Home About us Contact
|
Home About us Contact | ||
|
|
||
O2 Tension (o2 + tension)
Selected AbstractsNon-invasive measurements of the mean alveolar O2 tension from the oxygen uptake versus tidal volume curveACTA PHYSIOLOGICA, Issue 2 2007Hans Malte No abstract is available for this article. [source] Nitric oxide synthase inhibition in Thoroughbred horses augments O2 extraction at rest and submaximal exercise, but not during short-term maximal exerciseEQUINE VETERINARY JOURNAL, Issue S36 2006M. MANOHAR Summary Reason for performing study: Work is required to establish the role of endogenous nitric oxide (NO) in metabolism of resting and exercising horses. Objectives: To examine the effects of NO synthase inhibition on O2 extraction and anaerobic metabolism at rest, and during submaximal and maximal exertion. Methods: Placebo and NO synthase inhibition (with N,-nitro-L-arginine methyl ester [l -NAME] administered at 20 mg/kg bwt i.v.) studies were performed in random order, 7 days apart on 7 healthy, exercise-trained Thoroughbred horses at rest and during incremental exercise leading to 120 sec of maximal exertion at 14 m/sec on a 3.5% uphill grade. Results: At rest, NO synthase inhibition significantly augmented the arterial to mixed-venous blood O2 content gradient and O2 extraction as mixed-venous blood O2 tension and saturation decreased significantly. While NO synthase inhibition did not affect arterial blood-gas tensions in exercising horses, the exercise-induced increment in haemoglobin concentration and arterial O2 content was attenuated. In the l -NAME study, during submaximal exercise, mixed-venous blood O2 tension and haemoglobin-O2 saturation decreased to a greater extent causing O2 extraction to increase significantly. During maximal exertion, arterial hypoxaemia, desaturation of haemoglobin and hypercapnia of a similar magnitude developed in both treatments. Also, the changes in mixed-venous blood O2 tension and haemoglobin-O2 saturation, arterial to mixed-venous blood O2 content gradient, O2 extraction and markers of anaerobic metabolism (lactate and ammonia production, and metabolic acidosis) were not different from those in the placebo study. Conclusion: Endogenous NO production augments O2 extraction at rest and during submaximal exertion, but not the during short-term maximal exercise. Also, NO synthase inhibition does not affect anaerobic metabolism at rest or during exertion. Potential relevance: It is unlikely that endogenous NO release modifies aerobic or anaerobic metabolism in horses performing short-term maximal exertion. [source] Role of glutathione in the formation of the active form of the oxygen sensor FNR ([4Fe-4S]·FNR) and in the control of FNR functionFEBS JOURNAL, Issue 15 2000Quang Hon Tran The oxygen sensor regulator FNR (fumarate nitrate reductase regulator) of Escherichia coli is known to be inactivated by O2 as the result of conversion of a [4Fe-4S] cluster of the protein into a [2Fe-2S] cluster. Further incubation with O2 causes loss of the [2Fe-2S] cluster and production of apoFNR. The reactions involved in cluster assembly and reductive activation of apoFNR isolated under anaerobic or aerobic conditions were studied in vivo and in vitro. In a gshA mutant of E. coli that was completely devoid of glutathione, the O2 tension for the regulatory switch for FNR-dependent gene regulation was decreased by a factor of 4,5 compared with the wild-type, suggesting a role for glutathione in FNR function. In isolated apoFNR, glutathione could be used as the reducing agent for HS, formation required for [4Fe-4S] assembly by cysteine desulfurase (NifS), and for the reduction of cysteine ligands of the FeS cluster in FNR. Air-inactivated FNR (apoFNR without FeS) could be reconstituted to [4Fe-4S]·FNR by the same reaction as used for apoFNR isolated under anaerobic conditions. The in vivo effects of glutathione on FNR function and the role of glutathione in the formation of active [4Fe-4S]·FNR in vitro suggest an important role for glutathione in the de novo assembly of FNR and in the reductive activation of air-oxidized FNR under anaerobic conditions. [source] Hypoxia is an inducer of vasodilator agents in peritoneal macrophages of cirrhotic patientsHEPATOLOGY, Issue 5 2002Pilar Cejudo-Martín The aim of the investigation was to assess whether hypoxia induces the production