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PubMed1991

Protective effects of befunolol on hypoxic respiration-induced alterations in myocardial energy metabolism of rats.

The present study was undertaken to elucidate beta-adrenoceptor blocking effects of befunolol (BFE 60, CAS 39543-79-8) on changes in the myocardial metabolites induced by hypoxic respiration. When rats were subjected to hypoxic respiration, a significant increase in heart rate (about 13% increase) and a slight decline in mean aortic blood pressure (about 12% decrease) were observed at 1 min and 6 min after the onset of hypoxic respiration. The hypoxic respiration also elicited decreases in the myocardial ATP and creatine phosphate levels (each 18% decrease) and increases in the myocardial lactate (13% increase) and cyclic-AMP (20% increase) levels. In contrast, these changes were never observed throughout hypoxic respiration when rats had been treated with both reserpine and alpha-methyl-p-tyrosine methylester 20 to 22 h before experiment, suggesting that these metabolic alterations are mediated through beta-adrenoceptor stimulation. These hypoxic respiration-induced hemodynamic and metabolic changes were found to be suppressed by treatment with 1 and 10 micrograms/kg befunolol or 10 micrograms/kg propranolol to an appreciable degree. The results demonstrate protective action of befunolol, like propranolol, on hypoxia-induced changes in the myocardial energy metabolism.

Adenosine Triphosphate↗
PubMed1991

Effects of ouabain and digitoxin on the respiration of chick embryo cardiomyocytes in culture.

The effect of digitoxin (CAS 71-63-6) and ouabain (g-strophantin, CAS 630-60-4) on respiration, morphology and beating activity of cardiomyocytes in culture derived from embryonic chick hearts has been investigated. The drugs were applied in a perfusion system using a protein- and substrate-free perfusion medium (BSS) at two concentration of K+ (5.4 and 4 mmol/l). In either K+ concentration oxygen consumption was 0.13 +/- 0.05 nmol O2 h-1 per 1000 cells. During 3 h of perfusion with BSS oxygen consumption declines only slightly to 79 +/- 15% of the initial value. No relation was found between beating frequency and oxygen consumption. Increase in respiration ranged from 5 to 45% and lasted between 5 and 120 min. At concentrations being inhibitory to the Na+/K(+)-ATPase (greater than or equal to 1 mumol/l) ouabain stimulated respiration by about 20% at 4 mmol/l K+ and 10% at 5.4 mmol/l K+ while digitoxin was effective at 5.4 mmol/l only (a transient increase of 20%). At 0.1 nmol/l, (a concentration below the KD of the high affinity binding site of the Na+/K(+)-ATPase) ouabain caused a long lasting activation of respiration by about 30%, digitoxin induced a transient rise of up to 20% at 5.4 mmol/l K+. At 4 mmol/l K+ digitoxin did not affect respiration while ouabain caused a transient increase. The lowest concentration of ouabain inducing a reproducible activation of oxygen consumption was 0.1 pmol/l. At this concentration digitoxin was no longer effective. At 1 fmol/l respiration was stimulated only occasionally.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The mechanism of stimulation of respiration by fatty acids in isolated hepatocytes.

Addition of fatty acids to isolated hepatocytes raised respiration rate by 92% and raised mitochondrial membrane potential (delta psi m) in situ from 155 to 162 mV suggesting that the increased fuel supply had a greater effect on respiration rate than any increases in processes that consumed mitochondrial protonmotive force (delta p). The relationship between delta psi m and respiration rate was changed by addition of fatty acids or lactate, showing that there was also stimulation of delta p-consuming reactions. In the presence of oligomycin the relationship between delta psi m and respiration rate was unaffected by substrate addition, showing that the kinetics of delta p consumption by the H+ leak across the mitochondrial inner membrane were unchanged. The stimulation of delta p consumers by fatty acids therefore must be in the pathways of ATP synthesis and turnover. Inhibition of several candidate ATP-consuming reactions had little effect on basal or fatty acid-stimulated respiration, and the nature of the ATP turnover reactions in hepatocytes remains speculative. We conclude that fatty acids (and other substrates) stimulate respiration in hepatocytes in two distinct ways. They provide substrate for the electron transport chain, raising delta p and increasing the non-ohmic proton leak across the mitochondrial inner membrane and the rate of oxygen consumption. They also directly stimulate an unidentified delta p-consuming reaction in the cytoplasm. They do not work by uncoupling or by stimulation of intramitochondrial ATP-turnover reactions.

