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 577 records · Page 32Linked to original sources
PubMedDate not supplied

Respiration-related movements of the nose in dogs.

We studied the respiration-related movements of the canine nose by examining the respiratory oscillations of intranasal balloon pressure and EMG activities of the dilator nares in dogs. Under spontaneous respiration, balloon pressure decreased and EMG activities increased during the early inspiratory phase. These respiratory movements of the nose differed and changed reciprocally in strength between the two sides of the body spontaneously, after painful stimulation or intranasal histamine administration. When the muscle relaxant was administered and the respiration was controlled by the ventilation pump, the intranasal balloon pressure increased during the inspiratory phase. This phenomenon had a completely inverted pattern compared with that during spontaneous respiration. Furthermore, even when the ventilation pump was stopped, respiration-like spontaneous oscillations of the intranasal balloon pressure were recognized. These were abolished by sectioning of the ipsilateral cervical sympathetic nerve trunk. From these findings, the respiration-related movements of the nose were thought to be controlled not only by the cardiac output and the vagal nerve reflexes but also by respiratory activities in the nervous systems controlling the nose, which might be originated from the medullary respiratory centres.

Animals↗
PubMed1983

Electrophrenic respiration following anastomosis of phrenic with branchial nerve in the cat.

Patients with high spinal cord injuries may be totally dependent on artificial ventilation. Prolonged use of mechanical devices requires intensive care, which restricts the mobility of these patients. Electrophrenic respiration has been used with success to overcome this difficulty. However, a prerequisite for electrophrenic respiration is a viable phrenic nerve. Patients with spinal cord injuries at the C-3 to C-5 levels do not have a viable phrenic nerve due to gradual degeneration of axons in these nerves. In the present study on cats, the authors caused degeneration in one of the phrenic nerves by sectioning it low in the neck. Then the distal end of the phrenic nerve was anastomosed to the proximal segment of a sectioned brachial nerve. Sixteen to 32 weeks were allowed for the growth of brachial axons into the anastomosed phrenic nerve. Each cat served as its own control because one of the phrenic nerves was left intact. It was observed that pacing of the anastomosed phrenic nerve produced respiration comparable to spontaneous respiration or to respiration induced by pacing the intact phrenic nerve. Lack of rhythmic bursts of electrical activity in the anastomosed phrenic nerve and electromyographic activity in the ipsilateral hemidiaphragm confirmed that the anastomosed phrenic nerve remained disconnected from the respiratory motoneurons. Abundance of collagen matrix in the electron micrographs of the anastomosed phrenic nerve indicated that degeneration of the axons of phrenic motoneurons had occurred and the brachial nerve had grown into the phrenic nerve stump. These results indicate that electrophrenic respiration may be possible in patients with spinal cord injuries at the C-3 to C-5 vertebral levels if the phrenic nerve is kept viable by anastomosing it to a branch of the brachial nerve.

Animals↗
PubMed2000

[Regular respiration during sleep in children in the first months of life].

Regular respiration is an important parameter of quiet sleep in infants. At the earliest age, the periods of regular respiration are shorter as compared with the periods of EEG, EMG and EOG patterns of quiet sleep. The duration of periods with regular respiration significantly increases with age, and their coincidence with other parameters of quiet sleep becomes higher. The frequency of regular respiration significantly decreases with age. Very short periods of regular respiration, low coincidence with other parameters of quiet sleep, and very high frequency of regular respiration after the 12th week of life may indicate a delay in the central nervous system development.

Aging↗
PubMedDate not supplied

[Criteria for adequate respiratory support during transfer of patients to spontaneous respiration].

Time course of circulation, oxygen transport and consumption parameters were studied in patients with parenchymatous pulmonary diseases during their transfer to spontaneous respiration under conditions of pressure support ventilation after long forced ventilation of the lungs. The oxygen cost of respiration can serve as a reliable criterion of respiratory support adequacy when the use of a respirator is discontinued. With oxygen cost of respiration at least 14%, a decrease of respiratory support is hardly possible without decompensation of the respiration system and circulation, which dictates monitoring of this parameter during transfer of patients to spontaneous respiration.

