Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “RESPIRATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,297 records · Page 72Linked to original sources
PubMed1977

[Respiration of the cells and isolated mitochondria of the rat liver in the early stages of hepatocarcinogenesis].

Under study was the respiration of mitochondria and cell aggregates (slices) of rat liver during the process of chemical carcinogenesis, induced by 3'-Me-DAB and AAP. The study of the hepatic mitochondria respiration indicated no impairment of the mitochondria functions investigated at early stages of carcinogenesis. The examination of hepatic slices respiration has demonstrated that during the process of chemical carcinogenesis the stimulation of endogenic respiration affected by DNP is decreased, whereas such effect is not observed while using succinate as a substrate. During the carcinogens metabolism compounds are assumed to be formed, those are able to affect oxidative phosphorylation without forming any stable link with the respiratory chain components. Which of the carcinogens metabolites may render similar effects is the question to be discussed.

2-Acetylaminofluorene↗
PubMed1983

[Polarographic study of cell respiration in a tissue culture].

A simple procedure for measuring the cells respiration without their transformation into the suspension, is suggested: seven glass slides with the cell culture of PKEV (pork, kidney, embryo, versen) are placed into the polarographic cell. Under these conditions the oxygen electrode easily records the fall of oxygen tension in the polarographic cell due to the respiration of 10(5) cells. Oxygen consumption is linear in time at the O2 concentration within the range from 480 to 200 nanoatoms per 1 ml of medium. The respiration rate is found to be enhanced by uncoupler and suppressed by the inhibitors of the electron flow chain (NaCN, antimycin A, amytal, rotenone) and mitochondrial ATPase (oligomycin and diciclohexylcarbodiimide). The above approach enables to evaluate the mitochondrial respiration of any cell monolayer keeping the cells intact.

2,4-Dinitrophenol↗
PubMedDate not supplied

[Relation between cyanide-resistant respiration, effectiveness and rate of growth of Candida valida on ethanol].

The object of this work was to study the correlation between the growth rate of Candida valida and its cyanide-resistant respiration, as well as to investigate the effect of cyanide-resistant oxidase on biomass yield in the course of continuous cultivation of the yeast. The inhibition of cellular respiration by cyanide was shown to be directly correlated with the biomass yield. The intensity of cyanide-resistant respiration depended on the growth rate of the culture, and was lowest at the highest growth rates. It has been concluded that, when cyanide-resistant oxidase appears in the yeast cells, it functions simultaneously with the main respiratory chain. Cyanide-resistant respiration can be inhibited under the optimal conditions of the culture growth.

Candida↗
PubMed1982

[Respiration activity of frozen-thawed lymphoid cells].

The respiration and oxidative phosphorylation rate of lymphocytes were studied after their cryopreservation. The oxygen uptake of cells frozen in the freezing medium containing 20% serum and 10% PEO-400 or DMSO is higher than that of the native lymphocytes. 2,4-DNP has not demonstrated any stimulating effect on the frozen-thawed cell respiration. Succinate has significantly stimulated the respiration of cells frozen with PEO-400 and produces a slight stimulating effect on the respiration of cells frozen with DMSO. It is concluded that the mitochondria and plasma membranes of cryopreserved lymphocytes undergo considerable changes.

Animals↗
PubMed1982

Comparison of respirator protection factors measured by two quantitative fit test methods.

A comparison of measured respirator protection factors for a di-2-ethylhexyl phthalate (liquid aerosol challenge) respirator quantitative fit test method is made with a complementary sodium chloride (solid aerosol challenge) method. The United States Army XM-29 chemical warfare defense respirator was used in this evaluation. A subject pool of twelve individuals (two female and ten male) were fitted and tested on both respirator quantitative fit test methods on ten different occasions. An exercise protocol of six different breathing and head movement maneuvers was used in each test. The purpose of the comparison was to determine if there is a difference between the two fit test methods. The di-2-ethylhexyl phthalate method showed a significant order-interaction effect with respect to the exercise sequence and whether it preceded or followed testing with sodium chloride. The sodium chloride method did not show a similar phenomenon, and consistently measured smaller protection factors compared to the di-2-ethylhexyl phthalate method. It appears that the sodium chloride method is more sensitive.

Chemical Warfare↗
PubMedDate not supplied

[Effect of acute hypoxic hypoxia on rat liver mitochondrial respiration].