Adenosine Triphosphate↗
PubMed1990

Cellular energetics and the oxygen dependence of respiration in cardiac myocytes isolated from adult rat.

The oxygen dependence of mitochondrial respiration was investigated using suspensions of mitochondria and quiescent ventricular myocytes isolated from adult rat hearts. A new optical method was used to determine oxygen concentration in the suspending media. The P50 for respiration for coupled mitochondria at a high [ATP]/[ADP].[Pi] ratio and oxidizing glutamate/malate was 0.45 +/- 0.03 microM but was increased to 0.57 +/- 0.02 microM by the addition of succinate to the substrate mixture. This value was decreased to less than 0.06 +/- 0.01 microM when the ATP/ADP.Pi ratio was decreased with the uncoupler, carbonyl cyanide p-trifluoromethoxyphenylhydrazone. The P50 value in resting myocytes was 2.23 +/- 0.13 microM at a Vmax of 13.22 +/- 1.38 nmol of O2/g, dry weight/min. During resting conditions, the creatine phosphate/creatine and ATPfree/ADPfree ratios were high in these cells, 6.81 +/- 1.11 and 1131 +/- 185, respectively. Addition of 1 mM Ca2+ to the suspending media increased the P50 by 50% whereas respiration rose by only 10%. Respiratory rate was increased up to about 10-fold by uncoupling the cells, but the P50 increased by less than 3-fold. When these uncoupled cells were inhibited with Amytal to lower the rate of oxygen consumption to that of resting cells, the P50 fell to 1.25 +/- 0.14 microM. Diffusion models indicate that in resting myocytes, the oxygen concentration difference from sarcolemma to cell core was approximately 1.84 microM with an additional difference of about 0.27 microM attributed to the unstirred layer of media surrounding each cell. The intracellular oxygen diffusivity coefficient in myocytes was calculated to be 0.30 x 10(-5) cm2/s. The results show that the oxygen dependence of respiration is modulated by the cellular metabolic state. At near maximal levels of respiration or on recovery from hypoxic episodes, oxygen diffusion may become an important determinant of the oxygen dependence of myocardial respiration.

Animals↗
PubMed1975

Glucagon stimulation of mitochondrial respiration.

Acute glucagon treatment of intact rats has been found to cause a stimulation of hepatic mitochondrial respiration as measured by monitoring oxygen uptake polarographically. Rates of State 3 respiration with several NAD-linked substrates and succinate were increased significantly after hormonal treatment and isolation of mitochondria. This stimulation cannot be ascribed to a partial uncoupling effect since State 4 respiration as measured by monitoring oxygen uptake polarographically. Rates of State 3 respiration with either slightly increased or unchanged. Furthermore, rates of uncoupled respiration with these substrates were also stimulated after hormonal treatment. On the other hand, respiratory rates (State 3, 4, and uncoupled) with ascorbate-N,N,N',N'-tetramethyl-p-phenylenediamine as substrate were unaffected by glucagon treatment. The hormonally stimulated rates of respiration produced a corresponding increase in the rate of generation of high energy state as indicated in measurements of Ca2+ uptake by isolated mitochondria. Rates of Ca2+ uptake were monitored by two methods: measurement of initial rates of proton ejection following CaCl2 additions and measurement of disappearance of Ca2+ from the suspension medium using murexide as indicator in a dual wavelength spectrophotometer. A significant stimulation in the initial rate of succinate-dependent Ca2+ uptake was noted after glucagon treatment of animals and isolation of hepatic mitochondria. No effect of the hormonal treatment was seen on the extent of Ca2+ uptake or the stoichiometry of H+ ejected per Ca2+ taken up. That the hormonal effect on Ca2+ transport is at the level of the substrate-induced generation of high energy state is indicated by the observation that no effect of glucagon treatment is seen on ATP-dependent Ca2+ uptake. Glucagon-induced changes in the activities of substrate-metabolizing enzymes are considered unlikely for the following reasons: (a) previously published data showed a lack of a hormonal effect on pyruvate-metabolizing enzymes and (b) data in this study showing no effect of glucagon treatment on the activity of NAD-malate dehydrogenase as measured in mitochondrial lysates. All of these observations are consistent with either an activation of mitochondrial substrate transport and/or a stimulation of mitochondrial electron transport by glucagon treatment. Regardless of the exact mechanism involved, the effect of the hormonal treatment is to produce an increase in ATP synthetic and ion-pumping capability during a period of increased energy demand, i.e. increased gluconeogenesis.

