Biomedical subjects

Bruno Lévy

Publications and source records attributed to Bruno Lévy.

11 recordsLinked to original sources

PubMed2006

Vasopressin or norepinephrine in early hyperdynamic septic shock: a randomized clinical trial.

OBJECTIVE: To compare the effects of arginine-vasopressin (AVP) and norepinephrine (NE) on hemodynamic variables, organ dysfunction, and adverse events in early hyperdynamic septic shock. DESIGN AND SETTING: Randomized, controlled, open-label trial. PATIENTS AND PARTICIPANTS: Twenty-three patients with early (12h) hyperdynamic septic shock in two teaching hospitals. INTERVENTIONS: AVP (0.04-0.20 Umin(-1), n=13) as a single agent or NE (0.1-2.8microg kg(-1)min(-1), n=10) infusion for 48[Symbol: see text]h to achieve mean arterial pressure at or above 70mmHg. MEASUREMENTS AND RESULTS: Hemodynamic parameters and Sequential Organ Failure Assessment (SOFA) score were measured. AVP and NE equally increased mean arterial pressure over 48h, but NE was required in 36% of AVP patients at 48h. Compared to baseline, AVP increased systemic vascular resistance, decreased exposure to NE, decreased cardiac output by decreasing heart rate, increased creatinine clearance, and improved SOFA score. The PrCO(2) - PaCO(2) difference remained stable throughout the study. One AVP patient developed acute coronary syndrome with dose-dependent ECG changes. Three patients in both groups died during their ICU stay. CONCLUSION: In early hyperdynamic septic shock, the administration of high-dose AVP as a single agent fails to increase mean arterial pressure in the first hour but maintains it above 70mmHg in two-thirds of patients at 48h. AVP decreases NE exposure, has no effect on the PrCO(2) - PaCO(2 )difference, and improves renal function and SOFA score.

Arginine↗

PubMed2006

Modulation of the triggering receptor expressed on myeloid cells-1 pathway during pneumonia in rats.

BACKGROUND: Triggering receptor expressed on myeloid cells-1 (TREM-1) is a cell-surface molecule that has been identified on both human and murine polymorphonuclear neutrophils and mature monocytes. The activation of TREM-1 in the presence of microbial components amplifies the inflammatory response and may be responsible for the hyperresponsiveness observed during the initial stage of sepsis. The aim of the present study was to investigate the effect of the modulation of the TREM-1 pathway during experimental pneumonia in rats. METHODS: Adult male Wistar rats were intratracheally inoculated with Pseudomonas aeruginosa (PAO1 strain) and randomly treated or not treated with an analogue synthetic peptide derived from the extracellular moiety of TREM-1 (LP17). RESULTS: P. aeruginosa induced a severe pneumonia associated with signs of severe sepsis within the first 24 h. In septic rats, LP17 improved hemodynamic status, attenuated the development of lactic acidosis and hypoxemia, modulated lung and systemic inflammatory responses and coagulation activation, reduced lung histological damage, and improved survival. CONCLUSIONS: The modulation of the TREM-1 pathway by the use of such synthetic peptides as LP17 appears beneficial during P. aeruginosa pneumonia in rats in attenuating lung and systemic inflammatory responses.

Amino Acid Sequence↗

PubMed2006

Outcome value of Clara cell protein in serum of patients with acute respiratory distress syndrome.

OBJECTIVE: Injury to the alveolocapillary barrier characterizes ALI/ARDS; therefore determining levels of lung epithelium-specific small proteins in serum may help predict clinical outcomes. We examined whether serum Clara cell protein (CC-16) concentration is correlated with the outcome, mechanical ventilation duration, and incidence of nonpulmonary organ failure. DESIGN: Prospective multicenter observational study conducted by the Quebec Critical Care Network. MEASUREMENTS: Seventy-eight adult ARDS patients requiring mechanical ventilation were enrolled and 28-day mortality was the primary outcome. Ventilatory parameters were computed and blood was sampled daily. Clinical information collected included cause of death, duration of mechanical ventilation, number of ventilator-free days, and organ failures. RESULTS: Median serum levels of CC-16 were significantly higher in nonsurvivors than survivors on days 0-2 (19.93 microg/l, IQR 11.8-44.32, vs. 8.9, 5.66-26.38) and sustained up to day 14. CC-16 levels were correlated positively with the number of failing organs (rho 0.3623) and requirement for prolonged mechanical ventilation. Predictors of patient mortality included age, arterial carbon dioxide partial pressure, CC-16, and APACHE II score (odds ratios 1.35, 1.52, 1.37, 1.159, respectively). CONCLUSIONS: Higher initial CC-16 serum level is associated with increased risk of death, fewer ventilator-free days, and increased frequency of nonpulmonary multiple organ failure. CC-16 is a valuable biomarker of ARDS that may help predict outcome among ARDS patients with high-risk mortality.

Adult↗

PubMed2006

Modulation of the triggering receptor expressed on the myeloid cell type 1 pathway in murine septic shock.

