrithioxin or HV alone. HV appears to facilitate the neural effects of the drug by promoting its transfer into the CNS.

Aged↗
PubMedDate not supplied

Hyperventilation enhances transcapillary diffusion of sodium fluorescein.

Voluntary hyperventilation (HV) provokes hemoconcentration due to a loss of fluid from the intravascular space. In 10 healthy male volunteers the hypothesis was tested whether HV increases transcapillary fluid shift into the interstitial compartment. For this purpose, fluorescent light intensity (FLI) alterations after intravenous injection of sodium fluorescein (Na fluorescein) before and during 3 min of HV were determined. Concomitantly, temperature and microvascular skin flux (laser Doppler fluxmetry, LDF) were recorded continuously. Hematocrit and serum proteins, as markers of hemoconcentration, increased significantly from 41.2 +/- 2.3 to 42.7 +/- 2.0% (p = 0.0023) and from 69.5 +/- 3.4 to 72.9 +/- 3.0 g/l (p = 0.0005, respectively). Skin temperature and LDF showed no changes during HV compared to baseline levels. Interstitial FLI indicating transcapillary diffusion of Na fluorescein was significantly higher (p < 0.001) during HV compared to the values recorded during the baseline period. The exact mechanism of enhanced transcapillary diffusion of Na fluorescein is not known. The distinct increase in FLI without a significant change in microvascular skin flux suggests an HV-induced increase in capillary pressure or an enhancement in capillary permeability for water and small solutes.

Adult↗
PubMed1986

Cold-air isocapnic hyperventilation test in the study of the effects and duration of action of Duovent. Comparison with fenoterol, salbutamol, disodium cromoglycate and placebo.

The cold-air isocapnic hyperventilation (CAIH) test is a challenge test for non-specific bronchitis which was recently incorporated into the study of bronchial hyperreactivity. As it is easy to perform and to reproduce, the CAIH test is regarded as a valuable examination in clinical pharmacology. We carried out a study using this test in 12 atopic asthmatics in intercritical phase. The patients were treated for a few days before, under double-blind conditions and random order, with Duovent (80 micrograms ipratropium bromide + 200 micrograms fenoterol), fenoterol (400 micrograms), salbutamol (200 micrograms), disodium cromoglycate (DSCG) (10 mg) and placebo. All the drugs were administered by aerosol 30 min before the test which was repeated at intervals of 120, 240 and 360 min after intake of the drug. Certain parameters of respiratory function were measured by dry spirometry (Vicatest 2 C) before administration of the drug as well as before and 0, 3, 5, 15, 30 and 60 min after each test. For the sake of brevity only the FEV1 values are shown in the figures since the other parameters all revealed a similar pattern. After placebo, all the patients reacted to the CAIH test with significant falls after each of the 4 tests, but there was no statistically significant difference between the 4 tests; there were no statistically significant differences between the pretreatment values in FEV1 recorded before each treatment (verum or placebo).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Respiratory impedance measurements in a dose-response study of isocapnic hyperventilation with cold air.

Spirometry and impedance of the respiratory system were compared after increasing rates of isocapnic cold air hyperventilation (IHCA) in 10 asthmatics and 11 healthy nonsmokers. In the control group IHCA at 60% of indirect maximum breathing capacity (IMBC) resulted in a significant, equal increase in resistance at lower and higher frequencies, suggesting central airway constriction. In the asthmatics negative frequency dependence of resistance and a significant increase in resonant frequency and decrease in the reactance at 8 Hz were found at 40 and 60% IMBC. These changes suggest an increase in the resistance of the peripheral airways. The frequency dependence of resistance and resonant frequency were found to be the most sensitive measures to differentiate between normals and asthmatics. It is concluded that impedance measurements provide a suited method to assess the response in cold air provocation tests.

Adult↗
PubMed1996

Prevalence of severity of hypoxemia following clinical voluntary hyperventilation.