Adenosine Diphosphate↗
PubMed1987

Interactions between adenosine and alpha 1-adrenergic agonists in regulation of respiration in hamster brown adipocytes.

Respiration in brown adipocytes can be increased by beta-adrenergic receptor agonists or by alpha 1-adrenergic receptor agonists (phenylephrine and norepinephrine). Previous studies have shown that beta receptor-stimulated respiration is inhibited by adenosine and that enzymatic removal of adenosine produced by fat cells under normal incubation conditions enhances the respiratory response to beta receptor activation. The present experiments were performed to determine the effect of adenosine on the respiratory response elicited by agonists of alpha 1 receptors. The alpha-adrenergic agonists phenylephrine and norepinephrine (in the presence of the beta-adrenergic antagonist propranolol) stimulated respiration and the respiratory response to each agent was enhanced when endogenous adenosine was removed with adenosine deaminase. Addition of hydrolysis-resistant analogues of adenosine inhibited phenylephrine-stimulated respiration, and, since N6-phenylisopropyladenosine was more effective than was 5'-N-ethylcarboxamidoadenosine, we conclude that an A1 receptor is involved. In contrast, the P site agonist 2',5'-dideoxyadenosine did not inhibit phenylephrine-stimulated respiration but did cause some inhibition of isoproterenol-stimulated respiration. These results suggest that adenosine, acting via A1 receptors, modulates alpha 1-adrenergic effects on thermogenesis in brown fat cells, an action that is analogous to its inhibition of beta-adrenergic receptor-stimulated thermogenesis.

Adenosine↗
PubMed1987

Characteristics of farmers who have obtained personal dust respirators.

A postal survey was used to investigate the characteristics of farmers who have acquired dust respirators. In 1979 about a quarter of the farmers were using dust respirators, men more often than women. The more vocational training the farmer had and the larger the area of land under cultivation the more likely he was to own a dust respirator. Grain producers had purchased the protective devices more frequently than other farmers had. Farmers who participated in the occupational health intervention during 1980-82 had acquired dust respirators considerably more often than those in the control group. In the intervention group men under 30 years had most frequently purchased the dust respirators. Participation in the intervention influenced the acquisition of dust respirators more than did occurrence of symptoms of chronic bronchitis or farmer's lung.

Adult↗
PubMed1979

Effect of cephaloridine on respiration by renal cortical mitochondria.

The effects of the nephrotoxic antibiotic, cephaloridine, were studied in rabbit renal cortical mitochondria. Mitochondria from animals which received a toxic dose of 200 mg/kg of the drug 2 hr before sacrifice (in vivo exposure) had significantly decreased rates of respiration compared with those of mitochondria from untreated control animals. In vitro exposure of normal mitochondria to cephaloridine resulted in a qualitatively similar decrease of respiration. With both in vivo and in vitro exposure, inhibition was greatest with ADP-dependent respiration using succinate as substrate. The severity of in vitro inhibition of respiration showed some correlation to the degree of in situ cytotoxicity at different cephaloridine concentrations. The results are in agreement with the finding of a reduction of rates of respiration in renal tubule suspensions after similar in vivo and in vitro exposure to cephaloridine. These studies provide preliminary evidence that cephaloridine nephrotoxicity may be mediated through an inhibitory effect on mitochondrial respiration.

Adenosine Diphosphate↗
PubMed1983

[Functional coupling of creatine phosphokinase and adenylate kinase with adenine nucleotide translocase and its role in regulation of heart mitochondrial respiration].

