1,721,009 research outputs found
Injurious mechanical ventilation causes kidney apoptosis and dysfunction during sepsis but not after intra-tracheal acid instillation: an experimental study
No full textBackground: Intratracheal aspiration and sepsis are leading causes of acute lung injury that frequently necessitate mechanical ventilation (MV), which may aggravate lung injury thereby potentially increasing the risk of acute kidney injury (AKI). We compared the effects of ventilation strategies and underlying conditions on the development of AKI. Methods: Spraque Dawley rats were challenged by intratracheal acid instillation or 24 h of abdominal sepsis, followed by MV with a low tidal volume (LVT) and 5 cm H2O positive end-expiratory pressure (PEEP) or a high tidal volume (HVT) and no PEEP, which is known to cause more lung injury after acid instillation than in sepsis. Rats were ventilated for 4 hrs and kidney function and plasma mediator levels were measured. Kidney injury was assessed by microscopy; apoptosis was quantified by TUNEL staining. Results: During sepsis, but not after acid instillation, MV with HVT caused more renal apoptosis than MV with LVT. Increased plasma active plasminogen activator inhibitor-1 correlated to kidney apoptosis in the cortex and medulla. Increased apoptosis after HVT ventilation during sepsis was associated with a 40% decrease in creatinine clearance. Conclusions: AKI is more likely to develop after MV induced lung injury during an indirect (as in sepsis) than after a direct (as after intra-tracheal instillation) insult to the lungs, since it induces kidney apoptosis during sepsis but not after acid instillation, opposite to the lung injury it caused. Our findings thus suggest using protective ventilatory strategies in human sepsis, even in the absence of overt lung injury, to protect the kidney
Production of endothelin-1 and reduced blood flow in the rat kidney during lung-injurious mechanical ventilation
No full textINTRODUCTION: The mechanisms by which mechanical ventilation (MV) can injure remote organs, such as the kidney, remain poorly understood. We hypothesized that upregulation of systemic inflammation, as reflected by plasma interleukin-6 (IL-6) levels, in response to a lung-injurious ventilatory strategy, ultimately results in kidney dysfunction mediated by local endothelin-1 (ET-1) production and renal vasoconstriction. METHODS: Healthy, male Wistar rats were randomized to 1 of 2 MV settings (n = 9 per group) and ventilated for 4 h. One group had a lung-protective setting using peak inspiratory pressure of 14 cm H(2)O and a positive end-expiratory pressure of 5 cm H(2)O; the other had a lung-injurious strategy using a peak inspiratory pressure of 20 cm H(2)O and positive end-expiratory pressure of 2 cm H(2)O. Nine randomly assigned rats served as nonventilated controls. We measured venous and arterial blood pressure and cardiac output (thermodilution method), renal blood flow (RBF) using fluorescent microspheres, and calculated creatinine clearance, urine flow, and fractional sodium excretion. Histological lung damage was assessed using hematoxylin-eosin staining. Renal ET-1 and plasma ETA and IL-6 concentrations were measured using enzyme-linked immunosorbent assays. RESULTS: Lung injury scores were higher after lung-injurious MV than after lung-protective ventilation or in sham controls. Lung-injurious MV resulted in significant production of renal ET-1 compared with the lung-protective and control groups. Simultaneously, RBF in the lung-injurious MV group was approximateIN 40% lower (P < 0.05) than in the control group and 28%, lower (P < 0.05) than ill the lung-protective,e group. Plasma ET-1 and IL-6 levels did not differ among the groups and systemic hemodynamics, such as cardiac Output, were comparable. There was no effect oil creatinine clearance, fractional sodium excretion, urine Output, or kidney histology. CONCLUSIONS: Lung-injurious MV for 4 h in healthy rats results ill significant production of renal ET-1 and in decreased RBF, independent of IL-6. Decreased RBF has no observable effect on kidney function or histology
Mechanical ventilation activates renal endothelial cells in a rat model of acute respiratory distress syndrome
No full textBench-to-bedside review: Ventilation-induced renal injury through systemic mediator release - just theory or a causal relationship?