Adult↗
PubMed1975

Participation of the Breuer-Hering inflation reflex in regulation of respiration frequency in anaesthetized rats.

The respiration frequency and Breuer-Hering inflation reflex (BHIR) values were compared in anaesthetized rats after unilateral vagotomy. Nos significant differences were found in the decrease in respiration frequency after transection of the right of left vagus and there were no differences in BHIR values in correlation to conduction by the right or left vagus. With unilateral vagotomy and an inflation pressure of 20 cm H20 the BHIR values fell to about one fourth of the control values. Progressive cooling of the contralateral vagus led at 8-10 degrees C to a non-significant decrease in respiration frequency to 87% of the initial value; in this state the BHIR could not be elicited. Further cooling of the vagus to 0 degrees C reduced respiration frequency to the same values as in bilateral vagotomy. The discrepancy between the mild decrease in respiration frequency and simultaneous disappearance of the BHIR shows that changes in respiration frequency in anaesthetized rats are not directly correlated to the presence of the BHIR.

Anesthesia↗
PubMed1988

Automatic assessment of the interaction between respiration and heart rate variability signal.

The present paper introduces an original method of processing heart rate variability (HRV) and respiration signals as detected respectively through chest electrodes and thoracic belt in dogs under different experimental conditions. Signals are processed as time series synchronous with the occurrence of QRS complexes on ECG signal and auto and cross spectra are accordingly calculated. Two particular bands appear mainly of interest on the spectrum of HRV signal: one in correspondence with the respiration rate and another one at a lower frequency value. Values of power at these frequency bands together with coherence and phase between HRV signal and respiration complete the parameters which try to quantify a few aspects of the complex dynamic relationships between the original signals. In particular, controlled respiration in dogs was studied through the connection with an automatic ventilator, as well as the effects of drugs which interact with the neural regulatory systems (i.e. sympathetic and parasympathetic nervous system). Gain and phase relationships between heart rate variability and respiration, obtained with spectral analysis, could be used to provide a better understanding of the neural control mechanisms linking heart rate and respiration in various experimental conditions. The method described in this study is to be used both in physiological and clinical research.

Animals↗
PubMedDate not supplied

[Effect of cations of transition metals on respiration and H+ production in liver mitochondria].

Results obtained prove that respiration stimulation of mitochondria Ca2+, Sr2+, Mn2+ is determined by transport of these cations to the indicated subcellular structures with participation of Ca2(+)-uniporter. Effect of Cd2+ on respiration of mitochondria is of two-phase character. Concentration of Cd2+ being above 100 microM the stimulation phase is accompanied by the further inhibition of mitochondria respiration. La3+ inhibits respiration of mitochondria. However La3+ and Cd2+ stimulate H+ production by mitochondria, that is not blocked by ruthenium red (10 microM). Probably, the effect of La3+ and Cd2+ on respiration of mitochondria is determined by the change of proton conductivity of mitochondrion membrane. Direct inhibiting effect of Cd2+ on the respiration chain of mitochondria has been established.

Animals↗
PubMed1993

Inhibition of tumor cell mitochondrial respiration by macrophage cytotoxic mediators distinct from interferon-gamma.