The respiration of rabbit heart mitochondria in the presence of ATP is stimulated by ADP, AMP, creatine and glucose plus hexokinase. The values of V for mitochondrial phosphorylating respiration in the presence of corresponding stimulators are equal to 491 +/- 34, 460 +/- 12, 480 +/- 45 and 463 +/- 72 natoms O2 X min-1 X mg-1 of protein, 37 degrees C. The half-maximal stimulation of respiration is observed at 35 microM AMP, 60 microM ADP and 10 mM creatine in the absence of creatine phosphate. In the presence of creatine phosphate the maximal stimulation of heart mitochondrial respiration is achieved under a combined action of creatine and AMP. The inhibition type of mitochondrial respiration by palmitoyl-CoA depends on the nature of stimulators used. Thus, with ADP or glucose plus hexokinase the inhibition is competitive, while with AMP and creatine an uncompetitive and non-competitive inhibition was observed, respectively. The experimental results are indicative of functional coupling of heart mitochondrial adenylate kinase and creatine phosphokinase with ATP-ADP-translocase. It is assumed that creatine and AMP act as physiological regulators of heart mitochondrial respiration ("feed-back" signals from cytoplasm to mitochondria).

Adenylate Kinase↗
PubMed1983

The effect of CdCl2 on the respiration of rat small intestine mucosa.

Process of oxygen consumption of rat small intestine have already been studied at the level of whole intestinal wall or mucosa only by means of manometric or polarographic methods. The influence of cadmium on mucosal respiration of three sections of rat small intestine was determined because of its toxicological importance. Oxygen consumption was measured polarographically with Clark electrode at 38 degrees C in Krebs Ringer phosphate medium with 0.011 mol/l glucose. Control as well as cadmium affected respiration values were measured one after the other on the same mucosa. High cadmium concentration (applied as CdCl2) that is 2.2 and 1.4 . 10(-2) mol/l significantly inhibited the respiration in duodenum, jejunum and ileum. Observed inhibition of 80 and 50% on the average approximately for these two concentrations was related (similarly as following effects) to 100% value of control respiration. Concentrations 7.8 and 4.5. 10(-3) mol/l caused mostly lower inhibition of oxygen consumption (with the exception of significant 53% inhibition of jejunal respiration for 7.8. 10(-3) mol/l CdCl2). Low concentrations 10(-4) - 10(-6) mol/l CdCl2 had either no effect or stimulated oxygen uptake in intestinal mucosa. In older rats (weight 300-350 g) the respiration of duodenal and jejunal mucosa was inhibited with cadmium chloride concentration of 10(-6) mol/l.

Animals↗
PubMed1994

Stimulation of respiration in rat thymocytes induced by ionizing radiation.

The effect of X irradiation on the respiration of rat thymocytes was studied. An increase in the rate of O2 uptake was observed 1 h after cells were irradiated with doses of 6-10 Gy. The radiation-induced increase in respiration could be blocked by oligomycin, an inhibitor of mitochondrial ATP synthase, suggesting control by increased cytoplasmic ATP turnover. The stimulation of respiration was not associated with changes in the activity of mitochondrial electron transfer enzymes or permeability of the inner membrane. Several inhibitors of processes which used ATP were screened for their effects on the basal respiration rate and on the radiation response. In irradiated thymocytes, an enhancement of inhibition of respiration by ouabain, La3+ and cycloheximide was observed. These results indicate that the radiation-induced stimulation of respiration is due to changes in ion homeostasis and protein synthesis. The effect of X irradiation was shown to be independent of the redox status of nonprotein thiols and was not associated with detectable changes in some products of lipid peroxidation. The radiation-induced decrease in activity of superoxide dismutase suggests free radical involvement in deleterious effects of radiation.

Analysis of Variance↗
PubMed1993

[The effect of bovine serum albumin conjugates with polyalkylene oxides on the respiration of heart mitochondria].

The effect of polyalkylene oxides and pluronics (block copolymers of polyethylene oxide and polypropylene oxide) and their conjugates with bovine serum albumin (BSA) on respiration and oxidative phosphorylation in rat heart mitochondria has been studied. The pluronics and their conjugates with BSA stimulate state 4 respiration in mitochondria, inhibit state 3 respiration and 2,4-dinitrophenol-uncoupled state respiration, decrease the respiratory control, ADP/O ratio values and display weak uncoupling properties. The pluronics inhibit respiration and oxidative phosphorylation more effectively than their conjugates with BSA. The effect of the conjugate on the mitochondrial membrane is reversible, in contrast with that of the pluronics. The compounds under study act preferentially on the NADH-dehydrogenase complex of the respiratory chain. Inhibition of respiration in thymocytes by these compounds confirms their ability to penetrate into the cell membrane. The dependence of membranotropic properties of polyalkylene oxides and their conjugates with the protein on their structure is discussed.