No full textTHE ROLE OF POLY(ADP-RIBOSE) POLYMERASE 1 (PARP-1) IN ACUTE RENAL FAILURE ASSOCIATED WITH VENTILATOR INDUCED LUNG INJURY
No full textINTRODUCTION. Mechanical ventilation (MV) is a life-saving therapy for many patients
with respiratory failure but has detrimental consequences resulting in ventilator-induced lung
injury (VILI). MV can potentially lead to the development of an overwhelming inflammatory
response and multiple organ dysfunction syndrome (MODS). Acute renal failure (ARF) is the
most prevalent form of organ dysfunction in patients treated with MV. However, the factors
leading from mechanical stress to the initiation and propagation of VILI and ARF remain
uncertain. Poly (ADP-ribose) polymerase (PARP) enzyme has been shown to be overactivated
during VILI. Pharmacological inhibition of PARP by PJ-34 reduced lung injury and preserved
kidney function with a decreased renal apoptosis. We hypothesized that pharmacological
inhibition of PARP by PJ-34 mitigates kidney dysfunction by preserving endothelium
function.
METHODS. 24 Sprague Dawley rats (weight 310 ± 10 g) received intratracheal instillation
of lipopolysaccharide at 10 mg/kg, followed by 3.5 hrs mechanical ventilation with either
high tidal volume (Vt) of 19 ml/kg and PEEP 0 cmH 2 O (HV) in the presence or absence of
the PARP inhibitor PJ-34, or low Vt of 6 ml/kg and PEEP 5 cmH 2 O (LV) serving as a control
group. Arterial blood gases, hemodynamic measurements and urinary output were analyzed
hourly. Renal blood flow was assessed at the beginning and at the end of the experiment.
Kidney interlobar arteries were isolated thereafter and endothelium dependent vasodilation
was tested by incubating the arteries with acetylcholine.
RESULTS. As expected, we found that lung injury was increased in the HV group compared
to the LV group and PJ-34 treatment mitigates lung dysfunction in HV group. Kidney
endothelium function was tested by its ability to induce dilatation after acetylcholine stim-
ulation. Interlobar renal arteries isolated from the HV group showed an impaired ability to
dilate compared to the LV group. Endothelium dysfunction was also associated with reduction
in renal blood flow of approximately 80% in the HV group compared to the LV group and
with decreased urine production. Treatment with PJ-34 restored vascular reactivity, renal
blood flow, and preserved urine production. PJ-34 protective effect is probably due to its
ability to reduce NF-kB as shown by a decreased intensity of NF-kB nuclear staining in
kidney sections in PJ-34 treated group.
CONCLUSION. Application of PJ-34 reduces kidney dysfunction in a rat model of VILI by
preserving endothelium function, probably reducing NF-kB activation. Our study suggests a
novel potential therapeutic approach to mitigate the consequences of VILI by using the PARP
inhibitors.
GRANT ACKNOWLEDGEMENT. ECCRN Basic Science Award 2006
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Ventilator-induced coagulopathy in experimental Streptococcus pneumoniae pneumonia
No full textPneumonia, the main cause of acute lung injury, is characterised by a local pro-inflammatory response and coagulopathy. Mechanical ventilation (MV) is often required. However, MV can lead to additional injury: so-called ventilator-induced lung injury (VILI). Therefore, the current authors investigated the effect of VILI on alveolar fibrin turnover in Streptococcus pneumoniae pneumonia. Pneumonia was induced in rats, followed 48 h later by either lung-protective MV (lower tidal volumes (LVT) and positive end-expiratory pressure (PEEP)) or MV causing VILI (high tidal volumes (HVT) and zero end-expiratory pressure (ZEEP)) for 3 h. Nonventilated pneumonia rats and healthy rats served as controls. Thrombin-antithrombin complexes (TATc), as a measure for coagulation, and plasminogen activator activity, as a measure of fibrinolysis, were determined in bronchoalveolar lavage fluid (BALF) and serum. Pneumonia was characterised by local (BALF) activation of coagulation, resulting in elevated TATc levels and attenuation of fibrinolysis compared with healthy controls. LVT-PEEP did not Influence alveolar coagulation or fibrinolysis. HVT-ZEEP did intensity the local procoagulant response: TATc levels rose significantly and levels of the main inhibitor of fibrinolysis, plasminogen activator inhibitor-1, increased significantly. HVT-ZEEP also resulted in systemic elevation of TATc compared with LVT-PEEP. Mechanical ventilation causing ventilator-induced lung injury increases pulmonary coagulopathy in an animal model of Streptococcus pneumoniae pneumonia and results in systemic coagulopathy
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
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