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R Gäbler

Publications and source records attributed to R Gäbler.

10 recordsLinked to original sources
PubMed2005

Real-time detection of nitric oxide isotopes in lung function tests.

In lung function tests, the determination of the pulmonary diffusing capacity (D) using the single-breath method is a commonly applied technique. The calculation of D is performed on the basis of accurate measurements of indicator gas concentrations. In this chapter, we demonstrate the appropriateness of the stable nitric oxide (NO) isotopes 14NO and 15NO in revealing reliable data of D. We performed studies on animals (14NO) by using respiratory mass spectrometry (M3) and on humans (15NO) by applying laser magnetic resonance spectroscopy (LMRS). The equipment was characterized by sufficient detection limits of 70 parts/billion at [14NO] = 0.001% (M3) and 40 parts/billion at [15NO] = 0.002 % (LMRS), respectively. Lastly, we were able to show that D-values for 14NO indeed reveal the entire diffusive properties of the alveolar-capillary membrane and that 15NO is a useful indicator gas for reflecting disturbances of pulmonary gas exchange.

Animals↗
PubMed2004

Pulmonary 15NO uptake in interstitial lung disease.

Because lung nitric oxide (NO) diffusing capacity (DL) represents alveolar-capillary gas diffusion, we queried as to whether disturbances of pulmonary gas exchange in interstitial lung disease (ILD) are appropriately reflected by using NO. In this pilot study, we applied the (15)N-labeled stable isotope (15)NO (relative abundance 0.37% of total NO) in order to ignore the endogenous NO production. In 10 ILD-outpatients, we measured DL (15)NO by performing the single-breath method. Lung function parameters as well as arterial oxygen partial pressure (PaO(2)) were also tested. Values of DL (15)NO ranged within 50-151 ml (15)NO/(mmHg min). Ratios of DL (15)NO/reference were between 43 and 108% of predicted data as taken from our previous work on healthy volunteers [Eur. J. Physiol. 446 (2003) 256]. We found a significant reduction of DL (15)NO/reference in five patients. Additionally, values of PaO(2) were significantly correlated to ratios of DL (15)NO/reference (adjusted R2 +/-SEE=0.407+/-8.051). In conclusion, (15)NO represents an appropriate indicator gas for reflecting an ILD-induced impairment of alveolar-capillary gas exchange.

Adult↗
PubMed2003

Pulmonary 15NO uptake in man.

Nitric oxide (NO) is commonly thought to reveal more precise values of pulmonary gas uptake through alveolar-capillary membranes (DL) than the normally used carbon monoxide (CO). Since such measurements are influenced by a significant endogenous NO delivery within human airways, we propose the use of the naturally occurring (15)N-labelled stable nitric oxide isotope (15)NO. It occurs with a relative abundance of 0.37% of the dominating isotope (14)NO. Therefore, the endogenous (15)NO production can be neglected. In the present pilot study we demonstrate the workability of (15)NO in determining DL in healthy individuals. In seven female and 15 male volunteers, averaged values of DL increase with increasing mean alveolar volume as well as individual body height ( P=0.000001). Due to the very high significance level obtained from the multiple regression analysis, we conclude that the application of (15)NO establishes a novel approach to calculate standard values of DL. Such calculations can be employed to predict a reference for patients who suffer from pulmonary diffusion limitation.

Adolescent↗
PubMed2000

Herbivore-induced ethylene suppresses a direct defense but not a putative indirect defense against an adapted herbivore.

Herbivory induces both direct and indirect defenses in plants; however, some combinations of these defenses may not be compatible. The jasmonate signal cascade activated both direct (nicotine accumulations) and indirect (mono- and sesquiterpene emissions) whole-plant defense responses in the native tobacco Nicotiana attenuata Torr. Ex Wats. Nicotine accumulations were proportional to the amount of leaf wounding and the resulting increases in jasmonic acid (JA) concentrations. However, when larvae of the nicotine-tolerant herbivore, Manduca sexta, fed on plants or their oral secretions were applied to leaf punctures, the normal wound response was dramatically altered, as evidenced by large (4- to 10-fold) increases in the release of (i) volatile terpenoids and (ii) ethylene, (iii) increased (4- to 30-fold) accumulations of endogenous JA pools, but (iv) decreased or unchanged nicotine accumulations. The ethylene release, which was insensitive to inhibitors of induced JA accumulation, was sufficient to account for the attenuated nicotine response. Applications of ethylene and ethephon suppressed the induced nicotine response and pre-treatment of plants with a competitive inhibitor of ethylene receptors, 1-methylcyclopropene, restored the full nicotine response. This ethylene burst, however, did not inhibit the release of volatile terpenoids. Because parasitoids of Manduca larvae are sensitive to the dietary intake of nicotine by their hosts, this ethylene-mediated switching from direct to a putative indirect defense may represent an adaptive tailoring of a plant's defense response.

Acetates↗
PubMed1997

Cellulysin from the plant parasitic fungus Trichoderma viride elicits volatile biosynthesis in higher plants via the octadecanoid signalling cascade.

Cellulysin, a crude cellulase from the plant parasitic fungus Trichoderma viride, induces the biosynthesis of volatiles in higher plants (Nicotiana plumbaginifolia, Phaseolus lunatus, and Zea mays) when applied to cut petioles by the transpiration stream. The pattern of the emitted volatiles largely resembles that from a herbivore damage or treatment of the plants with jasmonic acid (JA) indicating that cellulysin acts via activation of the octadecanoid signalling pathway. The treatment with cellulysin raises the level of endogenous JA after 30 min and is followed by a transient emission of ethylene after 2-3 h. Volatile production becomes significant after 12-24 h. Inhibitors of the JA pathway effectively block the cellulysin-dependent volatile biosynthesis.

Cellulase↗