Female rats have been maintained at simulated altitudes 8,000-9,000 for 15-60 min. Under the hypoxic conditions there was noted an increase in the respiratory activity of fresh nonwashed liver mitochondria, using endogenous substrates in the uncoupled state, as well as coupling of the endogenous respiration with phosphorylation. After 40 min storage of the mitochondrial preparations from hypoxic animals in an ice-bath, an increase in the endogenous respiration and decrease in its coupling with phosphorylation occurred but the values did not reach the control level. Many parameters of respiration were increased in mitochondria hypoxic rats in presence of succinate: respiratory activity in the active metabolic state/V3/ and in the state V4, the respiratory control ratio, the rate of ADP phosphorylation, the coupling of respiration with phosphorylation in the state V4. All the changes found were considered as adaptive.

Acute Disease↗
PubMed1995

[Participation of SH-groups in regulating oxidative phosphorylation by malate and palmitate-uncoupled respiration in liver mitochondria].

The effect of malate on respiration in liver mitochondria has been studied during oxidation of succinate in the presence of rotenone both in state 3 and after palmitate addition. Malate was shown to stimulate the rate of mitochondrial respiration in the both respiratory states, its effect being increased in the presence of the NAD-dependent substrates of oxidation-glutamate and pyruvate or thiols (cysteine and thiourea) Preincubation of mitochondria for 5 min in the absence of respiratory substrates eliminated the stimulating effect of malate. However, this effect was manifested in the conditions when the NAD-dependent respiratory substrates or thiols were added after preincubation of mitochondria. p-Chloromercuribenzoate eliminated the stimulating effect of malate. Carboxyatractyloside and ATP inhibited mitochondrial respiration in the presence of palmitate. Malate did not influence the action of the first effector but eliminated that of the second effector. It is concluded that malate can regulate oxidative phosphorylation and palmitate-uncoupled respiration by affecting the adenine nucleotide transported. The SH-groups localized outside the mitochondria in the hydrophilic region play an important role in the realization of malate effects.

Adenosine Triphosphate↗
PubMed1994

Generation of superoxide radicals as byproduct of cellular respiration.

Cell respiration is associated with the risk of formation of oxygen radicals. Although various conditions of respiration have been described under which O2-radicals are generated it is not clear whether oxygen radical generation is an inevitable side effect of respiration. The answer is necessarily linked to an understanding of the mechanism and molecular site of oxygen radical generation. Redox-cycling ubiquinones of the mitochondrial respiratory chain have often been suggested to account for cellular O2-radical formation. However, there is an increasing body of evidence which refutes this assumption on thermodynamic grounds. The discovery of a novel respiratory enzyme of heart mitochondria, exogenous NADH-dehydrogenase, some years ago, has considerably aided understanding of mitochondrial O2-radical generation and the role of ubiquinones therein. This mitochondrial enzyme can be directly activated by cytosolic NADH. It has been shown that NADH consumption via this enzyme not only stimulates electron flow along components of the respiratory chain but that its activity is also linked to the release O2-. or the single electron reduction of adequate non-physiological oxidants. Anthraquinones which are increasingly used as antitumor drugs can enter this redox-shuttle and initiate radical chain reactions which may be partially responsible for the selective cardiotoxicity of these compounds. Metabolic conditions, causing abnormally high NADH levels in the cytosol, such as ischemia have been found to irreversibly transform intact mitochondria to active radical generators. The present review elucidates the finding of a general phenomenon which gives more insight into the mechanism and the site of O2-radical formation during normal cell respiration.(ABSTRACT TRUNCATED AT 250 WORDS)

Free Radicals↗
PubMed1993

How much work is expended for respiration?

The rate of work expended to move air in the respiratory system has been determined for five different airflow waveshapes, a non-linear respiratory model and five exercise levels. As expected, the rectangular waveshape was the most efficient. Model conditions were then changed one a time: (i) starting lung volume was allowed to vary, (ii) exhalation flow limitation was added, (iii) respiration was considered to be a metabolic burden determining part of the ventilation requirement and (iv) a respirator mask was added. Although there is no direct work advantage to varying initial lung volume, such volume changes appear to be dictated by the asymmetry of lung recoil pressure about the lung relaxation volume; allowing the work of respiration to become a metabolic burden clearly shows why respiratory waveforms change from rest to exercise; and, adding a respirator imposes a severe respiratory burden on the wearer engaging in moderate, heavy and very heavy exercise.

Biomedical Engineering↗
PubMed1993

Respirable industrial fibres: pathology in animal models.