The voluntary hyperventilation (VHV) test is used in many clinical examinations. However, arterial hypoxemia following a clinical VHV test is not a well-studied phenomenon. We analyzed the arterial blood gases (ABGs) of 61 patients during a VHV test. The ABG were taken prior to (PaO2-Prior), immediately following (PaO2-Immediate), and 5 min after (PaO2-After) the VHV test. The patients' average PaO2 rose significantly (p < 0.0001) from the PaO2-Prior (88 +/- 8 mm Hg; mean +/- SD) to the PaO2-Immediate (118 +/- 13 mm Hg) and then dropped significantly (p < 0.0001) to the PaO2-After (74 +/- 16 mm Hg). Two of the 20 patients who experienced an angina pectoris attack (AP(+)) following the VHV test showed severe arterial hypoxemia (PaO2-After < 60 mm Hg), whereas 9 of the 41 patients who did not experience an angina pectoris attack (AP(-)) showed a PaO2-After < 60 mm Hg. The PaO2-After did not correlate with the PaO2-Prior. The decrease in the PaO2-Prior to After did not correlate significantly with the left ventricular ejection fraction rate (n = 58, r = 0.18, not significant). However, the decrease in the PaO2-Prior to After correlated well with the degree of recovery of the PaCO2 following the VHV test (r = -0.69, p < 0.0001). The age, gender ratio, changes in arterial blood gases, number of patients who experienced PaO2-After < 60 mm Hg, and left-ventricular ejection fraction rate were not significantly different between the AP(-) and AP(+) groups. Posthyperventilation hypoxemia developed frequently following the VHV test during coronary angiography. Although this arterial hypoxemia was not directly correlated with the occurrence of AP attacks following VHV in this study, continuous SaO2 monitoring is recommended whenever a VHV test is used as a diagnostic technique to avoid the potentially deleterious effects of arterial hypoxemia.

Arteries↗
PubMed1986

Flunarizine treatment in dizzy patients with vestibular hyperreactivity and hyperventilation.

Flunarizine (10 mg/day) was given in an open pilot study to 14 patients with the primary complaint of dizziness, who showed vestibular hyperreactivity in the velocity step (VS) test and were proven to have a hyperventilation syndrome (HVS) without any other disease. The VS test was repeated after 4-6 weeks of treatment. Twelve of these HVS patients reported alleviation of dizziness. Objective evaluation of the results of treatment was attempted by defining suitable response parameters and comparing their values to those obtained in a control group of 14 healthy volunteers tested twice with the same interval. A significant decrease in right-left asymmetry in the VS responses of the patients on drug was found.

Adolescent↗
PubMedDate not supplied

Effects of hyperventilation and hypoventilation on cochlear blood flow and endocochlear direct-current potential.

To understand the importance of oxygen transport to the inner ear tissue, we studied, in guinea pigs, the relationship between cochlear blood flow and endocochlear direct-current potential (EP) under different respiratory conditions. EP, a functional parameter of the stria vascularis, was recorded by a microelectrode inserted into the lateral wall of the chochlea. To measure the cochlear blood flow (CoBF), we employed laser Doppler flowmetry and recorded the flow with a probe placed on the same spot on the lateral wall. During 3 min of asphyxia, CoBF and systemic blood pressure showed irregular biphasic increases, while the EP decreased to reach a negative value. In the hypoxemia experiment, which was induced by stepwise reduction of the respiratory rate to 60%, increases in CoBF and blood pressure were evident during hypoventilation with an intermediate position of EP in the positive range. The mechanisms of these increases in two parameters are discussed from the viewpoints of sympathicotonic activity in the autonomic nervous system and the vasodilating action of CO2 during hypercapnia. In the hyperoxemia experiment, which was induced by stepwise increase in the respiratory rate to 140%, CoBF and blood pressure were found to decrease during hyperventilation with no significant change of EP. The decrease in blood pressure was considered to be due to the increase in intrathoracic pressure caused by the increased rate of artificial respiration. As for the concomitant decrease in CoBF, chemical regulation of PCO2 in the vascular bed of the lateral wall of the cochlea was thought to be a contributory factor.

Animals↗
PubMed2004

Hyperventilation-induced hypotension during cardiopulmonary resuscitation.

