Influence de la fonction rénale sur la capacité de la procalcitonine à diagnostiquer une infection bactérienne en post-opératoire de chirurgie vasculaire aortique

La procalcitonine (PCT) est un marqueur spécifique d infection bactérienne. Dans une étude, prospective, observationnelle, monocentrique, nous avons testé l influence de l insuffisance rénale aigue (IRA) sur la valeur diagnostique d infection bactérienne post-opératoire de la PCT en chirurgie aortique abdominale.Les dosages de PCT ont été réalisés en pré-opératoire puis quotidiennement pendant 5 jours en post-opératoire. L IRA a été définie par une clairance de la créatinine inférieure à 50 ml/min en post-opératoire. Le diagnostic d infection était établi, a posteriori, par l analyse des dossiers cliniques par deux experts indépendants, en aveugle quant aux valeurs de PCT.Parmi 276 opérés, le diagnostic d infection a été porté chez 67 patients. La PCT était significativement plus élevée chez les patients infectés que chez les patients non infectés. Une IRA post-opératoire était objectivée chez 75 patients. La PCT était significativement plus élevée chez les patients insuffisants rénaux qu ils soient infectés ou non. La valeur seuil optimale de PCT était différente en fonction de la présence ou non d une IRA post-opératoire (2,57 vs 0,8 ng/ml ; P < 0,05). La valeur diagnostique d infection bactérienne de la PCT était plus discriminante si la valeur seuil de PCT prenait en considération l IRA. L augmentation de la PCT précédait de 2 jours le diagnostic d infection porté par le clinicien. La PCT est un marqueur diagnostique d infection bactérienne efficient après chirurgie aortique abdominale, mais la fonction rénale post-opératoire influence les valeurs seuils de PCT et doit être prise en compte pour l interprétation de sa valeur diagnostique.PARIS6-Bibl.Pitié-Salpêtrie (751132101) / SudocSudocFranceF

Utility of Cricoid Pressure—Reply

International audienc

Atorvastatin reduces β-Adrenergic dysfunction in rats with diabetic cardiomyopathy.

In the diabetic heart the β-adrenergic response is altered partly by down-regulation of the β1-adrenoceptor, reducing its positive inotropic effect and up-regulation of the β3-adrenoceptor, increasing its negative inotropic effect. Statins have clinical benefits on morbidity and mortality in diabetic patients which are attributed to their "pleiotropic" effects. The objective of our study was to investigate the role of statin treatment on β-adrenergic dysfunction in diabetic rat cardiomyocytes.β-adrenergic responses were investigated in vivo (echocardiography) and ex vivo (left ventricular papillary muscles) in healthy and streptozotocin-induced diabetic rats, who were pre-treated or not by oral atorvastatin over 15 days (50 mg.kg-1.day-1). Micro-array analysis and immunoblotting were performed in left ventricular homogenates. Data are presented as mean percentage of baseline ± SD.Atorvastatin restored the impaired positive inotropic effect of β-adrenergic stimulation in diabetic hearts compared with healthy hearts both in vivo and ex vivo but did not suppress the diastolic dysfunction of diabetes. Atorvastatin changed the RNA expression of 9 genes in the β-adrenergic pathway and corrected the protein expression of β1-adrenoceptor and β1/β3-adrenoceptor ratio, and multidrug resistance protein 4 (MRP4). Nitric oxide synthase (NOS) inhibition abolished the beneficial effects of atorvastatin on the β-adrenoceptor response.Atorvastatin restored the positive inotropic effect of the β-adrenoceptor stimulation in diabetic cardiomyopathy. This effect is mediated by multiple modifications in expression of proteins in the β-adrenergic signaling pathway, particularly through the NOS pathway

Effect of Cricoid Pressure Compared With a Sham Procedure in the Rapid Sequence Induction of Anesthesia