of endogenous vasoactive peptides in macrophages of cirrhotic patients with ascites because low tissue oxygenation is a relatively frequent event in these patients. Peritoneal macrophages were isolated from ascites, seeded on well plates, and cultured at different times under hypoxic (5% O2) or normoxic conditions (21% O2). Then, accumulation of vasoactive peptides sensitive to hypoxia including endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), and adrenomedullin (ADM) was measured. Only VEGF and ADM were constitutively secreted, and hypoxia further stimulated the release of these vasodilator peptides. In concordance, increased messenger RNA (mRNA) levels of VEGF and ADM were found at culturing macrophages in hypoxia. This characteristic response was not observed in circulating monocytes of either cirrhotic patients or healthy subjects. Next the expression of the transcription factor, hypoxia inducible factor 1 (HIF-1), was analyzed. Expression of HIF-1, and HIF-1, messengers and HIF-1, protein subunit remained unchanged regardless of O2 tension, whereas HIF-1, protein subunit was overexpressed under hypoxic conditions. Moreover, conditioned medium from macrophages cultured under hypoxic conditions promoted a larger nitric oxide (NO) release in endothelial cells than that of normoxic macrophages. In conclusion, these data indicate that hypoxia induces the synthesis of VEGF and ADM in macrophages of cirrhotic patients, likely through HIF-1,enhanced transcriptional activity. These data suggest that a local reduction in O2 tension could enhance the synthesis of macrophage-derived vasodilators, thus aggravating the circulatory disturbance of these patients. [source] Central venous oxygen saturation for the diagnosis of low cardiac output in septic shock patientsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2010A. PERNER Background: Simple diagnostic tests are needed to screen septic patients for low cardiac output because intervention is recommended in these patients. We assessed the diagnostic value of central venous oxygen saturation in the superior vena cava (ScvO2) for detecting low cardiac output in patients with septic shock. Methods: We conducted a prospective observational study in three general intensive care units (ICUs) of adult patients with septic shock, who were to have a catheter inserted for thermodilution measurement of cardiac index (CITD). Paired measurements of CITD and central venous oximetry values were obtained when the clinician first measured CITD. Results: We included 56 patients with septic shock and a mean sequential organ failure assessment score of 12 (range 3,20). Baseline CITD was 3.5 l/min/m2 (1.0,6.2) and ScvO2 of 70% (33,87). The best cut-off of ScvO2 for CITD>2.5 l/min/m2 (n=42) was a value ,64% with positive and negative predictive values of 91% (95% confidence interval 79,98) and 91% (59,100), respectively. The diagnostic values were not improved by using instead central venous O2 tension or the difference between arterial and central venous O2 saturation. Conclusions: This prospective, observational study found that a ScvO2 measurement of ,64% indicated CITD>2.5 l/min/m2 in ICU patients with septic shock. [source] On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle massTHE JOURNAL OF PHYSIOLOGY, Issue 2 2009José A. L. Calbet Peak aerobic power in humans () is markedly affected by inspired O2 tension (). The question to be answered in this study is what factor plays a major role in the limitation of muscle peak in hypoxia: arterial O2 partial pressure () or O2 content ()? Thus, cardiac output (dye dilution with Cardio-green), leg blood flow (thermodilution), intra-arterial blood pressure and femoral arterial-to-venous differences in blood gases were determined in nine lowlanders studied during incremental exercise using a large (two-legged cycle ergometer exercise: Bike) and a small (one-legged knee extension exercise: Knee) muscle mass in normoxia, acute hypoxia (AH) () and after 9 weeks of residence at 5260 m (CH). Reducing the size of the active muscle mass blunted by 62% the effect of hypoxia on in AH and abolished completely the effect of hypoxia on after altitude acclimatization. Acclimatization improved Bike peak exercise from 34 ± 1 in AH to 45 ± 1 mmHg in CH (P < 0.05) and Knee from 38 ± 1 to 55 ± 2 mmHg (P < 0.05). Peak cardiac