This paper discusses the general efficacy of the rat as a model for studying the pathogenicity of respirable fibres in humans. Rats show differences in lung structure from man and these could influence the pulmonary response to some degree, but they do develop interstitial fibrosis, carcinoma and mesothelioma when exposed to respirable fibres and these same types of lesions are found in fibre-exposed humans. Because of the importance of long fibres in causing pathological change, a substantial number of long respirable fibres must be used in inhalation studies if the relative pathogenicity of different fibre types is to be assessed. From data on the fibre burden in human disease and information on build-up of fibres in rat studies in a range of different fibres, a 1 year exposure to a cloud of 200 fibres ml-1 minimum, preferably more, is recommended. The rate of dissolution of the fibres within the lung milieu will be an an important factor in determining the pathogenicity. Many questions remain unanswered as to the mechanism of lung pathogenicity caused by respirable fibres particularly in the areas of durability, fibre shape, fibre surface chemistry and the exact mechanism, at the cellular level whereby fibres can cause pathological change. The use of rat inhalation studies, properly conceived and designed, remain a key approach whereby these questions can be answered.

Air Pollutants, Occupational↗
PubMed1993

Evidence that mitochondrial respiration is a source of potentially toxic oxygen free radicals in intact rabbit hearts subjected to ischemia and reflow.

Previous in vitro studies have shown that isolated mitochondria can generate oxygen radicals. However, whether a similar phenomenon can also occur in intact organs is unknown. In the present study, we tested the hypothesis that resumption of mitochondrial respiration upon reperfusion might be a mechanism of oxygen radical formation in postischemic hearts, and that treatment with inhibitors of mitochondrial respiration might prevent this phenomenon. Three groups of Langendorff-perfused rabbit hearts were subjected to 30 min of global ischemia at 37 degrees C, followed by reflow. Throughout ischemia and early reperfusion the hearts received, respectively: (a) 5 mM KCl (controls), (b) 5 mM sodium amobarbital (Amytal, which blocks mitochondrial respiration at Site I, at the level of NADH dehydrogenase), and (c) 5 mM potassium cyanide (to block mitochondrial respiration distally, at the level of cytochrome c oxidase). The hearts were then processed to directly evaluate oxygen radical generation by electron paramagnetic resonance spectroscopy, or to measure oxygen radical-induced membrane lipid peroxidation by malonyl dialdehyde (MDA) content of subcellular fractions. Severity of ischemia, as assessed by 31P-nuclear magnetic resonance measurements of cardiac ATP, phosphocreatine, and pH, was similar in all groups. Oxygen-centered free radical concentration averaged 3.84 +/- 0.54 microM in reperfused control hearts, and it was significantly reduced by Amytal treatment (1.98 +/- 0.26; p < 0.05), but not by KCN (2.58 +/- 0.96 microM; p = not significant (NS)), consistent with oxygen radicals being formed in the mitochondrial respiratory chain at Site I. Membrane lipid peroxidation of reperfused hearts was also reduced by treatment with Amytal, but not with KCN. MDA content of the mitochondrial fraction averaged 0.75 +/- 0.06 nM/mg protein in controls, 0.72 +/- 0.06 in KCN-treated hearts, and 0.54 +/- 0.05 in Amytal-treated hearts (p < 0.05 versus both groups). Similarly, MDA content of lysosomal membrane fraction was 0.64 +/- 0.09 nM/mg protein in controls, 0.79 +/- 0.15 in KCN-treated hearts, and 0.43 +/- 0.06 in Amytal-treated hearts (p < 0.05 versus both groups). Since the effects of Amytal are known to be reversible, in a second series of experiments we investigated whether transient mitochondrial inhibition during the initial 10 min of reperfusion was also associated with beneficial effects on subsequent recovery of cardiac function after wash-out of the drug. At the end of the experiment, recovery of left ventricular end-diastolic and of developed pressure was significantly greater in those hearts that had been treated with Amytal during ischemia and early reflow, as compared to untreated hearts.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1995

[The effect of p-chloromercuribenzoate on regulation of oxidative phosphorylation by ADP and ATP and stimulation of liver mitochondrial respiration by palmitate].

The effect of p-chloromercuribenzoate (pCMB) on oxidative phosphorylation and palmitate-stimulated respiration of liver mitochondria has been studied. pCMB (1 microM) does not affect oxidative phosphorylation but reduces the inhibiting effect of ATP on this process. Used at the same concentration, pCMB eliminates the inhibiting effect of ADP and ATP on mitochondrial respiration in the presence of 10 and 20 microM palmitate. pCMB has no effect on inhibition of oxidative phosphorylation by carboxyatractyloside or on palmitate-stimulated respiration of mitochondria. It is concluded that the SH-groups of mitochondria localized in the hydrophilic region outside the inner mitochondrial membrane participate in regulation of oxidative phosphorylation by ATP and in regulation of palmitate-stimulated respiration by ADP + ATP.