Macrophage-mediated inhibition of mitochondrial respiration in EMT-6 murine mammary adenocarcinoma cells can be mimicked in vitro by treatment of the cells with interferon-gamma (IFN-gamma) in combination with tumor necrosis factor, interleukin-1, or lipopolysaccharide. Conditioned supernatants obtained from activated macrophages appear to contain interferon-gamma, suggesting that inhibition of mitochondrial respiration in tumor cells was caused by synergy of IFN-gamma with other cytokines. To further characterize monokines that cause inhibition of mitochondrial respiration in tumor cells, EA13.5 macrophage-like cells were isolated and selected for inhibition of mitochondrial respiration in EMT-6 tumor cells. After stimulation with IFN-gamma and lipopolysaccharide, the EA13.5 cells released into conditioned supernatants a cytotoxic mediator that induced nitric oxide synthesis and caused lesions in the electron transport chain of EMT-6 cells similar to the lesions caused by activated peritoneal macrophages. Enzyme-linked immunosorbent assay demonstrated that the conditioned supernatants produced by EA13.5 macrophage cells did not contain IFN-gamma. Treatment of the EA13.5 cell-conditioned supernatants with neutralizing antibody against IFN-gamma did not abrogate the inhibition of mitochondrial respiration in EMT-6 cells caused by these conditioned supernatants. This study demonstrated that unidentified macrophage cytotoxic mediators distinct from IFN-gamma are involved in the induction of nitric oxide synthesis and inhibition of mitochondrial respiration in tumor cells.

Adenocarcinoma↗
PubMed1983

Regional cell count and respiration in the brain of Rana catesbeiana.

Cell counts were made in three divisions of the bullfrog brain: (1) olfactory lobestelencephalon, (2) diencephalon-mesencephalon, and (3) the hindbrain; average cellular respiration in potassium-enriched Ringer solution and the rate of respiration in sodium-free medium were tested for their possible relationship to the numbers of glia and numbers of neurons in each region. After restoring some of the sodium ions to sodium-free minces, the percent increase in respiration was plotted for each brain segment and compared to the percent of glia per brain division to determine the glial respiratory contribution. Where glial numbers were greater, the potassium-stimulated respiration was greater; where neuronal numbers were greater, the sodium-free respiration was most prominent. The respiration increased most above the sodium-free rate, when sodium ions were added or when the full amount of sodium was present, in the hindbrain, where the glia appear to metabolize more vigorously and the neurons least actively.

Animals↗
PubMed1997

Diverse cytoprotectants prevent cell lysis and promote recovery of respiration and ion transport.

Numerous agents have been reported to prevent cell lysis. However, little information is available concerning the ability of cytoprotectants to promote the return of physiological functions. The goal of this study was to determine whether a diverse group of cytoprotectants prevent cell lysis and promote the recovery of respiration and ion transport following anoxia (60 min)/reoxygenation (60 min) in rabbit renal proximal tubule (RPT) suspensions. Cell lysis (LDH release) was determined immediately following the anoxic and reoxygenation periods. Mitochondrial function (basal respiration) and active Na+ transport (ouabain-sensitive respiration) was determined after the reoxygenation period. LDH release increased to 75 +/- 11% after the anoxic period and did not increase further during the reoxygenation period. LDH release in controls was 6 +/- 1% and did not vary over time. Glycine (2 mM), strychnine (1 mM), nifedipine (100 microM) and niflumic acid (100 microM) added immediately prior to the anoxic period completely blocked LDH release. All cytoprotectants increased basal respiration from 39 +/- 7% of controls in the anoxic samples to 65-77% of controls. Glycine, strychnine and nifedipine increased ouabain-sensitive respiration from 10 +/- 3% of controls in anoxic samples to 51-77% of control. Niflumic acid did not increase ouabain-sensitive respiration. These results demonstrate that glycine, strychnine and nifedipine are "true' cytoprotectants preventing both cell lysis and promoting the recovery of mitochondrial function and ion transport after an anoxic insult.

Animals↗
PubMed2000

Abnormal mitochondrial respiration in failed human myocardium.