output and leg blood flow were reduced in hypoxia only during Bike. Acute hypoxia resulted in reduction of systemic O2 delivery (46 and 21%) and leg O2 delivery (47 and 26%) during Bike and Knee, respectively, almost matching the corresponding reduction in . Altitude acclimatization restored fully peak systemic and leg O2 delivery in CH (2.69 ± 0.27 and 1.28 ± 0.11 l min,1, respectively) to sea level values (2.65 ± 0.15 and 1.16 ± 0.11 l min,1, respectively) during Knee, but not during Bike. During Knee in CH, leg oxygen delivery was similar to normoxia and, therefore, also in spite of a of 55 mmHg. Reducing the size of the active muscle mass improves pulmonary gas exchange during hypoxic exercise, attenuates the Bohr effect on oxygen uploading at the lungs and preserves sea level convective O2 transport to the active muscles. Thus, the altitude-acclimatized human has potentially a similar exercising capacity as at sea level when the exercise model allows for an adequate oxygen delivery (blood flow ×), with only a minor role of per se, when is more than 55 mmHg. [source] Effects of hypoxia on diaphragmatic fatigue in highly trained athletesTHE JOURNAL OF PHYSIOLOGY, Issue 1 2007Ioannis Vogiatzis Previous work suggests that exercise-induced arterial hypoxaemia (EIAH), causing only moderate arterial oxygen desaturation (: 92 ± 1%), does not exaggerate diaphragmatic fatigue exhibited by highly trained endurance athletes. Since changes in arterial O2 tension have a significant effect on the rate of development of locomotor muscle fatigue during strenuous exercise, the present study investigated whether hypoxia superimposed on EIAH exacerbates the exercise-induced diaphragmatic fatigue in these athletes. Eight trained cyclists (: 67.0 ± 2.6 ml kg,1 min,1; mean ±s.e.m.) completed in balanced order four 5 min exercise tests leading to different levels of end-exercise (64 ± 2, 83 ± 1, 91 ± 1 and 96 ± 1%) via variations in inspired O2 fraction (: 0.13, 0.17, 0.21 and 0.26, respectively). Measurements were made at corresponding intensities (65 ± 3, 80 ± 3, 85 ± 3 and 90 ± 3% of normoxic maximal work rate, respectively) in order to produce the same tidal volume, breathing frequency and respiratory muscle load at each . The mean pressure time product of the diaphragm did not differ across the four exercise tests and ranged between 312 ± 28 and 382 ± 22 cmH2O s min,1. Ten minutes into recovery, twitch transdiaphragmatic pressure (Pdi,tw) determined by bilateral phrenic nerve stimulation, was significantly (P= 0.0001) reduced after all tests. After both hypoxic tests (: 0.13, 0.17) the degree of fall in Pdi,tw (by 26.9 ± 2.7 and 27.4 ± 2.6%, respectively) was significantly greater (P < 0.05) than after the normoxic test (by 20.1 ± 3.4%). The greater amount of diaphragmatic fatigue in hypoxia at lower leg work rates (presumably requiring smaller leg blood flow compared with normoxia at higher leg work rates), suggests that when ventilatory muscle load is similar between normoxia and hypoxia, hypoxia exaggerates diaphragmatic fatigue in spite of potentially greater respiratory muscle blood flow availability. [source] Determinants of Placental VascularityAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2004Donald S. Torry Problem:, Vascular growth during implantation and placentation is critical for successful gestation and it is thought that vascular insufficiencies during placentation contribute to a number of obstetrical complications. However, relatively little is known regarding the regulation of angiogenesis in the placenta. Method of study:, We review literature concerning the potential significance of inadequate placental vascularity as a contributor to the obstetrical complications of spontaneous abortion, fetal growth restriction and preeclampsia. Gene expression assays were used to compare fluctuations of placenta growth factor (PlGF) and PlGF receptor expression in normal and preeclamptic trophoblast in vitro. Results:, Studies have shown that common obstetrical complications manifest altered placental vascularity. Both intrinsic defects (gene knockouts) and extrinsic factors (O2 tension, cytokines, etc) may be responsible for the defects. Some of these factors have been shown to influence trophoblast vascular endothelial growth factor (VEGF)/PlGF expression suggesting this particular family of