RDW is elevated in overweight and reflects the inflammatory state. RDW potentially represents an additional and cost-effective tool to indicate inflammation. Future studies are needed to understand the differential influences of nutrition and overweight on RDW.

Objectives: Orthogonal polarized spectral imaging-and sidestream darkfield-technique have enabled visual evaluation of the microcirculation. Different investigators described microcirculatory alterations, especially in surgical patients suffering from septic shock. We investigated the sublingual microcirculation in non-surgical patients admitted to our medical, intensive care unit (ICU).Methods: In 24 severely ill (APACHE-II Score: 27.8 ± 11.3), intubated patients admitted to our ICU the sublingual microcirculation was recorded with a handheld intravital microscope. Sublingual vessels were categorized according to their size (small: 10-25 µm; medium: 26-50 µm; large: 51-100 µm) and the flow in semiquantitative categories (0: no flow; 1: intermittent flow; 2: sluggish flow; 3: continuous flow).Results: Patients with cardiogenic shock (n = 7) had lower microflow compared with patients without cardiogenic shock (small p < 0.001, medium p < 0.001, large p = 0.003). Several other diseases, including diabetes and arterial hypertension, age, gender, had no influence. In general, patients with a flow less than 3 in the small vessels showed higher arterial blood lactate levels (p = 0.043) compared to continuous flow.Conclusions: A consequence of cardiogenic shock is the impairment of microcirculation with organ hypoperfusion. We observed that cardiac output is correlated to disturbance in microflow in the smallest vessels. On-line evaluation of microcirculation in vivo may be a valid tool for optimizing therapeutic measures in high risk patients.Additional online material may be found at: http://www.kim1.uniklinik-jena.de/Microcirculation.html.

Degenerative aortic stenosis (AS) is the most frequent form of acquired valvular heart disease. AS is known to entail endothelial dysfunction caused by increased mechanical shear stress leading to elevated circulatory levels of microparticles. Endothelial and platelet microparticles (EMP and PMP) are small vesicles that originate from activated cells and thrombocytes. We sought to evaluate whether transcatheter aortic valve implantation (TAVI) procedure would elicit effects on circulating EMP and PMP. 92 patients undergoing TAVI procedure for severe AS were included in this study. Samples were obtained at each visit before TAVI, 1 week post-procedure and at 1, 3 and after 6 months after TAVI and were evaluated using flow cytometry. A 12 month clinical follow-up was also performed. CD62E+ EMP concentration before TAVI was 21.11 % (±6.6 % SD) and declined to 20.99 % (±6.8 % SD) after 1 week, to 16.63 % (±5.4 % SD, p < 0.0001) after 1 month, to 17.08 % (±4.6 % SD, p < 0.0001) after 3 months and to 15.94 % (±5.4 % SD, p < 0.0001) after 6 months. CD31+/CD42b−, CD31+/Annexin+/− EMP remained unchanged. CD31+/CD41b+ PMP evidenced a slight, but statistically significant increase after TAVI and remained elevated during the entire follow-up. Apart from a procedure-related improvement in echocardiographic parameters, TAVI procedure led also to a decline in CD62E+ EMP. The reduction in pressure gradients with less hemodynamic shear stress seems also to have beneficially affected endothelial homeostasis.Electronic supplementary materialThe online version of this article (doi:10.1007/s00380-016-0885-z) contains supplementary material, which is available to authorized users.

These experimental results show that temporary hypoxic conditions can trigger the release of CD31+/ Annexin+ EMP also in healthy volunteers. In our previous studies we have shown that apoptotic bodies can confer pro-survival signals to cardiomyocytes during myocardial ischemia. Based on the experimental results of this current study we believe that the release of CD31+/Annexin+ EMP during hypoxia might act as an endogenous survival signal.

Hypoxia frequently associated with certain physiologic and pathologic conditions influences numerous cellular functions. Because the effects of short-term hypoxia are incompletely understood, we examined phagocytosis and cytokine production as well as the activation of the transcription factors HIF-1 and NFκB in peripheral blood cells of healthy volunteers exposed to an oxygen concentration equivalent to that found at a height of 5500 m. Furthermore, we analysed plasma HIF-1 and serum concentrations of various HIF-1-dependent genes. Results showed that short-term hypoxia increased phagocytosis in neutrophils without affecting monocyte phagocytosis. Hypoxia decreased basal TNFα concentration in monocytes and basal interferon γ concentration in CD4+ T lymphocytes. In contrast, plasma HIF and serum VEGF concentrations were not affected by hypoxia, although serum EPO concentration was raised. In PBMC, hypoxia increased cytosolic HIF-1 concentration without affecting nuclear HIF-1 concentration and led to a rise in the nuclear NFκB in PBMC. Our results show that short-term hypoxia affects immune functions in healthy individuals. Furthermore, we speculate that the effects of hypoxia are not due to HIF-1, but are caused by the activation of NFκB .