Adenosine Diphosphate↗
PubMedDate not supplied

[The correlation of liver mitochondrial respiration in mammals and reptiles at different temperatures].

In the experiments with isolated mitochondria in vitro (25 degrees C) it was shown that the respiration rate in mice was 3-5 times higher compared with agamas; in this case both animal species exhibited close body mass. At the comparison of mice and tortoises with the body mass 25-30 times exceeding the one of mice 4-10 times difference in mitochondrial respiration was found. In addition this difference was more pronounced with caprilate and pyruvate than with succinate used as substrates. High rates of respiration for mice mitochondria are shown to persist at wide temperature range in vitro. However respiration parameters for mice and agamas are close in vitro at the temperature of 37 degrees C for mice mitochondria (the optimal mouse body temperature is about 37 degrees C) and the temperature of 42 degrees C for agama mitochondria (the optimal life temperature for agamas is about 42 degrees C).

Animals↗
PubMed1995

Potential for respirable quartz exposure from North Carolina farm soils.

Sandy-loam soils from six active farms in the coastal plains of North Carolina (USA) were analyzed for aerodynamic equivalent diameter and quartz content and compared with results to similar analyses of clay soils of the Piedmont and sandy soils from the sand hills of North Carolina to see whether respirable quartz content varies with soil type. The respirable fraction of sandy loam-soils averaged 0.04 (SD 0.02) versus 0.13 (SD 0.03) for clay soils and 0.04 (SD 0.03) for sandy soils. Quartz content in the 4.25 mu m fraction of sandy-loam soils averaged 15.2 (SD 4.1) % versus 2.2 (SD 0.8) % in clay soils and 29.0 (SD 11.1) % in sandy soils. The mass of respirable quartz in sandy-loam soils averaged 0.7 (SD 0.4)% versus 0.3 (SD 0.1)% in clay soils and 1.0 (SD 0.4) % in sandy soils. These results suggest that, during dusty farm activities, there is a potential for greater respirable quartz exposures associated with work with sandy or sandy-loam soils than from work with clay soils.

Agriculture↗
PubMedDate not supplied

[Detection of cyanide resistant respiration among Candida lipolytics yeasts].

Conditions causing cyanide-resistant respiration were studied in the yeast Candida lipolytica. This type of respiration was found when the culture growing on glucose, glycerol, hexadecane, or acetate exhuasted the substrate and passed from the logarithmic to stationary growth phase; the same phenomenon can be induced by exhaustion of phosphorus or nitrogen in the glucose medium. The yeast culture growing on lactate, ethanol, pyruvate, alpha-ketoglutarate, malate, or succinate is characterized by cyanide-resistant respiration even at the beginning of the logarithmic growth phase. The values of pH in the incubation medium have no effect on the time of manifestation of cyanide-resistant respiration.

Candida↗
PubMed1989

Effects of respiration and vasodilation on venous volume in animals and man, as measured with an impedance catheter.

Venous return determines cardiac preload and is in turn affected by respiration and vasodilation. The purpose of the present study was to examine the dynamics of venous return and venous volume, using impedance volume measurements in the venous system. In order to develop a methodology for the assessment of venous volume and venous return in man, we first studied 17 endotracheally intubated and ventilated anesthetized closed-chest dogs. We measured central venous and inferior vena cava (IVC) pressure (micromanometer) and volume (impedance catheter). Studies were done above and below the diaphragm with normal ventilation, with positive end-expiratory pressure (PEEP), and with beta-adrenergic blockade and i.v. nitroglycerin. Intrathoracic IVC volume fell and extrathoracic IVC volume rose with lung inflation, while PEEP raised extrathoracic IVC volume and lowered intrathoracic IVC volume. Nitroglycerin lowered intrathoracic IVC volume. Beta blockade did not affect IVC volume, ventilatory variation, or response to PEEP and nitroglycerin. We performed similar studies in 14 human subjects during normal quiet respiration, with measurements above and below the diaphragm, and with interventions including Valsalva maneuver and i.v. nitroglycerin. Intrathoracic IVC volume fell and extrathoracic IVC volume rose with expiration and Valsalva maneuver. Nitroglycerin again lowered intrathoracic IVC volume. We conclude that venous volume and the dynamics of venous return can be assessed in animals and man with an impedance catheter. Specifically, we show the divergent effects of respiration, ventilation, PEEP, and nitroglycerin on IVC volumes above and below the diaphragm. Beta-adrenergic blockage does not appear to play a role in altering any of these effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed2002

Effects of prolonged mechanical ventilation on respiratory muscle ultrastructure and mitochondrial respiration in rabbits.

