Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GASES”

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 847 records · Page 47Linked to original sources

Changes in arterial blood gases during and after a period of oxygen breathing in patients with chronic hypercapnic respiratory failure and in patients with asthma.

1. Ten patients with chronic hypercapnic respiratory failure (group 1) and eight patients with asthma (group 2) breathed pure O2 from an MC mask for 60 min. Blood gases were measured during this period and for the subsequent 45 min. 2. In mine of ten patients in group 1 and in all eight patients in group 2 arterial O2 tension (Pa,O2) fell to values lower than had been obtained before O2 was given. 3. These undershoots in Pa,O2 are unrelated to changing CO2 stores or to hypoventilation, and are more likely due to persistence of altered ventilation-perfusion ratios associated with O2 breathing. 4. Magnitude of the undershoots is usually small, and periods of less than 15 min of O2 are unlikely to be harmful.

Adolescent↗

Influence of blood gases, Ca2+-entry blockade and angiotensin converting enzyme inhibition on pressor responses to alpha-adrenoceptor agonists: evidence in vivo for subtypes of response independent of receptor subtype?

The pressor responses in the pithed rat to alpha-adrenoceptor agonists can be modified by alterations in arterial blood gas levels or by drugs which interfere with excitation-contraction coupling processes in the vascular smooth muscle, e.g. Ca2+-entry blockers or angiotensin converting enzyme (ACE) inhibitors. However, the extent of these influences depends on which agonist is used. The pressor response to intravenous injection of alpha-adrenoceptor agonists consists of two phases: an initial rapid but transient response (phase I) is followed by a response of slower onset but longer duration (phase II). We have examined the effects of manipulation of arterial blood gases, a Ca2+-entry blocker, nifedipine, and an ACE inhibitor, teprotide, on the pressor responses to a series of alpha-adrenoceptor agonists. In each case, the effects showed selectivity for one or other of the two phases and the differences in susceptibility between agonists could be explained by the relative sizes of the two phases in their responses. In general, phase II was more susceptible to alkalosis, nifedipine and teprotide, so that drugs in which this component predominated were more susceptible to these factors. In contrast there was no direct correlation with the receptor subtypes activated by the agonists.

Adrenergic alpha-Agonists↗

Human alveolar gas-mixing efficiency for gases of differing diffusivity in health and airflow limitation.

1. Incomplete mixing of alveolar gas may be expressed as an equivalent alveolar dead space serving a remaining alveolar space in which mixing is regarded as complete. Calculation of this dead space during multiple-breath, inert gas wash-in or wash-out leads to an estimate of 'multiple-breath alveolar mixing efficiency' (MBME). 2. We measured MBME in 25 healthy subjects and six patients with chronic airflow limitation (CAL), and in three asthmatic patients before and after bronchial provocation with histamine aerosol, from successive breaths during open-circuit, multiple-breath wash-in of a mixture containing helium (He) and sulphur hexafluoride (SF6). The simultaneous use of a light and a heavy gas helps to identify diffusive mechanisms. 3. MBME fell almost linearly with log Z, the proportion of total wash-in remaining uncompleted. For a given Z, MBME was always lower for SF6 than for He in the same subject. In health the lowest MBME (52.2%) was seen for SF6 in a man aged 21 years. The same wash-in yielded a ventilation distribution with an extreme range of specific ventilation of less than 1 decade. MBME of this order is thus consistent with estimates of ventilation distribution in health. 4. Patients with CAL showed a big increase in the volume of the conducting airways or 'series dead space' (VDS) for both gases, and VDS was always bigger for SF6 than for He. This very large VDS appears to be the main reason for wash-in delay in these patients, followed by impaired diffusive mixing in the peripheral air spaces. Ventilation maldistribution may play little part in the mixing defect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Excessive exercise ventilation in moderate left heart dysfunction. Influence of postural changes in central haemodynamics and blood gases.

