Simultaneous measurement of eight foreign gases in blood by gas chromatography

Wagner, P. D.; Naumann, Patrick; Laravuso, Raymond B.

doi:10.1152/jappl.1974.36.5.600

Cited by 329 publications

(166 citation statements)

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“…Buffers equilibrated by bubbling with CO 2 -free or high CO 2 air were perfused via Teflon tubing into the well used for calcium imaging (see Supporting Text), then collected 3-5 seconds later in an airtight glass syringe, to estimate the final CO 2 concentration to which stomata were exposed (48,57). CO 2 -free air (6-9 ml) was introduced into the syringe, and the [CO 2 ] in the buffer and air was equilibrated by shaking for 5 min.…”

Section: Determination Of [Co2] In Perfused Buffersmentioning

confidence: 99%

“…The [CO 2 ] of the equilibrated air was then measured by using a Li-6400 gas exchange analyzer (Li-Cor, Lincoln, NE). The CO 2 content of the buffer was calculated by performing calibration measurements and a mass balance as described (57 Fig. 9, which is published as supporting information on the PNAS web site).…”

Section: Determination Of [Co2] In Perfused Buffersmentioning

confidence: 99%

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CO ₂ signaling in guard cells: Calcium sensitivity response modulation, a Ca ²⁺ -independent phase, and CO ₂ insensitivity of the gca2 mutant

Young

Mehta²,

Israelsson³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

178

246

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. These changes in leaf CO 2 concentrations occur as a result of photosynthesis and respiration. Furthermore, atmospheric CO 2 is predicted to double in the present century (1). Many studies have been carried out to determine the effects of atmospheric CO 2 increases on plant gas exchange, carbon fixation, and growth and the resulting impact this will have on natural and agricultural ecosystems (2-6). One of the mechanisms by which increased atmospheric CO 2 affects plants is CO 2 regulation of stomatal apertures. Reports show that a doubling of atmospheric [CO 2 ] causes significant stomatal closure by 20-40% in diverse plant species (7-9).Stomata experience diurnal changes in [CO 2 ] inside the leaf during light͞dark transitions. In the dark, CO 2 is produced in leaves by cellular respiration. The [CO 2 ] shifts caused by illumination changes are rapid and large, with [CO 2 ] in the stomatal cavity ranging from 200 to 650 ppm (10).Stomatal aperture is controlled by the turgor pressure in the guard cells surrounding the stomatal pore. Guard cell turgor pressure is mediated by the ion and organic solute concentration in guard cells. Elevated CO 2 has been shown to enhance potassium efflux channel and S type anion channel activities that mediate extrusion of ions during stomatal closure (11,12). In correlation with these findings, chloride release from guard cells is triggered by CO 2 elevation (13), and high CO 2 causes depolarization of guard cells (14, 15). Furthermore, CO 2 activation of R type anion channel currents was found in a subset of Vicia faba guard cells (12).Little is known about the CO 2 signal transduction mechanisms that function upstream of ion channels in guard cells (16)(17)(18)(19). CO 2 -induced stomatal movements were previously found to be absent in two mutants that affect the stomatal closure signaling network for the drought stress hormone abscisic acid (ABA): abi1-1 and abi2-1 (20). Conditional CO 2 responsiveness was reported in these mutants by using different experimental conditions (21,22 (16-18, 24, 26-32). Furthermore, some studies have also indicated a role for calcium increases in the opposing response of stomatal opening (33)(34)(35). It is unclear how these opposite responses could be directed via elevations in the same second messenger, Ca 2ϩ .CO 2 is a particularly interesting stomatal stimulus with respect to cytosolic Ca 2ϩ responses, as demonstrated in the present study. CO 2 can induce stomatal opening or closing depending on its concentration (36). Studies in animal and plant cells have shown that different patterns of repetitive calcium transients modulate responses (29,(37)(38)(39). Although previous studies have shown a role for calcium in CO 2 signaling in guard cells (24,25), changes in repetitive calcium transient patterns have not yet been studied in guard cells in response to CO 2 . The present study demonstrates CO 2 modulation of repetitive calcium transient patterns in Arabidopsis guard cells and characterizes roles of Ca 2ϩ in CO 2 -regulated stomatal ope...