The triggering receptor expressed on myeloid cell type 1 (TREM-1) is a cell surface molecule that has been identified on both human and murine polymorphonuclear neutrophils and mature monocytes. The activation of TREM-1 in the presence of microbial components amplifies the inflammatory response and may be responsible for the hyperresponsiveness observed during the initial stage of sepsis. To investigate the effect of the modulation of the TREM-1 pathway during experimental murine sepsis, we used analogue synthetic peptides derived from the extracellular moiety of TREM-1. The TREM-1 ligand was expressed on both peritoneal and peripheral neutrophils during experimental peritonitis in mice. The TREM-1 peptides inhibited the recognition by TREM-1 of its ligand and protected endotoxinic mice from death. In septic rats, the TREM-1 peptides improved the hemodynamic status, attenuated the development of lactic acidosis, modulated the production of such proinflammatory cytokines as tumor necrosis factor alpha and interleukin-1beta, and improved survival. The protective effect of these peptides on arterial pressure could partly be explained by a decreased production of nitric oxide. These data suggest that in vivo modulation of TREM-1 might be a suitable therapeutic tool for the treatment of sepsis.

Adaptor Proteins, Signal Transducing↗

PubMed2005

Surface triggering receptor expressed on myeloid cells 1 expression patterns in septic shock.

OBJECTIVE: To analyze the pattern of cell-surface expression of the triggering receptor expressed on myeloid cells (TREM) 1 during septic shock. DESIGN AND SETTING: Prospective clinical study in an adult 16-bed medical ICU. PATIENTS AND METHODS: 25 septic shock patients, 15 patients with shock of noninfectious origin and 7 healthy volunteers. Arterial blood was drawn within 12 h of admission and subjected to flow cytometry analysis after staining with anti-TREM-1 and anti-CD14 antibodies. Repeated sampling was performed on days 2, 3, 5, 7, and 14 in septic shock patients. RESULTS: Monocytic TREM-1 expression was significantly higher in septic shock patients (mean fluorescence intensity 2.3+/-0.2) than in nonseptic patients (1.0+/-0.1), and healthy volunteers (1.0+/-0.1). There was no difference in monocytic TREM-1 expression between nonseptic patients and healthy volunteers or between any of the three groups with respect to TREM-1 expression on neutrophils. The time course of TREM-1 expression on monocytes diverged significantly by day 3 between survivors and ns. CONCLUSIONS: The specificity of TREM-1 regulation by infection is highlighted. Moreover, surface TREM-1 expression on monocytes may prove useful in allowing the follow-up of septic patients during the course of the disease.

Aged↗

PubMed2005

Risk factors of relative adrenocortical deficiency in intensive care patients needing mechanical ventilation.

OBJECTIVE: To study the factors associated with relative adrenocortical deficiency in mechanically ventilated, critically ill patients. DESIGN AND SETTING: Prospective observational study in a multidisciplinary ICU of a university-affiliated teaching hospital. PATIENTS: Sixty-two consecutive, acutely ill patients needing mechanical ventilation for more than 24 h. MEASUREMENTS AND RESULTS: A high-dose short corticotropin test 24 h after endotracheal intubation. Relative adrenocortical deficiency ("nonresponder" group of patients) was defined by a rise in cortisol less than 90 microg/l after stimulation. Twenty-seven patients were classified as nonresponders and 35 as responders. On univariate analysis nonresponders were more often men, had lower mean arterial pressure, required vasoactive agents more often, had lower creatinine clearance, higher SAPS II, higher organ dysfunction scores, and received etomidate as a single bolus for endotracheal intubation more often than responders. On multivariate analysis, only etomidate administration was related to relative adrenocortical deficiency (OR 12.21; 95% CI 2.99-49.74) while female gender was protective (OR 0.13; 95% CI 0.03-0.57). CONCLUSIONS: A single bolus infusion of etomidate could be a major risk factor for the development of relative adrenocortical deficiency in ICU patients for at least 24 h after administration. Female gender is an independent protective factor.

Addison Disease↗

PubMed2004

[Myocardial dysfunction and septic shock].

Myocardial dysfunction frequently accompanies severe sepsis and septic shock. It is now clear that such a myocardial depression, as evidenced by biventricular alteration, is present during the early phase of sepsis in most patients. Myocardial depression exists despite a fluid loading-dependent hyperdynamic state and usually recovers within 7 to 10 days in survivors. Myocardial dysfunction does not appear to be due to irreversible structural abnormalities nor to myocardial hypoperfusion, but rather linked to many circulating mediators including cytokines. At a cellular level, reduced myocardial contractility could be related in part to apoptosis and induced by both nitric oxide-dependent and nitric oxide-independent mechanisms. However, whatever the mechanism involved, it leads to calcium homeostasis abnormality. The present review describes both the diagnosis procedure and the molecular and cellular pathways of sepsis-induced myocardial depression.

Cardiomyopathies↗

PubMed2003

Baseline cortisol levels, cortisol response to corticotropin, and prognosis in late septic shock.