angiogenic proteins play an important role in placental angiogenesis. Conclusion:, Placental vascularization reflects a complex interaction of regulatory factors. Understanding the regulation of vascular growth in the placenta will provide much needed insight into placenta-related vascular insufficiencies. [source] Hepatocyte Function in a Radial-flow Bioreactor Using a Perfluorocarbon Oxygen CarrierARTIFICIAL ORGANS, Issue 11 2005Martin J. Nieuwoudt Abstract:, The aims of this study were, first, to indicate the metabolic activity of hepatocytes in a radial-flow polyurethane foam matrix bioreactor relative to monocultures, and second, to evaluate the effect on the hepatocytes of including a synthetic perfluorocarbon (PFC) oxygen carrier to the recirculating medium. The efficient O2 -carrying ability of PFCs may be beneficial to bioreactors employed in stressed cellular environments. Thus, they may also be useful in the treatment of an acute liver failure patient with a bioartificial liver support system (BALSS). Data on the function of three-dimensional (3-D) hepatocyte cultures exposed to emulsified PFCs are lacking. Results: the metabolic functions of the 3-D hepatocyte cultures were improved relative to monocultures. Three-dimensional cultures with and without PFC behaved similarly, and no adverse effects could be detected when PFC was included in the recirculating medium. The addition of PFC significantly improved lidocaine clearance possibly due to the presence of higher O2 tension in the medium. Imaging indicated that large aggregates formed and that seeding had followed flow through the matrix. Simulations indicated first, that the cell numbers used in this study had been insufficient to challenge the bioreactor O2 supply explaining the similarity in performance of the 3-D cultures, and second, that the benefit of adding PFC would be more pronounced at the cell densities likely to be used in a BALSS bioreactor. [source] Review: Correlations between oxygen affinity and sequence classifications of plant hemoglobins,BIOPOLYMERS, Issue 12 2009Benoit J. Smagghe Abstract Plants express three phylogenetic classes of hemoglobins (Hb) based on sequence analyses. Class 1 and 2 Hbs are full-length globins with the classical eight helix Mb-like fold, whereas Class 3 plant Hbs resemble the truncated globins found in bacteria. With the exception of the specialized leghemoglobins, the physiological functions of these plant hemoglobins remain unknown. We have reviewed and, in some cases, measured new oxygen binding properties of a large number of Class 1 and 2 plant nonsymbiotic Hbs and leghemoglobins. We found that sequence classification correlates with distinct extents of hexacoordination with the distal histidine and markedly different overall oxygen affinities and association and dissociation rate constants. These results suggest strong selective pressure for the evolution of distinct physiological functions. The leghemoglobins evolved from the Class 2 globins and show no hexacoordination, very high rates of O2 binding (,250 ,M,1 s,1), moderately high rates of O2 dissociation (,5,15 s,1), and high oxygen affinity (Kd or P50 , 50 nM). These properties both facilitate O2 diffusion to respiring N2 fixing bacteria and reduce O2 tension in the root nodules of legumes. The Class 1 plant Hbs show weak hexacoordination (KHisE7 , 2), moderate rates of O2 binding (,25 ,M,1 s,1), very small rates of O2 dissociation (,0.16 s,1), and remarkably high O2 affinities (P50 , 2 nM), suggesting a function involving O2 and nitric oxide (NO) scavenging. The Class 2 Hbs exhibit strong hexacoordination (KHisE7 , 100), low rates of O2 binding (,1 ,M,1 s,1), moderately low O2 dissociation rate constants (,1 s,1), and moderate, Mb-like O2 affinities (P50 , 340 nM), perhaps suggesting a sensing role for sustained low, micromolar levels of oxygen. © 2009 Wiley Periodicals, Inc. Biopolymers 91: 1083,1096, 2009. This article was originally published online as an accepted preprint. The "Published Online" date corresponds to the preprint version. You can request a copy of the preprint by emailing the Biopolymers editorial office at biopolymers@wiley.com [source] Nitric oxide availability affects microvascular O2 tensionsACTA PHYSIOLOGICA, Issue 3 2006Frank B. Jensen No abstract is available for this article. [source] | ||||||||||||||||