To evaluate the relative importance of pulmonary congestion and peripheral hypoxia as causes for the excessive exercise ventilation in left heart dysfunction, seven patients with excessive ventilation and distinct left heart dysfunction during moderate exercise (LHD), and seven control patients with essentially normal exertional functions (CTR), had ventilation, central haemodynamics, arterial and mixed venous blood gases examined at rest and exercise, 32 W (25-40) in the LHD group and 44 W (33-49) in the CTR group, in lying and sitting positions. Change from lying to sitting exercise, led to fall in pulmonary artery wedge pressure (PAWP) from 31.0 +/- 5.5 to 8.8 +/- 5.0 mmHg in the LHD group, compared with from 13.7 +/- 1.0 to 2.1 +/- 2.4 mm Hg in the controls, while ventilation/O2 intake ratio (V/VO2) and physiological dead space/tidal volume ratio (VD/VT) showed a tendency to rise, from 36.3 +/- 8.8 to 39.2 +/- 7.4, and from 0.35 +/- 0.11 to 0.39 +/- 0.09, respectively, in the LHD group, and from 27.5 +/- 3.1 to 28.7 +/- 5.3, and from 0.19 +/- 0.09 to 0.21 +/- 0.12 in the controls. Mixed venous O2 tension (PvO2) showed a marked decline from 3.60 +/- 0.33 to 3.26 +/- 0.36 kPa in the LHD group, as compared with from 3.94 +/- 0.28 to 3.71 +/- 0.29 kPa in the controls, while the calculated physiologic shunt (Qs/Qt) suggested improved alveolo-arterial gas exchange. The data fit in with recent studies ascribing the excessive exercise ventilation to a combination of signals from hypoxia-induced changes, particularly in the exercising muscles, and augmented ergoreflex and central and peripheral chemoreceptor activity, partly to changes in the integrated control of ventilation and circulation, not to mechanisms related to pulmonary congestion.

Aged↗

Staff exposure to anaesthetic gases in theatre and non theatre areas.

Environmental monitoring of anaesthetic gases was carried out in theatre areas in eight hospitals as well as in Delivery suites, radiology, radiotherapy and Dental suites. High staff exposures occurred in nontheatre areas although exposures in theatres were generally satisfactory. Environmental control measures are required where staff exposures exceed legal standards.

Air↗

Effect of medroxyprogesterone on pulmonary arterial pressure, exhaled nitric oxide, ECG and arterial blood gases.

OBJECTIVES: To evaluate the effect of medroxyprogesterone acetate (MPA) therapy on pulmonary arterial pressure (PAP), exhaled nitric oxide (NO), electrocardiogram (ECG), and on arterial blood gases (ABG). DESIGN: A double-blind randomized placebo-controlled cross-over trial. SETTING: University hospital in Turku, Finland. SUBJECTS: Fourteen postmenopausal women with respiratory impairment. INTERVENTIONS: A 2-week placebo and a 2-week MPA period (60 mg day -1) followed by 6-week placebo or MPA washout periods. MAIN OUTCOME MEASURES: The systolic PAP was estimated by Doppler echocardiography. PAP, ECG, NO and ABG were monitored at baseline, after 2-week placebo and MPA periods, and after 3- and 6-week placebo and MPA washout periods. RESULTS: The mean PaCO2 at baseline was 5.4 +/- 0.6 kPa (mean +/- SD). The average decrease of PaCO2 on MPA was -0.8 +/- 0.3 kPa (P < 0.001) and 0.3 +/- 1.0 kPa (P = 0.007) at the 3-week washout. The mean systolic PAP at baseline was 44.3 +/- 14.5 mm Hg. MPA did not change PAP until the 6-week washout, when the average increase of + 6.9 +/- 19.8 mm Hg (P = 0.002) was observed. No changes occurred in PaO2, exhaled NO or the ECG axes. The PR interval was shorter only on MPA (15.9 +/- 27.0 ms, P = 0.020) whereas the QRS duration remained shorter up to 3-week washout (3.9 +/0 5.5 ms, P = 0.008 and 4.0 +/- 14.3 ms, P = 0.032). The systolic and diastolic BP and the heart rate did not change. CONCLUSIONS: Despite prolonged decrease in PaCO2, short-term MPA had no effect on exhaled NO and did not decrease systolic PAP in postmenopausal women with respiratory impairment. MPA shortened the PR interval and the QRS duration, the latter effect being sustained at least up to 3 weeks.

Aged↗

Lung function, blood gases, pH and serum electrolytes of small-scale miners exposed to chrome ore dust on the Great Dyke in Zimbabwe.