Animals↗
PubMed1997

Nitric oxide inhibition of cytochrome oxidase and mitochondrial respiration: implications for inflammatory, neurodegenerative and ischaemic pathologies.

Nitric oxide (NO) at high levels is cytotoxic, and may be involved in a range of inflammatory, neurodegenerative, and cardiovascular/ischaemic pathologies. The mechanism of NO-induced cytotoxicity is unclear. Recently we and others have found that low (nanomolar) levels of NO reversibly inhibit mitochondrial respiration by binding to the oxygen binding site of cytochrome oxidase in competition with oxygen. This raises the apparent K(m) for oxygen of mitochondrial respiration into the physiological range, potentially making respiration sensitive to the oxygen level. The NO inhibition of oxygen consumption was seen in isolated cytochrome oxidase, mitochondria, brain nerve terminals, and cultured cells. Cultured astrocytes activated to express the inducible from of NO synthase produced up to 1 microM NO and strongly inhibited their own cellular respiration rate. This respiratory inhibition was rapidly reversed by removing the NO, and was due to the inhibition of cytochrome oxidase. These results suggest that any cell producing high levels of NO will inhibit its own respiration and that of surrounding cells, and make the respiration rate sensitive to the oxygen level. This inhibition of energy metabolism may contribute to cytotoxicity or cytostasis in some pathologies.

Animals↗
PubMed1998

Laboratory performance evaluation of N95 filtering facepiece respirators, 1996.

In 1995, CDC's National Institute for Occupational Safety and Health (NIOSH) introduced a new classification scheme for particulate air-purifying respirators. Most health-care workers use type N95 half-mask filtering facepiece respirators (i.e., N95 respirators) to prevent occupational transmission of tuberculosis. As a result, NIOSH received inquiries about how well N95 respirators fit, whether they need to be fit tested, and whether they can be quantitatively fit tested. In response to these inquiries, NIOSH evaluated the performance of 21 N95 respirator models on a 25-person panel. This report summarizes the results of this evaluation, which indicate that fit testing is needed to ensure at least the expected level of protection (i.e., the concentration of airborne contaminants inside the respirator is < or =10% of ambient levels).

Adult↗
PubMed1985

Coronary sinus blood flow determination by the thermodilution technique: influence of catheter position and respiration.

By measuring the coronary sinus blood flow using the thermodilution technique the influence of "thermodilution catheter" withdrawal from the great cardiac vein to the ostium of the coronary sinus was investigated in 41 patients. In addition, the influence of normal and forced respiration on coronary sinus blood flow was measured in 16 of the patients. Mean great cardiac vein flow was measured to 54 +/- 25 ml X min-1. Catheter withdrawal revealed coronary sinus blood flows of 80 +/- 32, 103 +/- 35, 145 +/- 39 and 213 +/- 61 ml X min-1 when the catheter was moved by steps of 1 cm towards the coronary sinus ostium. The coronary sinus blood flow changed between 116 +/- 34 ml X min-1 and 128 +/- 41 ml X min-1 on expiration or inspiration during normal respiration, respectively, when the catheter was placed in a mid-coronary sinus position. Forced respiration changed the coronary sinus blood flow from 98 +/- 41 ml X min-1 during expiration to 196 +/- 76 ml X min-1 during inspiration. The data show that coronary sinus blood flow changes from 23 to 68 ml X min-1 per cm catheter movement, the nearer the ostium the greater the change. Therefore comparison of coronary sinus blood flow between groups of patients would be a comparison between different catheter positions. Normal respiration moves, as judged by the coronary sinus blood flow, the thermodilution catheter by less than 0.5 cm while forced respiration moves the catheter up to 2 cm within the coronary sinus.

Adult↗
PubMed1977

Phrenic and vagal nerve activities during spontaneous respiration and positive-pressure ventilation.