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Section: Determination Of [Co2] In Perfused Buffersmentioning

confidence: 99%

Section: Determination Of [Co2] In Perfused Buffersmentioning

confidence: 99%

CO ₂ signaling in guard cells: Calcium sensitivity response modulation, a Ca ²⁺ -independent phase, and CO ₂ insensitivity of the gca2 mutant

Young

Mehta²,

Israelsson³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

178

246

View full text Add to dashboard Cite

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“…V '/Q ' relationships were determined by means of the MIGET [21,22] using constant infusion of a dilute solution of six inert gases (sulphur hexafluoride, ethane, cyclopropane, halothane, diethyl ether and acetone) dissolved in 5% dextrose as described by WAGNER and coworkers [21,22]. The gas extraction method of WAGNER et al [21] was used to determine inert gas tensions and solubilities in blood samples.…”

Section: Inert Gas Exchange Measurementsmentioning

confidence: 99%

Pulmonary NO synthase inhibition and inspired CO2: effects on V ′/Q ′ and pulmonary blood flow distribution

Brogan¹,

Hedges²,

McKinney³

et al. 2000

Eur Respir J

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Inhaled carbon dioxide decreases ventilation/perfusion ratio (V '/Q ') heterogeneity in dogs. The aim of this study was to test whether inhaled CO 2 improves the V '/Q ' by inhibition of nitric oxide production and whether inhibition of endogenous NO production in the lung alters gas exchange and V '/Q ' matching.Eleven healthy dogs were anaesthetized and mechanically ventilated. The multiple inert gas elimination technique (MIGET) was used to measure V '/Q ' heterogeneity and regional pulmonary blood flow heterogeneity was assessed in five dogs using fluorescent microspheres. In a separate set of five dogs, exhaled NO levels were measured via chemiluminescence. All dogs were studied before and after 4.8% inspired CO 2 , and then given the NO synthase inhibitor N v -nitro-L-arginine methyl ester (L-NAME, 10 mg . kg -1 ) via nebulization, after which they were studied again with room air and inhaled CO 2 .CO 2 and L-NAME improved arterial and alveolar oxygen tension, but the improvements with L-NAME did not reach statistical significance. Improved V '/Q ' matching, as assessed by the MIGET, occurred under all experimental conditions. Exhaled NO levels were reduced by 40% with CO 2 and 70% with L-NAME. The standard deviation of regional pulmonary blood flow assessed via microspheres decreased only with inhaled CO 2 . Fractal analysis of pulmonary blood flow distributions revealed that regional blood flow was highly correlated with flow to neighbouring pieces of lung in all four conditions with no changes in the fractal dimension.Inspired carbon dioxide improves ventilation perfusion ratio matching and is associated with a more homogeneous distribution of pulmonary blood flow. Although inspired carbon dioxide causes a reduction in exhaled nitric oxide, the differences in pulmonary perfusion distributions found between carbon dioxide and N v -nitro-Larginine methyl ester suggest that the carbon dioxide effect is not mediated by a reduction in nitric oxide production. The improved ventilation perfusion ratio matching with inhibition of nitric oxide synthase suggests the intriguing possibility requiring further study that endogenous production of nitric oxide in the lung does not subserve ventilation perfusion ratio regulation. Eur Respir J 2000; 16: 288±295. Addition of low concentrations (2±5%) of carbon dioxide to inspired gas improves gas exchange and arterial oxygenation in normal lungs [1,2]. Using the multiple inert gas elimination technique (MIGET), it was demonstrated that inspired CO 2 reduces ventilation/perfusion ratio (V '/Q ') heterogeneity even with constant ventilation [3]. Although CO 2 has many effects on the lungs that may promote V '/Q ' matching [4,5], it remains unknown how and at what site(s) CO 2 decreases V '/Q ' heterogeneity.Changes in CO 2 concentration or the accompanying pH may affect airways, parenchyma or vessels directly or indirectly through modulation of effector substances such as prostaglandins [6] or calcium [7]. Of considerable interest, also, is nitric oxide, which is ...

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“…Thus, SF 6 , being the least soluble and second heaviest of the six MIGET gases, will correspondingly exhibit the lowest intravascular diffusivity, which, in the presence of an increased intravascular distance, may be sufficient to result in its failure to achieve equilibration within the blood phase and, hence, between blood and alveolar gas. Indeed, consistent with this proposed mechanism is the simple but pertinent observation that, when compared with more soluble inert gases, SF 6 takes a substantially longer time to achieve complete pressure equilibration when exposed to a body of blood in a closed system [25]. There is also experimental evidence that, even in the normal lung, small but measurable diffusion limitation does occur for the respiratory elimination of some intravenously infused inert gases [26].…”

Section: Discussionmentioning

confidence: 71%

Pulmonary vascular dilatation and diffusion-dependent impairment of gas exchange in liver cirrhosis