BACKGROUND: A clinical observational study revealed that rescuers consistently hyperventilated patients during out-of-hospital cardiopulmonary resuscitation (CPR). The objective of this study was to quantify the degree of excessive ventilation in humans and determine if comparable excessive ventilation rates during CPR in animals significantly decrease coronary perfusion pressure and survival. METHODS AND RESULTS: In humans, ventilation rate and duration during CPR was electronically recorded by professional rescuers. In 13 consecutive adults (average age, 63+/-5.8 years) receiving CPR (7 men), average ventilation rate was 30+/-3.2 per minute (range, 15 to 49). Average duration per breath was 1.0+/-0.07 per second. No patient survived. Hemodynamics were studied in 9 pigs in cardiac arrest ventilated in random order with 12, 20, or 30 breaths per minute. Survival rates were then studied in 3 groups of 7 pigs in cardiac arrest that were ventilated at 12 breaths per minute (100% O2), 30 breaths per minute (100% O2), or 30 breaths per minute (5% CO2/95% O2). In animals treated with 12, 20, and 30 breaths per minute, the mean intrathoracic pressure (mm Hg/min) and coronary perfusion pressure (mm Hg) were 7.1+/-0.7, 11.6+/-0.7, 17.5+/-1.0 (P<0.0001), and 23.4+/-1.0, 19.5+/-1.8, and 16.9+/-1.8 (P=0.03), respectively. Survival rates were 6/7, 1/7, and 1/7 with 12, 30, and 30+ CO2 breaths per minute, respectively (P=0.006). CONCLUSIONS: Professional rescuers were observed to excessively ventilate patients during out-of-hospital CPR. Subsequent animal studies demonstrated that similar excessive ventilation rates resulted in significantly increased intrathoracic pressure and markedly decreased coronary perfusion pressures and survival rates.

Adult↗
PubMed1988

Nonspecific bronchial hyperresponsiveness to inhaled histamine and hyperventilation of cold dry air in subjects with respiratory symptoms of uncertain etiology.

Fifty adult subjects referred to a respiratory function laboratory of a tertiary care hospital for respiratory symptoms of uncertain etiology were investigated prospectively by means of a questionnaire, isocapnic inhalation of dry cold air (-20 degrees C), histamine inhalation tests, monitoring of peak expiratory flow rates, total eosinophil counts, and total IgE. Wheezing, tightness in the chest, dyspnea, and cough were reported by 35, 23, 41, and 30 subjects, respectively. FEV1 values less than 80% pred were found in only 2 subjects. Twenty-nine subjects had a PC20 histamine less than or equal to 16 mg/ml. Twenty, 15, and 10% falls in FEV1 were found in 10, 18, and 26 subjects, respectively, using hyperventilation of cold air. Significant eosinophilia and increased total IgE levels were seen in 5 and 18 subjects, respectively. Eight subjects had daily changes in PEFR greater than 20% on at least 1 day of monitoring. There was no significant association between specific responses to the respiratory questionnaire or the presence of rhinitis on the one hand and bronchial responsiveness to histamine and cold air on the other hand. The 10 subjects who demonstrated a greater than 20% change in FEV1 after cold air inhalation also had a PC20 less than 16 mg/ml, and 5 of them reacted at a concentration less than or equal to 2 mg/ml. Two subjects who had a PC20 less than or equal to 2 mg/ml demonstrated a less than 20% change in FEV1 after inhaling cold air. There was no association between the increase in total eosinophils or IgE and bronchial hyperresponsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Dissociation of temperature-gradient and evaporative heat loss during cold gas hyperventilation in cold-induced asthma.