We measured and compared lung function indices and some blood parameters (gases, electrolytes, glucose, pH, red cell indices) of 54 male small-scale miners (SSM) chronically exposed to chrome ore dust to those of 50 nonmining control subjects (NMC) and 46 large-scale chrome miners (LSM) who had taken internationally recommended precautionary measures (secondary control). The respirable dust level in the SSM environment (6.0 +/- 0.5 mg/m3) was significantly higher (P < 0.001) than in the NMC and LSM environments (0.3 +/- 0.1 mg/m3 and 0.5 +/- 0.3 mg/m3, respectively). There were no significant differences in neither dust levels nor lung function status between NMC and LSM environments. The values of FVC, FEV1, PEFR and FEV1% of the SSM were 3.5 +/- 0.09 l, 2.61 +/- 0. 09 l, 6.07 +/- 0.36 l/second and 76.19 +/- 2.36%, respectively. These values were significantly lower than those of NMC (P < 0.01, respectively). However, the blood parameters of the SSM and NMC were not significantly different. The results are indicative of both restrictive and obstructive ventilatory defects in the SSM which may be attributed exposure to chrome ore dust in the environment. Associated risk factors appear to be advancing age, prolonged exposure to chrome ore dust and acid base disturbance.

Adult↗

Arterial blood gases in extraperitoneal laparoscopic urethrocystopexy.

BACKGROUND: The aim of this study was to investigate the effects of extraperitoneal laparoscopy and carbon dioxide insufflation on hemodynamic parameters, arterial blood gases and complications in urethrocystopexy operations. METHODS: Twenty-five female patients who underwent extraperitoneal laparoscopic mesh urethrocystopexy operation for the correction of urinary incontinence were allocated to the study. Hemodynamic parameters were noted and blood gas analyzes were performed before the induction of anesthesia, 10 min after induction, 5 and 10 min after the beginning of carbon dioxide insufflation, at the end of carbon dioxide insufflation and 30 min after exsufflation. RESULTS: There was no significant change in mean arterial pressure, peripheral oxygen saturation, arterial carbon dioxide pressure, and arterial oxygen saturation compared to preinsufflation and preinduction values. End-tidal carbon dioxide pressure did not increase above 45 mm/Hg during carbon dioxide insufflation. Arterial oxygen saturation and partial oxygen pressure did not decrease. Subcutaneous emphysema, pneumothorax, pneumomediastinum and pleural effusion were not noted in any patient. CONCLUSION: We conclude that, extraperitoneal laparoscopic urethrocystopexy is not associated with hemodynamic and respiratory impairment.

Blood Gas Analysis↗

Arterial blood gases during exercise: validity of transcutaneous measurements.

OBJECTIVE: To investigate the validity of transcutaneous measurements of blood gas tensions for the assessment of partial arterial pressure of oxygen (PaO(2)) and carbon dioxide (PaCO(2)) during treadmill exercise. DESIGN: Experimental, self-controlled against a reference standard. SETTING: Lung function laboratory. PATIENTS: Eighty-one patients with various lung diseases. INTERVENTIONS: At rest and at symptom-limited peak exercise, puncture of the radial artery with concurrent transcutaneous measures of blood gases. MAIN OUTCOME MEASURES: Arterial blood samples were analyzed with a radiometer to measure PaO(2) and PaCO(2). A microgas apparatus was used to measure gas tensions transcutaneously. Values obtained transcutaneously (TcPO(2), TcPCO(2)) were compared with those obtained by blood sample. TcPO(2) was adjusted as close as possible to the PaO(2) obtained in the same conditions, with the correction factor of the apparatus. Values obtained transcutaneously were compared with those obtained by blood sample to establish the sensitivity and specificity of the noninvasive method. RESULTS: Mean differences +/- standard deviation between transcutaneous and arterial tension at peak exercise were 0.4 +/- 7.0mmHg and 2.1 +/- 3.3mmHg for PaO(2) and PaCO(2), respectively. The transcutaneous device enabled us to predict a decrease in PaO(2) (>or=2mmHg) from rest to exercise with a sensitivity of 92.1% and a specificity of 90% and an increase in PaCO(2) with a sensitivity of 88% and a specificity of 58.9%. CONCLUSIONS: Although transcutaneous measurement are sufficiently sensitive and specific to detect patients whose PaO(2) decreases during exercise, its precision is not sufficient for gas exchange calculations.

Adolescent↗

[An electrolyte-adapted heparin solution for the determination of blood gases and electrolytes in whole blood].