Crawford¹,

Regnis²,

Laks³

et al. 1995

Eur Respir J

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the actual presence of diffusion-limitation for oxygen. Thus, significant inequality of alveolar ventilationperfusion ratios (V'A/Q') could equally explain a marked improvement in arterial Pa,O 2 with 100% oxygen breathing. Indeed, recent studies using the multiple inert gas elimination technique (MIGET), an analysis which can indirectly detect oxygen diffusion-limitation, have attributed the arterial hypoxaemia in patients with liver cirrhosis to V'A/Q' inequality and intrapulmonary shunting [9][10][11]. However, none of these MIGET studies has providedany direct evidence of actual pulmonary vascular dilatation; and, hence, they do not, by themselves, invalidate the specific hypothesis that diffusionlimitation for oxygen can occur as a direct consequence of abnormal dilatation of interalveolar vessels.To adequately test the above hypothesis requires an experimental approach that has the power to simultaneously Eur Respir J, 1995, 8, 2015-2021 DOI: 10.1183 ABSTRACT: To test the hypothesis that diffusion-limitation for oxygen is due to abnormal vascular dilatation and significantly contributes to the arterial hypoxaemia of liver cirrhosis requires an experimental approach that detects both diffusion-limitation for oxygen and the presence of abnormal dilatation of pulmonary vessels exposed to alveolar gas. We therefore studied the gas exchange of a 64 year old man with alcoholic liver cirrhosis and severe resting arterial hypoxaemia (arterial oxygen tension (Pa,O 2 ) 7.5 kPa) whilst breathing air and 100% O 2 using conventional blood gas (CBG) analysis, the multiple inert gas elimination technique (MIGET) and whole body scintigraphy (WBS) following the i.v. administration of radiolabelled boli of macroaggregates with a minimum diameter of 15 µM.During air breathing, there was a consistently positive difference between the arterial oxygen tension predicted by MIGET and that actually measured (P-M Pa,O 2 , average 0.9 kPa). During O 2 breathing, P-M Pa,O 2 became negative, (average -12.2 kPa), and shunt estimated by the O 2 method (% of Q') was consistently less than that measured by MIGET. Whereas both O 2 method and MIGET estimates of shunt never exceeded 25%, the WBS shunt was 40%, indicating that a substantial fraction of cardiac output flowed through abnormally dilated pulmonary vessels, some of which were exposed to alveolar gas and, hence, participated in gas exchange.Although our observations pertain to one subject, we believe they provide the most convincing in vivo evidence to date that abnormal dilatation of interalveolar vessels may, per se, result in a significant diffusion impairment for O 2 . Furthermore, in view of the consistently negative P-M Pa,O 2 observed during oxygen breathing, we speculate that such abnormal vascular dilatation may also have produced a significant diffusive impairment of one or more of the less soluble inert gases used in the MIGET analysis. Eur Respir J., 1995Respir J., , 8, 2015Respir J., -2021

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Simultaneous measurement of eight foreign gases in blood by gas chromatography

Cited by 329 publications

References 0 publications

CO ₂ signaling in guard cells: Calcium sensitivity response modulation, a Ca ²⁺ -independent phase, and CO ₂ insensitivity of the gca2 mutant

CO ₂ signaling in guard cells: Calcium sensitivity response modulation, a Ca ²⁺ -independent phase, and CO ₂ insensitivity of the gca2 mutant

Pulmonary NO synthase inhibition and inspired CO2: effects on V ′/Q ′ and pulmonary blood flow distribution

Pulmonary vascular dilatation and diffusion-dependent impairment of gas exchange in liver cirrhosis

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Simultaneous measurement of eight foreign gases in blood by gas chromatography

Cited by 329 publications

References 0 publications

CO 2 signaling in guard cells: Calcium sensitivity response modulation, a Ca 2+ -independent phase, and CO 2 insensitivity of the gca2 mutant

CO 2 signaling in guard cells: Calcium sensitivity response modulation, a Ca 2+ -independent phase, and CO 2 insensitivity of the gca2 mutant

Pulmonary NO synthase inhibition and inspired CO2: effects on V ′/Q ′ and pulmonary blood flow distribution

Pulmonary vascular dilatation and diffusion-dependent impairment of gas exchange in liver cirrhosis

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Product

Resources

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CO ₂ signaling in guard cells: Calcium sensitivity response modulation, a Ca ²⁺ -independent phase, and CO ₂ insensitivity of the gca2 mutant

CO ₂ signaling in guard cells: Calcium sensitivity response modulation, a Ca ²⁺ -independent phase, and CO ₂ insensitivity of the gca2 mutant