OBJECTIVE: To investigate in rabbits whether prolonged mechanical ventilation (PMV) leads to ultrastructural changes in respiratory muscles and alters diaphragm mitochondrial respiration. DESIGN AND SETTING: Experimental prospective study in a university laboratory. ANIMALS AND INTERVENTIONS: We studied respiratory muscles of seven rabbits after 49+/-1 h of controlled mechanical ventilation. Ten nonventilated rabbits were used as a control group. MEASUREMENTS AND RESULTS: After mechanical ventilation electron-microscopic observations of the diaphragm and the external intercostal muscles revealed disrupted myofibrils, increased number of lipid vacuoles in the sarcoplasm, and smaller mitochondria with focal membrane disruptions. Volumetric and numerical densities of the mitochondria were significantly lower in the PMV group than the control group. Mitochondrial respiration was quantified in isolated diaphragm muscle-cell mitochondria using two respiratory substrates. There was no difference in oxygen consumption values in the three states of mitochondrial respiration between the two groups except for state 2 (basal state) with pyruvate/malate parameter (53.5+/-20 for the ventilated group vs. 33.8+/-10.2 nmol atom O/mg per minute for the control group). There was no significant difference between groups in ADP/O ratio or respiratory control ratio. CONCLUSIONS: PMV leads to respiratory muscle cell degeneration and minor changes in oxidative phosphorylation coupling in diaphragmatic mitochondria. These phenomena may mediate part of damage of respiratory muscles after inactivity related to PMV.

Animals↗
PubMed2004

[Cardiac efficiency in patients with Cheyne-Stokes respiration as a result of heart insufficiency during long-term nasal respiratory treatment with adaptive servo ventilation (AutoSet CS)].

Cheyne-Stokes respiration (CSR) is known to be an important negative predictor of outcome in patients with congestive heart failure. The goal of this study was to investigate whether the use of adaptive servo ventilation (AutoSet CS) would permit sufficient suppression of this pathological breathing pattern and improve cardiac function in longterm use over 1 year. Inclusion criteria for the study were congestive heart failure (left ventricular ejection fraction 20-50%), proven CSR with a central apnea-hypopnea index (AHI) > 15/h and stable clinical status with standard medical therapy. Patients with obstructive sleep apnea and COPD were excluded. Twenty consecutive patients (16 male) age 65.5 years (range 48-77) were followed with full blood counts, blood gas analysis, lung function tests and questionnaires for cardiopulmonary capacities (Minnesota, MRC Scale) and sleepiness (Epworth Sleepiness Scale). In addition, we performed 6-min walk distance (6MWD), echocardiography and polysomnography just before and after adjusting to adaptive servo ventilation and 3 and 12 months later. Mean usage of adaptive servo ventilation was sufficient (4.3 +/- 2.1 h/day at 12 months). No significant changes in blood gas analysis, blood counts and pulmonary function were detectable. CSR disappeared almost completely in all patients (AHI pre-study 44.3 +/- 13.4/h vs 3.4 +/- 8.0/h at 12 months; p < 0.0001). Saturation normalized steadily over the course of the study. The desaturation index decreased from 45.3 +/- 17.8/h to 5.2 +/- 11.5/h at 12 months (p < 0.0001). Mean saturation increased with the first night of sleep with adaptive servo ventilation from 92.0 +/- 2.5% to 93.0 +/- 1.6% (p < 0.05) and then to 94.1 +/- 1.9% at 3, and 94.2 +/- 1.9% at 12 months (p < 0.001). Quality of sleep was significantly improved with an increase of slow-wave sleep from 4.5 +/- 4.6% to 13.7 +/- 6.9% at 12 months (p < 0.0001). The arousal index concomitantly decreased from 29.8 +/- 17.9/h pre-study to 12.0 +/- 10.3/h at 12 months (p < 0.01). REM-sleep and sleep efficiency remained unchanged. The Epworth Sleepiness Scale showed only a trend to improvement. Cardiac function improved significantly during the course of the study. The ejection fraction increased from mean 37.1 +/- 12.5% pre-study to 41.7 +/- 8.8% at 12 months (p < 0.05). The 6-min walk distance increased from 192 +/- 110 m to 277 +/- 130 m at 12 months (p < 0.01). The MRC and Minnesota score were not significantly different pre- and post-study. We conclude that long-term respirator therapy with adaptive servo ventilation has sufficiently suppressed CSR and improved cardiac function in patients with congestive heart failure. Thus, safety and feasibility of this respirator therapy could be demonstrated. However, due to methodological reasons (no control group, no randomization) a direct effect on cardiac function could not be confirmed.

Aged↗