Chronic heart failure (HF) is associated with morphologic abnormalities of cardiac mitochondria including hyperplasia, reduced organelle size and compromised structural integrity. In this study, we examined whether functional abnormalities of mitochondrial respiration are also present in myocardium of patients with advanced HF. Mitochondrial respiration was examined using a Clark electrode in an oxygraph cell containing saponin-skinned muscle bundles obtained from myocardium of failed explanted human hearts due to ischemic (ICM, n=9) or idiopathic dilated (IDC, n=9) cardiomyopathy. Myocardial specimens from five normal donor hearts served as controls (CON). Basal respiratory rate, respiratory rate after addition of the substrates glutamate and malate (V(SUB)), state 3 respiration (after addition of ADP, V(ADP)) and respiration after the addition of atractyloside (V(AT)) were measured in scar-free muscle bundles obtained from the subendocardial (ENDO) and subepicardial (EPI) thirds of the left ventricular (LV) free wall, interventricular septum and right ventricular (RV) free wall. There were no differences in basal and substrate-supported respiration between CON and HF regardless of etiology. V(ADP)was significantly depressed both in ICM and IDC compared to CON in all the regions studied. The respiratory control ratio, V(ADP)/V(AT), was also significantly decreased in HF compared to CON. In both ICM and IDC, V(ADP)was significantly lower in ENDO compared to EPI. The results indicate that mitochondrial respiration is abnormal in the failing human heart. The findings support the concept of low myocardial energy production in HF via oxidative phosphorylation, an abnormality with a potentially impact on global cardiac performance.

Adult↗
PubMed1992

An Escherichia coli mutant containing only demethylmenaquinone, but no menaquinone: effects on fumarate, dimethylsulfoxide, trimethylamine N-oxide and nitrate respiration.

The mutant strain AN70 (ubiE) of Escherichia coli which is known to lack ubiquinone (Young IG et al. 1971), was analyzed for menaquinone (MK) and demethylmenaquinone (DMK) contents. In contrast to the wild-type, strain AN70 contained only DMK, but no MK. The mutant strain was able to grow with fumarate, trimethylamine N-oxide (TMAO) and dimethylsulfoxide (DMSO), but not with nitrate as electron acceptor. The membranes catalyzed anaerobic respiration with fumarate and TMAO at 69 and 74% of wild-type rates. DMSO respiration was reduced to 38% of wild-type activities and nitrate respiration was missing (less than or equal to 8% of wild-type), although the respective enzymes were present in wild-type rates. The results complement earlier findings which demonstrated a role for DMK only in TMAO respiration (Wissenbach et al. 1990). It is concluded, that DMK (in addition to MK) can serve as a redox mediator in fumarate, TMAO and to some extent in DMSO respiration, but not in nitrate respiration. In strain AN70 (ubiE) the lack of ubiquinone (Q) is due to a defect in a specific methylation step of Q biosynthesis. Synthesis of MK from DMK appears to depend on the same gene (ubiE).

Anaerobiosis↗
PubMed1987

Brain cellular and mitochondrial respiration in media of altered pH.

This study was designed to investigate the effects of altered pH on cellular aerobic energy metabolism in the immature and adult rat cerebral cortex. Cerebral cortical slice respiration was measured polarographically in acid and alkaline media. In separate experiments, the extracellular pH was changed by altering the HCO3- concentration or the intracellular pH and extracellular pH were changed by altering the CO2. Respiratory rates and oxidative phosphorylation in adult rat cerebral mitochondria also were measured in media with an altered pH. Increased intracellular pH inhibited respiratory rates in cortical slices from immature rats more than in tissue from adults. Decreasing the pH to 6.7 produced no changes in respiration in mature cortical slices and moderate inhibition of immature tissue respiration. In cerebral mitochondria, altered pH caused inhibition of State 3 respiration, respiratory control ratios, and ADP/O ratios. These changes were greater and occurred with smaller pH changes in the alkaline compared to the acid direction. From the results of these studies, we conclude that brain cellular respiration is not affected by moderate decreases in intracellular pH. With increased pH, there is inhibition of cellular and mitochondrial respiration, which may be the mechanism for the rise in lactic acid previously observed to result from hypocarbia in vivo.