Afferent vagal nerve activity from stretch-receptors in the lung and efferent phrenic nerve activity were recorded during spontaneous respiration and during positive-pressure ventilation with three different types of ventilators. During spontaneous respiration the efferent phrenic nerve activity slightly preceded the afferent vagal nerve activity. Volume-controlled ventilation did not alter the phrenic nerve activity when the ventilation was set at a rate equal to that during spontaneous respiration, but afferent vagal volleys increased in duration. At higher frequencies of insufflation spontaneous inspiration was inhibited. An increase in afferent vagal nerve activity and a concomitant slight decrease in efferent phrenic nerve activity were obtained during animal triggered pressure-controlled ventilation. High-frequency positive-pressure ventilation (HFPPV) gave rise to basal, non-grouped activity in vagal afferents, causing inhibition of inspiration. During HFPPV, spontaneous respiration can take place on activation of other afferents to the respiratory centre. Clinical aspects of respirator treatment from a neurophysiological standpoint are discussed.

Afferent Pathways↗
PubMed1992

Coordination of deglutition and phases of respiration: effect of aging, tachypnea, bolus volume, and chronic obstructive pulmonary disease.

The effects of aging, tachypnea, bolus volume, and chronic obstructive pulmonary disease on the coordination of swallowing with the phases of respiration were studied by concurrent respirography and submental surface electromyography. Study findings showed that in young healthy volunteers, during rest, there is preferential coupling of subconscious swallowing with the expiratory phase of continuous respiration. This preferential coupling of swallowing with expiration was found to increase relative to other phases of respiration during water swallows and tachypnea (P < 0.05). Respiratory phase occurrence of swallowing and postdeglutitive resumption of respiration during exacerbation of chronic obstructive pulmonary disease was found to be significantly different compared with the basal state (P < 0.05). Respiratory phase occurrence of subconscious swallowing in the elderly was found to be different from the young (P < 0.05). Position had no significant effect on the coordination of swallowing and phases of respiration. We concluded that in resting young volunteers the majority of deglutitions are coupled with the expiratory phase of swallowing. This coupling is increased in frequency by the presence of a liquid bolus and tachypnea. And finally, age and chronic obstructive pulmonary disease alter this coordination significantly.

Adult↗
PubMed1989

The effect of oxygen on respiration and sleep in patients with congestive heart failure.

STUDY OBJECTIVE: To determine the effect of supplemental oxygen on Cheyne-Stokes respiration, nocturnal oxygen saturation (SaO2), and sleep in male patients with severe, stable congestive heart failure. DESIGN: Randomized, single-blind, placebo-controlled crossover study. SETTING: Patients referred from outpatient cardiology clinics of two teaching hospitals. PATIENTS: Sequential sample of nine outpatients with severe, stable congestive heart failure. INTERVENTIONS: For each patient, sleep studies (after an adaptation night) from two consecutive randomized nights were compared; one study was done while the patient breathed compressed air and the other while the patient breathed oxygen (O2). Compressed air and oxygen were both administered through nasal cannulae at 2 to 3 L/min. MEASUREMENTS AND MAIN RESULTS: Cheyne-Stokes respiration, defined as periodic breathing with apnea or hypopnea, was found in all patients. Low-flow oxygen significantly reduced the duration of Cheyne-Stokes respiration (50.7% +/- 12.0% to 24.2% +/- 5.4% total sleep time), mainly during stage 1 NREM (non-rapid eye movement) sleep (21.3% +/- 7.1% to 6.7% +/- 2.3% total sleep time) with no significant change during stage 2 sleep, slow-wave sleep, or REM (rapid eye movement) sleep. Although patients had normal SaO2 (96.0% +/- 1.7%) while awake, severe sleep hypoxemia was common; breathing oxygen reduced the amount of time that SaO2 was less than 90% from 22.3% +/- 8.0% to 2.41% +/- 1.93% of total sleep time. Sleep, disrupted to a variable extent in all patients, improved with oxygen therapy: There was an increase in total sleep time from 275.3 min +/- 36.6 to 324.6 min +/- 23.3; a reduction in the proportion of stage 1 sleep (27.6% +/- 5.8% total sleep time to 15.2% +/- 2.6% total sleep time); and a reduction in the number of arousals (30.4/h +/- 8.0 to 13.8/h +/- 1.9). The apnea-hypopnea index was reduced from 30.0 +/- 4.7 to 18.9 +/- 2.4 with oxygen breathing. CONCLUSION: In severe, stable congestive heart failure, nocturnal oxygen therapy reduces Cheyne-Stokes respiration, corrects hypoxemia, and consolidates sleep by reducing arousals caused by the hyperpneic phase of Cheyne-Stokes respiration. Correction of nocturnal hypoxemia and sleep disruption may improve the clinical status of these patients.

Adult↗