An electrochemical nitric oxide generator for in-home inhalation therapy in pulmonary artery hypertension

Figures

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  Fig. 1. Design, configuration, and schematic of a novel ENG model. A Appearance, size, and configuration of the ENG. B Detailed positioning of each unit inside the highly integrated NO generator. C Schematic diagram of the ENG that consists of 4 sequentially connected units and two work modes controlled by a switch valve. The NO generator was connected to the ventilator pipeline and supervised by the circuit board

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  Fig. 2. NO production and NO2 monitoring with the ENG. A NO concentration monitoring in the solution with different levels of applied current. B The linear relationship between the calibrated NO concentration and applied currents. C NO levels generated for five consecutive time periods. D NO2 levels under therapeutic doses of NO

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  Fig. 3. Establishment of a porcine PAH model. A EVG elastic staining of the lungs shows the pathological changes in piglets with MCT-induced PAH and the vehicle-treated group. The arrows indicate uneven thickening of the middle layer of the pulmonary arteries, with lumen stenosis, muscularized pulmonary arterioles, and lung interstitial thickening with inflammatory cell infiltration. B Immunofluorescence staining of Ki67 and α-SMA in paraffin-embedded sections of lung tissue from piglets with MCT-induced PAH or the vehicle-treated group. Scale bars, 50 μm. C H&E staining and Masson staining of the right ventricular myocardium of piglets with MCT-induced PAH or the vehicle-treated group. Scale bars, 50 μm for H&E staining and 100 μm for Masson staining. D EVG staining of the tunica media of the main pulmonary artery of piglets with MCT-induced PAH or the vehicle-treated group. Scale bars, 2 mm. E Representative images and quantification of eNOS expression in the lung tissues of piglets with MCT-induced PAH or the vehicle-treated group by western blotting. F Hemodynamic data for the pulmonary circulation, including sPAP, dPAP, mPAP, SV, CO, CI, PVR, and PVRI, were measured and calculated…

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  Fig. 4. The ENG effectively alleviated hypoxemia and improved pulmonary hemodynamics in the porcine PAH model. A A schematic of the connection of the ENG to the ventilator and the acquisition of hemodynamic data. B Western blotting for sGC and PKG in the lung tissues of piglets with PAH in the presence or absence of NO inhalation (n=6/group). C PaO2 detection in piglets with PAH in the presence or absence of NO inhalation or the sham group at the indicated timepoint (n=6/group). D–F The measurement of PAP (D); SV, CO, and CI (E); and PVR and PVRI (F). * P<0.05, ** P<0.01; compared to the PAH group, as analyzed by Student’s t test (B) or two-way ANOVA with repeated measures (C–F)

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  Fig. 5. Examination of physiological indicators and lung pathology after NO inhalation with the ENG. A–D Comparison of blood cells (A); hepatic and renal function (B); procoagulant function (C); and methemoglobin (D) between piglets with PAH treated with the ENG and those not treated with the ENG; compared to the PAH group, as analyzed by Student’s t test. E H&E staining of paraffin sections of bronchioles (scale bars, 500 μm) and terminal bronchi (scale bars, 50 μm)