Aging↗
PubMed1996

Vitality fertilization of Scots pine stands growing along a gradient of heavy metal pollution: short-term effects on microbial biomass and respiration rate of the humus layer.

In 1992 forest vitality fertilization experiments were established on a heavy metal deposition gradient with four treatments in three replications at distances of 0.5, 4 and 8 km from a Cu-Ni smelter in order to estimate their impact on the disturbed forest ecosystem. The increase in Cu concentration in the humus (F/H) layer of the Calluna site type Scots pine (Pinus sylvestris) stands from ca. 300 to 8000 mg kg(-1) d.m. (dry matter) along the 8 km long transect towards the smelter resulted in declining soil microbial biomass and soil respiration activity. Three independent measurements of microbial biomass: C(mic)-FE (fumigation extraction), C(mic)-SIR (substrate induced respiration), and ATP have been used together with an indicator of fungal biomass (ergosterol) and microbial activity (soil respiration). Within this Cu pollution range, all the measured microbial biomass levels declined to 10%-28% of the control plot values and activity assessed by respiration was lowered to 16%. Liming has increased the C(mic)-SIR and respiration rate. Treatments with test fertilizer, made from grounded apatite, did not result in different microbial biomass and respiration rate values compared to the respective controls along the whole gradient. Nitrogen + lime treatments resulted in similar changes to lime alone. No changes, as compared to the respective control, could be detected with nitrogen fertilization at the less polluted end of the gradient.

Journal Article↗
PubMed2001

The impact of the thermal sensitivity of cytochrome c oxidase on the respiration rate of Arctic charr red muscle mitochondria. pierre_blier@uqar.qc.ca.

To assess if cytochrome c oxidase could determine the response of mitochondrial respiration to changes in environmental temperature in ectotherms, we performed KCN titration of the respiration rate and cytochrome c oxidase activity in mitochondria from Arctic charr (Salvelinusfontinalis) muscle at four different temperatures (1 degrees C, 6 degrees C, 12 degrees C, and 18 degrees C). Our data showed an excess of cytochrome c oxidase activity over the mitochondrial state 3 respiration rate. Mitochondrial oxygen consumption rates reached approximately 12% of the cytochrome c oxidase maximal capacity at every temperature. Also, following titration, the mitochondrial respiration rate significantly decreased when KCN reached concentrations that inhibit almost 90% of the cytochrome c oxidase activity. This strongly supports the idea that the thermal sensitivity of the maximal mitochondrial respiration rate cannot be dictated by the effect of temperature on cytochrome c oxidase catalytic capacity. Furthermore, the strong similarity of the Q10s of mitochondrial respiration and cytochrome c oxidase activity suggests a functional or structural link between the two. The functional link could be coevolution of parts of the mitochondrial system to maintain optimal functions in most of the temperature range encountered by organisms.

Animals↗
PubMed1991

A possible mechanism of mitochondrial dysfunction during cerebral ischemia: inhibition of mitochondrial respiration activity by arachidonic acid.

The dramatic increase in the arachidonic acid (AA) level in the brain is a well-known molecular event during cerebral ischemia. As mitochondria are known to be one possible site of the cell damage, the effects of AA on the respiratory activity of rat brain mitochondria were investigated in vitro using an oxygen electrode. In NAD-linked respiration, respiratory control ratio was decreased significantly by AA, with an IC50 of 6.0 microM. AA had the dual effect on mitochondrial respiration, a decrease in state 3 and uncoupled state and an increase in state 4 (i.e., uncoupling) as reported by Hillered and Chan (J. Neurosci. Res. 19, 94-100, 1988). Furthermore, we found that other unsaturated long-chain free fatty acids (C18:1-C18:3, C20:1-C20:5) also showed such a dual effect. Cyclooxygenase metabolites of AA such as prostaglandins (D2, E2, F2 alpha, E1) and thromboxane B2, and lipoxygenase metabolites such as leukotrienes (D4, B4) and 5- or 12-hydroperoxyeicosatetraenoic acid had no significant effect. The inhibition of the uncoupled state by AA was more marked in NAD-linked than that in FAD-linked respiration, while the degree of uncoupling by AA were the same in both respirations. In spectrophotometrical measurement, the reduction of cytochromes and flavo-protein was markedly inhibited by AA in NAD-linked respiration, but not in the FAD-linked one. In addition, the activity of cytochrome c oxidase was scarcely inhibited by AA. These data suggest that AA itself, not its metabolites, may inhibit mitochondrial ATP production during brain ischemia and that AA may act on the site(s) closely related to NAD-linked respiration, but not the FAD-linked one, in addition to its uncoupling effect.

