Characterization and In Vitro Behavior of PEO Coated Mg Modified with Antibacterial Ag(I) and Cu(II) Complexes.

The use of Mg-based biomaterials with a number of their advantageous properties are overshadowed by uncontrollable metal corrosion. Moreover, the use of implants goes alongside with the threat of pathogens-associated complications. In this study, PEO coated Mg biomaterial loaded with antibacterial Ag(I) and Cu(II) complexes is produced and tested to meet both appropriate protective characteristics as well as sufficient level of antibacterial activity. To achieve a suitable level of anticorrosion protection phosphate and fluoride-phosphate electrolytes are used in the PEO process. Investigation of the surface thickness and morphology done by means of cross-section analysis and scanning electron microscopy (SEM), as well as electrochemical impedance spectroscopy (EIS) assay show precedence of the fluoride containing PEO coating and make it the material of choice for further modification with Ag(I) and Cu(II) complexes. The presence of the complexes on the PEO surface is confirmed by energy dispersive X-ray spectroscopy (EDX). X-ray photoelectron spectroscopy (XPS), transmission electron microscopy (TEM) and glow discharge optical emission spectroscopy (GDOES) are used to estimate the complexes' chemical state and depth of penetration in the coating surface. Based on the results of antibacterial assay, the modified coatings are found to be active against both Gram-positive and Gram-negative bacteria.

Bone cells influence the degradation interface of pure Mg and WE43 materials: Insights from multimodal in vitro analysis.

In this study, the interaction of pure Mg and WE43 alloy under the presence of osteoblast (OB) and osteoclast (OC) cells and their influence on the degradation of materials have been deeply analyzed. Since OB and OC interaction has an important role in bone remodeling, we examined the surface morphology and dynamic changes in the chemical composition and thickness of the corrosion layers formed on pure Mg and WE43 alloy by direct monoculture and coculture of pre-differentiated OB and OC cells in vitro. Electrochemical techniques examined the corrosion performance. The corrosion products were characterized using a combination of the focused ion beam (FIB), scanning electron microscopy (SEM), and energy-dispersive X-ray spectroscopy (EDX). Cell viability and morphology were assessed by fluorescent microscopy and SEM. Our findings demonstrate cell spread and attachment variations, which differ depending on the Mg substrates. It was clearly shown that cell culture groups delayed degradation processes with the lowest corrosion rate observed in the presence of OBOC coculture for the WE43 substrate. Ca-P enrichment was observed in the outer-middle region of the corrosion layer but only after 7 days of OBOC coculture on WE43 and after 14 days on the pure Mg specimens. STATEMENT OF SIGNIFICANCE: Magnesium metallic materials that can degrade over time provide distinct opportunities for orthopedic application. However, there is still a lack, especially in elucidating cell-material interface characterization. This study investigated the influence of osteoblast-osteoclast coculture in direct Mg-material contact. Our findings demonstrated that pre-differentiated osteoblasts and osteoclasts cocultured on Mg substrates influenced the chemistry of the corrosion layers. The cell spread and attachment were Mg substrate-dependent. The findings of coculturing bone cells directly on Mg materials within an in vitro model provide an effective approach for studying the dynamic degradation processes of Mg alloys while also elucidating cell behavior and their potential contribution to the degradation of these alloys.

Tetrastarch sustains pulmonary microvascular perfusion and gas exchange during systemic inflammation.

OBJECTIVE: According to Fick's law of diffusion, gas exchange depends on the size and thickness of the blood perfused alveolocapillary membrane. Impairment of either one is tenuous. No data are available concerning the impact of hydroxyethyl starches and saline on pulmonary microperfusion and gas exchange during systemic inflammation. DESIGN: Prospective, randomized, controlled experimental study. SETTING: University research laboratory. SUBJECTS: Thirty-two anesthetized rabbits assigned to four groups (n = 8). INTERVENTIONS: Except for the control group, systemic inflammation was induced by lipopolysaccharide. Fluid resuscitation was performed with saline alone or in conjunction with tetrastarch or pentastarch. Pulmonary microcirculation was analyzed at 0 hr and 2 hrs using intravital microscopy. Thickness of the alveolocapillary membrane was measured using electron microscopy. MEASUREMENTS AND MAIN RESULTS: Macrohemodynamics were stable in all groups. In pulmonary arterioles, lipopolysaccharide reduced the erythrocyte velocity and impeded the microvascular decrease of the hematocrit in the saline and pentastarch group. In contrast, infusion of tetrastarch normalized these perfusion parameters. In capillaries, lipopolysaccharide decreased the functional capillary segment density and the capillary perfusion index, which was prevented by both starches. However, compared with saline and pentastarch, treatment with tetrastarch prevented the lipopolysaccharide-induced reduction of the capillary erythrocyte flux and inversely reduced the erythrocyte capillary transit time. Thickening of alveolocapillary septae after lipopolysaccharide application was solely observed in the saline and pentastarch group. In contrast to pentastarch and saline, the application of tetrastarch prevented the lipopolysaccharide-induced increase of the alveoloarterial oxygen difference. CONCLUSIONS: Tetrastarch sustains pulmonary gas exchange during experimental systemic inflammation more effectively than saline and pentastarch by protecting the diffusion distance and the size of the microvascular gas exchange surface. Improved capillary perfusion resulting from tetrastarch therapy, which is typically applied to increase blood pressure, may according to the Ohm's law locally decrease hydrostatic perfusion pressures in the pulmonary microvasculature during systemic inflammation.

Glycocalyx degradation causes microvascular perfusion failure in the ex vivo perfused mouse lung: hydroxyethyl starch 130/0.4 pretreatment attenuates this response.

The endothelial glycocalyx (GLX) is pivotal to vascular barrier function. We investigated the consequences of GLX degradation on pulmonary microvascular perfusion and, prompted by evidence that hydroxyethyl starch (HES) improves microcirculation, studied the effects of two HES preparations during GLX diminution. C57 BL/6 black mice lungs were explanted and perfused with 1-mL/min buffer solution containing autologous erythrocytes (red blood cells) at a hematocrit of 5%. Microvessel perfusion was quantified by video fluorescence microscopy at 0 and 90 min. To register interstitial edema, alveolar septal width was quantified. Pulmonary artery pressure (PAP), airway pressure, and left atrial pressure were recorded continuously. Lungs were randomly assigned to four groups (each n = 5): (i) control: no treatment, (ii) HEP1: heparinase I (1 mU/mL) was injected for GLX degradation, (iii) HES 130, and (iv) HES 200: one third of perfusion fluid was exchanged for 6% HES 130/0.4 or 10% HES 200/0.5 before GLX degradation. Analysis of variance on ranks and pairwise multiple comparisons were used for statistics, P < 0.05. Compared with control, GLX degradation effected perfusion failure in microvessels, increased PAP, and facilitated interstitial edema formation after a 90-min period of perfusion. In contrast to HES 200/0.5, pretreatment with HES 130/0.4 attenuated all of these consequences. Sequelae of GLX degradation in lung include perfusion failure in microvessels, interstitial edema formation, and increase in PAP. We assume that these effects are a consequence of vascular barrier dysfunction. Beneficial effects of HES 130/0.4 are presumably a result of its lower red blood cell bridging capacity compared with HES 200/0.5.