The prognostic value of basal and corticotropin-stimulated cortisol concentration in patients with sepsis remains a controversial issue. In a retrospective cohort study, 82 consecutive patients with septic shock underwent a short corticotropin test performed more than 24 h after the onset of vasopressor therapy. Forty-one (50%) patients died within 28 days after the onset of septic shock. The mean (SD) basal cortisol level was 22.7 (10.6) microg/dL. With threshold values of 7 and 9 microg/dL maximal increases in cortisol level, 28 (34%) and 31 (38%) patients were, respectively, classified as nonresponders to the short corticotropin test. On multivariate analysis, a cortisol level >20 microg/dL (P = 0.0002), a maximal response to corticotropin <9 microg/dL (P = 0.044), abnormal lactate values (P = 0.0098), and positive blood cultures (P = 0.004) were independent predictors of 28-day mortality. In conclusion, high basal cortisol and low increase on corticotropin stimulation are predictors of a poor outcome in late septic shock. The underlying mechanisms of these prognostic patterns remain to be elucidated.

Adrenocorticotropic Hormone↗

PubMed2002

Mechanical ventilation-induced pneumoprotein CC-16 vascular transfer in rats: effect of KGF pretreatment.

After air-blood barrier injury, "pneumoproteins" specific to lung epithelial distal airspaces reaching the bloodstream are putative markers of lung hyperpermeability. The contribution of mechanical ventilation (MV) to this leakage is unknown. To explore this issue, 16-kDa Clara cell protein (CC-16) concentration was quantified in bronchoalveolar lavages (BALFs) and/or sera of rats first exposed either to ambient air or to 48 h of hyperoxia-induced acute lung injury and then ventilated for 2 h according to one of the following strategies: 1) spontaneous ventilation (SV), 2) very-low-volume high PEEP (VLVHP, where PEEP is positive end-expiratory pressure), 3) low-volume zero PEEP, 4) moderate-volume low PEEP, and 5) high-volume zero PEEP (HVZP). Results show that total proteins in BALFs increased with time and MV, with little impact from hyperoxia preexposure. CC-16 content decreased in BALFs but increased in the bloodstream during MV, suggesting intravascular leakage. Lung overdistension may result either from high-volume (HVZP) or high-PEEP (VLVHP) MV, and it was the most potent inducer of CC-16 leakage (P < 0.05 vs. SV). In the VLVHP group, pretreatment with keratinocyte growth factor was efficient in reducing blood CC-16 transfer.

Animals↗

PubMedDate not supplied

Distributed shared memory for roaming large volumes.

We present a cluster-based volume rendering system for roaming very large volumes. This system allows to move a gigabyte-sized probe inside a total volume of several tens or hundreds of gigabytes in real-time. While the size of the probe is limited by the total amount of texture memory on the cluster, the size of the total data set has no theoretical limit. The cluster is used as a distributed graphics processing unit that both aggregates graphics power and graphics memory. A hardware-accelerated volume renderer runs in parallel on the cluster nodes and the final image compositing is implemented using a pipelined sort-last rendering algorithm. Meanwhile, volume bricking and volume paging allow efficient data caching. On each rendering node, a distributed hierarchical cache system implements a global software-based distributed shared memory on the cluster. In case of a cache miss, this system first checks page residency on the other cluster nodes instead of directly accessing local disks. Using two Gigabit Ethernet network interfaces per node, we accelerate data fetching by a factor of 4 compared to directly accessing local disks. The system also implements asynchronous disk access and texture loading, which makes it possible to overlap data loading, volume slicing and rendering for optimal volume roaming.

Computer Graphics↗

PubMedDate not supplied

Representing higher-order singularities in vector fields on piecewise linear surfaces.

Accurately representing higher-order singularities of vector fields defined on piecewise linear surfaces is a non-trivial problem. In this work, we introduce a concise yet complete interpolation scheme of vector fields on arbitrary triangulated surfaces. The scheme enables arbitrary singularities to be represented at vertices. The representation can be considered as a facet-based "encoding" of vector fields on piecewise linear surfaces. The vector field is described in polar coordinates over each facet, with a facet edge being chosen as the reference to define the angle. An integer called the period jump is associated to each edge of the triangulation to remove the ambiguity when interpolating the direction of the vector field between two facets that share an edge. To interpolate the vector field, we first linearly interpolate the angle of rotation of the vectors along the edges of the facet graph. Then. we use a variant of Nielson's side-vertex scheme to interpolate the vector field over the entire surface. With our representation, we remove the bound imposed on the complexity of singularities that a vertex can represent by its connectivity. This bound is a limitation generally exists in vertex-based linear schemes. Furthermore, using our data structure, the index of a vertex of a vector field can be combinatorily determined. We show the simplicity of the interpolation scheme with a GPU-accelerated algorithm for a LIC-based visualization of the so-defined vector fields, operating in image space. We demonstrate the algorithm applied to various vector fields on curved surfaces.

Journal Article↗