International audienceImportance: The use of cricoid pressure (Sellick maneuver) during rapid sequence induction (RSI) of anesthesia remains controversial in the absence of a large randomized trial.Objective: To test the hypothesis that the incidence of pulmonary aspiration is not increased when cricoid pressure is not performed.Design, setting, and participants: Randomized, double-blind, noninferiority trial conducted in 10 academic centers. Patients undergoing anesthesia with RSI were enrolled from February 2014 until February 2017 and followed up for 28 days or until hospital discharge (last follow-up, February 8, 2017).Interventions: Patients were assigned to a cricoid pressure (Sellick group) or a sham procedure group.Main outcomes and measures: Primary end point was the incidence of pulmonary aspiration (at the glottis level during laryngoscopy or by tracheal aspiration after intubation). It was hypothesized that the sham procedure would not be inferior to the cricoid pressure. The secondary end points were related to pulmonary aspiration, difficult tracheal intubation, and traumatic complications owing to the tracheal intubation or cricoid pressure.Results: Of 3472 patients randomized, mean (SD) age was 51 (19) years and 1777 (51%) were men. The primary end point, pulmonary aspiration, occurred in 10 patients (0.6%) in the Sellick group and in 9 patients (0.5%) in the sham group. The upper limit of the 1-sided 95% CI of relative risk was 2.00, exceeding 1.50, failing to demonstrate noninferiority (P = .14). The risk difference was -0.06% (2-sided 95% CI, -0.57 to 0.42) in the intent-to-treat population and -0.06% (2-sided 95% CI, -0.56 to 0.43) in the per protocol population. Secondary end points were not significantly different among the 2 groups (pneumonia, length of stay, and mortality), although the comparison of the Cormack and Lehane grade (Grades 3 and 4, 10% vs 5%; P 30 seconds, 47% vs 40%; P <.001) suggest an increased difficulty of tracheal intubation in the Sellick group.Conclusions and relevance: This large randomized clinical trial performed in patients undergoing anesthesia with RSI failed to demonstrate the noninferiority of the sham procedure in preventing pulmonary aspiration. Further studies are required in pregnant women and outside the operating room.Trial registration: ClinicalTrials.gov Identifier: NCT02080754

General characteristics of healthy and diabetic treated (<i>atorvastatin</i>, 50 mg. kg^-1.day^-1) and control rats.

<p>General characteristics of healthy and diabetic treated (<i>atorvastatin</i>, 50 mg. kg^-1.day^-1) and control rats.</p

Atorvastatin reduces β-Adrenergic dysfunction in rats with diabetic cardiomyopathy - Fig 3

<p><b>Representative western blot and densitometric data reflecting protein expressions of β1-adrenoceptor (Panel A) and β3-adrenoceptor (Panel B) in left ventricles homogenates of healthy or diabetic rats, treated or not by atorvastatin (50 mg kg-1.day-1) during 15 days.</b> Western blot experiments were normalized using proteins using Ponceau S solution. Data are means ± SD (n = 4 to 9). *: <i>p</i><0.05 versus healthy untreated rats; †: <i>p</i><0.05 diabetic statin versus diabetic untreated rats.</p

Active force (% of baseline value) variation of left ventricle papillary muscle exposed to isoproterenol in diabetic rats pretreated with statin (atorvastatin, 50 mg kg-1 day-1) during 15 days (8 rats per group) with or without L-NAME administration.

<p>Control refers to diabetic rats not receiving statin. AF/s = active force normalized per cross-sectional area during isometric contraction. Data are expressed as mean ± SD. NS: non-significant.</p

Effects of atorvastatin on the transcriptome of left ventricles of healthy or diabetic rats.

<p>Panel A-B Heat Map of RNA expression profiles in diabetic versus healthy left ventricles (Panel A) or in statin diabetic versus untreated diabetic left ventricles (Panel B); Color scale indicate relative expression ratio for each gene in diabetic versus healthy left ventricle (Panel A) or in statin versus untreated diabetic left ventricle. Panel C-D Volcano Plot for the modification of genes expression by diabetes in heart ventricle (Panel C) and by atorvastatin in diabetic left ventricle (Panel D). The vertical axis represents the <i>p</i> value (-log¹⁰ <i>p</i> value) and the horizontal axis range the fold change (log² ratio) between diabetic and healthy left ventricles (Panel C) or statin diabetic versus untreated diabetic left ventricles (Panel D) (by t-test). Genes in the area delimited in red have a fold change greater than 1.5 with a <i>p</i> value < 0.05. Genes in the area delimited in green have a fold change greater than -1.5 (ratio <0.67) with a <i>p</i> value < 0.05. Panel E Venn diagram representing the differently expressed genes in diabetic versus healthy left ventricles in blue and in statin diabetic versus untreated diabetic left ventricles in red (<i>p</i><0.05). D is for down-regulation in diabetic versus healthy left ventricles, U for up-regulation. The overlapping part represents the genes modified by diabetes as well as statin, with up- or down-regulation for each comparison.</p

Representative Western Blot and densitometric data reflecting protein expressions of multidrug resistance protein 4 (MRP4) in left ventricles homogenates of healthy or diabetic rats, treated or not by atorvastatin (50 mg kg-1.day-1) during 15 days.

<p>Western blot experiments were normalized using GAPDH (37kDa). Data are means ± SD (n = 6). *: <i>p</i><0.05 versus healthy untreated rats; †: <i>p</i><0.05 diabetic statin versus diabetic untreated rats.</p