Blood gases, pH, sodium, potassium, chloride, and ionised calcium in whole blood samples can be determined simultaneously in modern instruments. Preparing syringes with conventional heparin solutions causes a relevant bias of the electrolyte concentrations (especially K+ and Ca2+) by dilution of the sample. Additionally, ionised calcium is decreased by binding to heparin. The solution described in the present paper yields a final heparin concentration of 4-6 mU/l, thus eliminating the calcium binding effect. The dilution effects are antagonised by an electrolyte composition that is similar to normal plasma. The heparin solution is commercially available.

Blood Gas Analysis↗

Effects of controlled frequency breathing during exercise on blood gases and acid-base balance.

The purpose of this study was to determine the effect of a reduced ventilatory frequency (Vf) on blood gases and acid-base changes during three intensities of cycling exercise. VO2max and lactate threshold workload (LaT) of six subjects were assessed on a Monark ergometer. Experimental rides were performed 1) with no restriction on Vf (NB) and 2) with a prescribed Vf of 10/min (CFB). Each exercise period consisted of 8 min at 10% of VO2max below the LaT (WI), followed immediately by 8 min at LaT (WII), followed immediately by 8 min at 10% of VO2max above LaT (WIII). Blood was taken from a heated fingertip at the end of each load and analyzed for lactate concentration, pH, PO2, and PCO2. Respiratory exchange was monitored continuously using open circuit indirect calorimetry. Minute ventilation (VE) was significantly reduced by CFB at all three workloads. The reduced VE resulted in lower (p less than 0.05) blood PO2 at each workload (p less than 0.05), however, neither blood lactate nor VO2 were significantly different between CFB and NB for the three loads. Blood [H+] was significantly higher in CFB than NB at all three loads with the greatest difference between trials at WIII (NB: 37.93 +/- 0.68 nM: CFB: 44.77 +/- 1.02 nM). This was accounted for by a significantly higher PCO2 during CFB in WII and WIII (WII, NB: 33.0 +/- 1.4 mmHg, CFB: 35.7 +/- 2.7 mmHg; WIII, NB: 31.2 +/- 1.7 mmHg, CFB: 38.9 +/- 2.4 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

Effects of warm-up on blood gases, lactate and acid-base status during sprint swimming.

A standardized 200-m front crawl sprint swim (SpS) was used to evaluate the effects of warm-up on pH, blood gases, and the concentrations of lactate ([La-]) and bicarbonate ([HCO3-]) in arterialized and venous blood. Eight trained male swimmers performed two randomly assigned 200-m front crawl swims at previously determined intensities corresponding to 120% VO2max. One swim was preceded by a warm-up (WU trial) which consisted of a 400-m front crawl swim (82% VO2max), 400-m flutter kicking (45% VO2max), and 4 x 50-m front crawl sprints (111% VO2max). The second was performed without warm-up (NWU trial). Blood was sampled from a hyperemized earlobe and an antecubital vein before the warm-up, 9 min after the warm-up (1 min before the swim), immediately following the SpS, and at 2, 5, 10, and 20 min after the SpS. The warm-up exercise resulted in a higher pre-SpS [La-] in arterialized blood (3.1 +/- 0.4 and 1.7 +/- 0.4 mmol x l-1, p less than 0.05), a higher hydrogen ion concentration ([H+]) in venous blood (45.9 +/- 0.9 and 42.2 +/- 0.8 nmol x l-1, p less than 0.001), and a lower arterialized blood [HCO3-] (25.1 +/- 0.9 and 22.2 +/- 0.8 mmol x l-1, p less than 0.05). The SpS was accompanied with higher heart rates during the WU trial (178 +/- 3 and 169 +/- 3 bpm; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Cord blood gases and abnormal fetal biophysical assessment in preterm premature rupture of the membranes.

The relationship between cord blood gases and infection outcome was determined in 53 consecutive patients with preterm premature rupture of the membranes who were delivered because of abnormal fetal biophysical assessment. Measures of infection outcome included the presence of clinical amnionitis, possible neonatal sepsis, and neonatal sepsis. Fetal acidosis at birth, as defined by cord arterial pH less than 7.20, was found in six fetuses; five of these developed neonatal sepsis and the other was born to a mother who had intrapartum clinical amnionitis. The mean cord blood pH (artery and vein) of fetuses with neonatal sepsis was significantly less than in fetuses with possible neonatal sepsis or no sepsis; however, two thirds (10 of 15) of the neonates with sepsis had normal acid-base status at birth. These data suggest that the fetal biophysical assessment becomes abnormal before the development of fetal acidosis. The possible mechanisms by which fetal infection diminishes fetal biophysical activities prior to the development of acidosis are discussed.