We examined temperature-gradient and evaporative energy losses during cold gas inhalation challenges in patients with exercise-induced asthma by using gases with similar water-carrying capacities but significantly different volume heat capacities. Seven subjects were asked to hyperventilate mixtures of 80% helium/20% oxygen (HeO2) or 80% sulfur hexafluoride/20% oxygen (SF6O2) for 5 min at a fixed target minute ventilation of 20 x FEV1 and an inspired gas temperature of 0 degrees C. Each subject equilibrated his or her lungs with the appropriate gas mixture prior to testing: PETCO2 and FIO2 were monitored and maintained at constant values (CO2 = 0.05; O2 = 0.20) by CO2 scrubbing and addition of compressed gas to the system. Gas composition, inspired and expired flow rates, and gas temperatures at the airway opening were recorded in real time using a computer-based data collection system that calculated respiratory heat loss on a per breath basis. Bronchoconstriction was quantitated using specific airway conductance measured before and serially after each challenge. The degree of bronchoconstriction correlated closely with evaporative respiratory heat loss (r = 0.658 p less than 0.05), but poorly with both temperature-gradient (r = 0.114, p greater than 0.20) and total (r = 0.268, p greater than 0.15) heat loss. These findings suggest that total respiratory heat loss is not the primary stimulus in exercise-induced asthma, and further suggest that total water loss, or focal heat/water loss, may be important in inducing bronchospasm in this subset of asthmatics.

Adult↗
PubMed1992

Lack of bronchial hyperresponsiveness to methacholine and to isocapnic dry air hyperventilation in heart/lung and double-lung transplant recipients with normal lung histology. The Paris-Sud Lung Transplant Group.

To investigate whether survivors of heart/lung and double-lung transplantations have normal or increased nonspecific bronchial responsiveness, nine heart/lung and four double-lung transplant recipients with normal lung histology underwent methacholine challenge and voluntary isocapnic dry air hyperventilation (VIH) in a randomized order at a mean time of 14.8 +/- 12.1 months after surgery. Transplant recipients were compared with 10 normal subjects and 11 patients with mild asthma. Asthmatic patients had a mean provocative concentration of methacholine inducing a 20% fall (PC20) in FEV1 of 3.4 +/- 3.6 mg/ml (SD). Seventy seven percent of the transplant recipients and 70% of the normal subjects had PC20 superior to 32 mg/ml. The percentage fall from baseline FEV1 after VIH was 12.6 +/- 10.4% in asthmatic patients as compared with 1.9 +/- 2.9% in transplant recipients (p = 0.002) and 0.45 +/- 1.2% in normal subjects (p = 0.001). The decrease in FEV1 after VIH was similar in transplant recipients and normal subjects (p = 0.14). These results show that heart/lung or double-lung transplant recipients with normal lung histology have a normal response to nonspecific bronchial stimulation.

Adult↗
PubMed1992

Amelioration of sleep apnea by salicylate-induced hyperventilation.

It is well documented that upper airway (UAW) muscle activity is augmented in response to increased respiratory drive, the overall effect being an improvement in UAW patency. We have recently shown that salicylate-induced ventilatory stimulation increased UAW muscle electrical activity and decreased UAW resistance and collapsibility in anesthetized dogs. In the present study, we evaluated the effect of respiratory stimulation produced by high therapeutic doses of aspirin on sleep in nine patients with previously diagnosed sleep apnea. A control, all-night, polysomnographic sleep study, including oximetry and ventilatory monitoring by inductive plethysmography, was compared with a second study undertaken after patients ingested 8 to 10 g of aspirin over a period of 4 to 5 h. Aspirin ingestion resulted in high therapeutic salicylate serum levels (33 +/- 2.5 mg/dl, mean +/- SE) the following morning and was associated with marked ventilatory stimulation. Mean sleep duration and the relative partitioning of sleep stages were not affected by aspirin. However, aspirin-induced hyperventilation was associated with a significant non-rapid decrease in periodic breathing and the frequency of both obstructive and mixed apneas in all non-rapid eye movement (REM) sleep stages. The total number of apneas over the whole night was reduced in all subjects and on average fell from a control rate of 42 +/- 7 to 28 +/- 7 apneas/h (p less than 0.01). Similarly, the mean duration of apneas fell from 23 +/- 2 to 20 +/- 1 s (p less than 0.05), and the overall time spent in apneas decreased from 17 +/- 3 to 10 +/- 3 min/h (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