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The design of an electrochemical permeation device on a tensile machine has allowed to control the hydrogen flux and to isolate the effects of trapped and mobile hydrogen on the hydrogen embrittlement of a martensitic steel. Based on a local approach of fracture, tensile tests on several notched specimens were completed in order to investigate the impact of hydrostatic stress, equivalent plastic strain, hydrogen concentration and flux on the damage processes. Analysis of the fracture surfaces revealed that trapped hydrogen favors ductile fracture, enhancing nucleation and growth of voids by reducing the interface energy between precipitates/inclusions and matrix. Mobile hydrogen leads to quasi-cleavage along the substructure (lath and/or blocks) boundaries at mainly the {101} planes. For both mechanisms, the mutual interaction between hydrogen and dislocations (drag process increasing hydrogen diffusion and hydrogen favoring dislocations mobility) has a large contribution to the hydrogen embrittlement of the martensitic steel. Image, graphical abstract [ABSTRACT FROM AUTHOR]

A specific dependency of elastic tensile stress on the hydrogen solubility is identified for martensitic steels. The lattice hydrogen concentration under applied stress may be underestimated when predicted by a classical law which associates hydrostatic stress with the partial molar volume of hydrogen. We have explored the impact of elastic distortions on hydrogen solubility from two different sources: internal stresses arising from heterogeneous microstructures and elastic fields around vacancy clusters. Only the latter seems to be in reasonable agreement with our results. [ABSTRACT FROM AUTHOR]

Understanding hydrogen transport and trapping phenomena is a key feature to revisit the hydrogen embrittlement (HE) models proposed in the literature. Both aspects can be affected by stress-strain states at different microstructural scales. Elastic distortion and plastic strain are both aspects of the mechanical states associated with defects (vacancies, dislocations), metallurgical elements (grain boundaries, precipitates), internal stresses and applied stresses, which can modify the diffusion and solubility of hydrogen. In the present work we first explore the effects of a tensile stress applied on martensitic steel membrane on the hydrogen concentration and mobility. In a second part, we analyse the impact of mobile and trapped hydrogen on HE using local approach of fracture under hydrogen flux. [ABSTRACT FROM AUTHOR]

Cardiovascular effects of an essential oil from the aerial parts of Mentha x villosa (OEMV) were tested in rats using a combined in vivo and in vitro approach. In non-anesthetized normotensive rats, OEMV (1, 5, 10, 20, 30 mg kg(-1) body wt., i.v.) induced a significant and dose-dependent hypotension (-3 +/- 1.8%; -6 +/- 0.7%; -40 +/- 6.7%; -58 +/- 3.8%; -57 +/- 2.1%, respectively) associated with decreases in heart rate (-1 +/- 0.3%; -9 +/- 0.9%; -17 +/- 3.2%; -72 +/- 3.1%; -82 +/- 1.4%, respectively). The hypotensive and bradycardic responses evoked by OEMV were attenuated and blocke by pre-treatment of the animals with atropine (2 mg kg(-1) body wt., i.v.). In isolated rat atrial preparations, OEMV (10, 100, 300, 500 microg ml(-1)) produced concentration-related negative chronotropic and inotropic effects (IC50 value = 229 +/- 17 and 120 +/- 13 microg ml(-1), respectively). In isolated rat aortic rings, increasing concentrations of OEM (10, 100, 300, 500 microg ml(-1)) were able to antagonize the effects of phenylephrine (1 microM), prostaglandin F2alpha (10 microM) and KCl (80 mM)-induced contractions (IC50 value = 255 +/- 9, 174 +/- 4 and 165 +/- 14 microg ml(-1), respectively). The vasorelaxant activity induced by OEMV was attenuated significantly by either endothelium removal (IC50 value = 304 +/- 9 microg ml(-1)), NG-nitro L-arginine methyl ester (L-NAME) 100 microM (IC50 value=359 +/- 18 microg ml(-1)), L-NAME 300 microM (IC50 value = 488 +/- 20 microg ml(-1)) or indomethacin 10 microM (IC50 value = 334 +/- 18 microg ml(-1)). However, it was not affected by atropine 1 microM (IC50 value = 247 +/- 12 microg ml(-1)). Furthermore, the hypotensive response induced by OEMV was attenuated significantly after nitric oxide (NO) synthase blockade (L-NAME, 20 mg kg(-1) body wt., i.v.), while bradycardia was not altered. The results suggest that the hypotensive effect induced by OEMV is probably due to its direct cardiodepressant action and peripheral vasodilation, which can be attributed to both endothelium-dependent (via EDRFs, at least NO and prostacyclin) and endothelium-independent mechanisms (such as Ca2+ channel blockade). [ABSTRACT FROM AUTHOR]