TY - JOUR A1 - Lehmann, Martin A1 - Oehler, Beatrice A1 - Zuber, Jonas A1 - Malzahn, Uwe A1 - Walles, Thorsten A1 - Muellenbach, Ralf M. A1 - Roewer, Norbert A1 - Kredel, Markus T1 - Redistribution of pulmonary ventilation after lung surgery detected with electrical impedance tomography JF - Acta Anaesthesiologica Scandinavica N2 - Background: Regional ventilation of the lung can be visualized by pulmonary electrical impedance tomography (EIT). The aim of this study was to examine the post‐operative redistribution of regional ventilation after lung surgery dependent on the side of surgery and its association with forced vital capacity. Methods: In this prospective, observational cohort study 13 patients undergoing right and 13 patients undergoing left‐sided open or video‐thoracoscopic procedures have been investigated. Pre‐operative measurements with EIT and spirometry were compared with data obtained 3 days post‐operation. The center of ventilation (COV) within a 32 × 32 pixel matrix was calculated from EIT data. The transverse axis coordinate of COV, COVx (left/right), was modified to COVx′ (ipsilateral/contralateral). Thus, COVx′ shows a negative change if ventilation shifts contralateral independent of the side of surgery. This enabled testing with two‐way ANOVA for repeated measurements (side, time). Results: The perioperative shift of COVx′ was dependent on the side of surgery (P = .007). Ventilation shifted away from the side of surgery after the right‐sided surgery (COVx′‐1.97 pixel matrix points, P < .001), but not after the left‐sided surgery (COVx′‐0.61, P = .425). The forced vital capacity (%predicted) decreased from 94 (83‐109)% (median [quartiles]; [left‐sided]) and 89 (80‐97)% (right‐sided surgery) to 61 (59‐66)% and 62 (40‐72)% (P < .05), respectively. The perioperative changes in forced vital capacity (%predicted) were weakly associated with the shift of COVx′. Conclusion: Only after right‐sided lung surgery, EIT showed reduced ventilation on the side of surgery while vital capacity was markedly reduced in both groups. KW - electrical impedance tomography KW - general anaesthesia KW - one‐lung ventilation KW - postoperative complications KW - pulmonary function tests KW - pulmonary surgical procedures Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-213575 VL - 64 IS - 4 ER - TY - JOUR A1 - Oehler, Beatrice A1 - Kloka, Jan A1 - Mohammadi, Milad A1 - Ben-Kraiem, Adel A1 - Rittner, Heike L. T1 - D-4F, an ApoA-I mimetic peptide ameliorating TRPA1-mediated nocifensive behaviour in a model of neurogenic inflammation JF - Molecular Pain N2 - Background High doses of capsaicin are recommended for the treatment of neuropathic pain. However, low doses evoke mechanical hypersensitivity. Activation of the capsaicin chemosensor transient receptor potential vanilloid 1 (TRPV1) induces neurogenic inflammation. In addition to the release of pro-inflammatory mediators, reactive oxygen species are produced. These highly reactive molecules generate oxidised phospholipids and 4-hydroxynonenal (4-HNE) which then directly activate TRP ankyrin 1 (TRPA1). The apolipoprotein A-I mimetic peptide D-4F neutralises oxidised phospholipids. Here, we asked whether D-4F ameliorates neurogenic hypersensitivity in rodents by targeting reactive oxygen species and 4-HNE in the capsaicin-evoked pain model. Results Co-application of D-4F ameliorated capsaicin-induced mechanical hypersensitivity and allodynia as well as persistent heat hypersensitivity measured by Randell–Selitto, von Frey and Hargreaves test, respectively. In addition, mechanical hypersensitivity was blocked after co-injection of D-4F with the reactive oxygen species analogue H2O2 or 4-HNE. In vitro studies on dorsal root ganglion neurons and stably transfected cell lines revealed a TRPA1-dependent inhibition of the calcium influx when agonists were pre-incubated with D-4F. The capsaicin-induced calcium influx in TRPV1-expressing cell lines and dorsal root ganglion neurons sustained in the presence of D-4F. Conclusions D-4F is a promising compound to ameliorate TRPA1-dependent hypersensitivity during neurogenic inflammation. KW - TRPA1 KW - capsaicin KW - reactive oxygen species KW - oxidised lipids KW - pain KW - targeting Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-236061 VL - 16 ER -