Animals↗
PubMed1975

Energy-dependent accumulation of iron by isolated rat liver mitochondria. V. Effect of factors controlling respiration and oxidative phosphorylation.

1. Depending on the metabolic state, the addition of iron(III)-sucrose induces an inhibition or a stimulation of the respiration rate when added to isolated rat liver mitochondria. 2. Under conditions identical to those used in the accumulation studies (Romslo, I. and Flatmark T. (1973) Biochim. Biophys. Acta 305, 29-40), the ferric complex induces a decrease in the oxygen uptake concomitant to an oxidation of cytochromes c (+c1) and a(+a3). These results suggest that ferric iron is reduced to ferrous iron by the respiratory chain prior to or simultaneously with its energy-dependent accumulation. 3. On the other hand, the addition of iron(III)-sucrose induces a stimulation of respiration in State 4 and State 3 provided Mg-2+ is present in the suspending medium. In contrast to Ca-2+, iron stimulates State 4 respiration in a cyclic process only within narrow concentration limits; at concentrations of iron above 100 mu M the respiration remains in the activated state until anaerobiosis. The stimulation of State 4 respiration is more pronounced with succinate than with NAD-linked substrates, a difference which partly may be attributed to a stimulation of the succinate dehydrogenase complex. 4. The stimulation of respiration by iron is approx. 3 times higher in State 3 than in State 4 and this difference can be attributed to a stimulation of the adenine mucleotide exchange reaction in State 3 with a concomitant increase in the rate of oxidative phosphorylation, although the P/O ration is slightly diminished.

Adenine Nucleotides↗
PubMed1992

Regulation of fat body mitochondrial respiration in Periplaneta americana by a novel factor from the corpus cardiacum.

Respiration of fat body (Periplaneta americana) mitochondria is increased by pretreatment of the tissue with corpus cardiacum (CC) extract. The magnitude of the increase depends on the type of substrate supplied for oxidation. With 5 mM pyruvate the respiration increased 22%, decreasing to 0 with 1 mM pyruvate. In contrast, 50 microM and 0.2 mM palmitic acid supported an increase in CC-stimulated respiration of 14 and 44%, respectively. Unlike crude CC extract, the synthetic hyperglycemic peptides CCI and CCII failed to alter the respiratory activity of fat body mitochondria. In common with the action of CC extract pretreatment of the fat body in vitro with 10(-5) M cyclic AMP, 10(-5) M 8-bromo-cyclic AMP, or 10(-5) M forskolin increased mitochondrial respiration approximately 30%. Octopamine (10(-4) M) elicited a response similar to that obtained with CC extract. Neither 10(-5) M cyclic AMP nor 10(-5) M 8-bromo-cyclic AMP stimulated respiration when applied directly to the mitochondria. These results suggest that the factor in CC extract manifests its effect intracellularly through the activation of a cyclic AMP-dependent protein kinase. This interpretation is also based on the finding that diamide, an inhibitor of protein kinase, inhibits CC-dependent and cyclic AMP-dependent mitochondrial respiration. The physiological role of the CC factor responsible is not known.

8-Bromo Cyclic Adenosine Monophosphate↗