Bicarbonates↗

Umbilical cord blood gases for term healthy newborns.

Examination of paired umbilical arterial and umbilical venous blood gases for 147 term, healthy newborns revealed a strong correlation of pH, bicarbonate, and base excess with the 1-minute Apgar score. Although significantly different from each other, a strong correlation existed between the gas measurements of the two vessels. The lower limit of pH for the umbilical artery was 7.12 and for the vein, 7.25. The arterial-venous difference for bicarbonate but not pH, oxygen or carbon dioxide tension, or base excess was correlated with the 1-minute Apgar score.

Apgar Score↗

[Effect of almitrine and oxygen on arterial blood gases in chronic respiratory insufficiency].

In patients with respiratory failure, almitrine causes an increase in arterial O2 partial pressure (paO2) by stimulating peripheral chemoreceptors. Since such patients often require long-term O2 therapy inhibiting peripheral chemoreceptor activity, the effect on arterial blood gases by almitrine (100 mg orally) and increasing amounts of nasally supplied O2 was studied. In ten patients with severe chronic airways obstruction and pulmonary emphysema, almitrine produced a mean increase of paO2 by 5.2 mm Hg both while breathing normal air and during nasal administration of O2 (0.5-2.0 l/min), whereas paCO2 levels remained constant. In 4 patients with pulmonary fibrosis almitrine did not change the paO2. These results show that patients with chronic airways obstruction and pulmonary emphysema respond to a single dose of 100 mg almitrine by an increase of paO2 equivalent to that achieved by administering 1.0 l/min of O2 via the nose.

Almitrine↗

[Cimetidine and ranitidine in intensive care patients. Double-blind randomized cross-over study on intravenous administration: hemodynamics, plasma coagulation, blood gases and acid-base status].

Intravenous cimetidine 200 mg, and ranitidine 50 mg were administered as 2 minute infusions to 50 intensive-care patients. Cimetidine and ranitidine differed significantly in their effect on systolic arterial blood pressure measured during the second minute (alpha = 0.01). In the case of cimetidine the haemodynamic parameters measured over 10 minutes revealed a clearly defined fall in systolic, diastolic and mean arterial blood pressure as well as a rise in heart rate. The initial values were regained 5 minutes after drug application. Adverse effects of ranitidine on haemodynamics were much less than those of cimetidine. Neither drug produced any essential change in clotting parameters (partial thromboplastin time, plasma thrombin time, thromboplastin time and fibrinogen) measured before and 5 minutes after application, nor had they any effect on blood-gases or acid-base status.

Acid-Base Equilibrium↗

Compressibility and specific heats of heavier condensed rare gases near the liquid-vapor critical point.

This study concerns the way to describe some physical properties of simple liquids by using the Bogoliubov-Born-Green-Kirkwood-Yvon hierarchy. It constructively analyzes the recent contribution of Sarkisov [G. N. Sarkisov, J. Chem. Phys. 119, 373 (2003)] on the structural behavior of a simple fluid near the liquid-vapor critical point. His work, already compared with computer simulation studies, is here brought into direct contact for the heavier condensed rare gases Ar, Kr, and Xe with (a) experiment and (b) earlier theoretical investigations. Directions for future studies then emerge.

Journal Article↗

Exciton dynamics of GaSe nanoparticle aggregates.

Time-resolved and static spectroscopic results on GaSe nanoparticle aggregates are presented to elucidate the exciton relaxation and diffusion dynamics. These results are obtained in room-temperature TOP/TOPO solutions at various concentrations. The aggregate absorption spectra are interpreted in terms of electrostatic coupling and covalent interactions between particles. The spectra at various concentrations may then be interpreted in terms of aggregate distributions calculated from a simple equilibrium model. These distributions are used to interpret concentration-dependent emission anisotropy kinetics and time-dependent emission spectral shifts. The emission spectra are reconstructed from the static emission spectra and decay kinetics obtained at a range of wavelengths. The results indicate that the aggregate z axis persistence length is about 9 particles. The results also show that the one-dimensional exciton diffusion coefficient is excitation wavelength dependent and has a value of about 2 x 10(-5) cm(2)/s following 406 nm excitation. Although exciton diffusion results in very little energy relaxation, subsequent hopping of trapped electron/hole pairs occurs by a Forster mechanism and strongly red shifts the emission spectrum.

Journal Article↗