Aims:  To assess the ability of Listeria monocytogenes to form biofilm on different food‐contact surfaces with regard to different temperatures, cellular hydrophobicity and motility. Methods and Results:  Forty‐four L. monocytogenes strains from food and food environment were tested for biofilm formation by crystal violet staining. Biofilm levels were significantly higher on glass at 4, 12 and 22°C, as compared with polystyrene and stainless steel. At 37°C, L. monocytogenes produced biofilm at significantly higher levels on glass and stainless steel, as compared with polystyrene. Hydrophobicity was significantly (P < 0·05) higher at 37°C than at 4, 12 and 22°C. Thirty (68·2%) of 44 strains tested showed swimming at 22°C and 4 (9·1%) of those were also motile at 12°C. No correlation was observed between swimming and biofilm production. Conclusions:  L. monocytogenes can adhere to and form biofilms on food‐processing surfaces. Biofilm formation is significantly influenced by temperature, probably modifying cell surface hydrophobicity. Significance and Impacts of the Study:  Biofilm formation creates major problems in the food industry because it may represent an important source of food contamination. Our results are therefore important in finding ways to prevent contamination because they contribute to a better understanding on how L. monocytogenes can establish biofilms in food industry and therefore survive in the processing environment.

BackgroundPeak first derivative of femoral artery pressure (arterial dP/dtmax) derived from fluid-filled catheter remains questionable to assess left ventricular (LV) contractility during shock. The aim of this study was to test if arterial dP/dtmax is reliable for assessing LV contractility during various hemodynamic conditions such as endotoxin-induced shock and catecholamine infusion.MethodsVentricular pressure-volume data obtained with a conductance catheter and invasive arterial pressure obtained with a fluid-filled catheter were continuously recorded in 6 anaesthetized and mechanically ventilated pigs. After a stabilization period, endotoxin was infused to induce shock. Catecholamines were transiently administrated during shock. Arterial dP/dtmax was compared to end-systolic elastance (Ees), the gold standard method for assessing LV contractility.ResultsEndotoxin-induced shock and catecholamine infusion lead to significant variations in LV contractility. Overall, significant correlation (r = 0.51; p < 0.001) but low agreement between the two methods were observed. However, a far better correlation with a good agreement were observed when positive-pressure ventilation induced an arterial pulse pressure variation (PPV) ≤ 11% (r = 0.77; p < 0.001).ConclusionWhile arterial dP/dtmax and Ees were significantly correlated during various hemodynamic conditions, arterial dP/dtmax was more accurate for assessing LV contractility when adequate vascular filling, defined as PPV ≤ 11%, was achieved.

Morimont P, Lambermont B, Ghuysen A, Gerard P, Kolh P, Lancellotti P, Tchana-Sato V, Desaive T, D'Orio V. Effective arterial elastance as an index of pulmonary vascular load. Am J Physiol Heart Circ Physiol 294: H2736-H2742, 2008. First published April 18, 2008 doi:10.1152/ajpheart.00796.2007.-The aim of this study was to test whether the simple ratio of right ventricular (RV) endsystolic pressure (Pes) to stroke volume (SV), known as the effective arterial elastance (E a), provides a valid assessment of pulmonary arterial load in case of pulmonary embolism-or endotoxin-induced pulmonary hypertension. Ventricular pressure-volume (PV) data (obtained with conductance catheters) and invasive pulmonary arterial pressure and flow waveforms were simultaneously recorded in two groups of six pure Pietran pigs, submitted either to pulmonary embolism (group A) or endotoxic shock (group B). Measurements were obtained at baseline and each 30 min after injection of autologous blood clots (0.3 g/kg) in the superior vena cava in group A and after endotoxin infusion in group B. Two methods of calculation of pulmonary arterial load were compared. On one hand, Ea provided by using three-element windkessel model (WK) of the pulmonary arterial system [Ea(WK)] was referred to as standard computation. On the other hand, similar to the systemic circulation, Ea was assessed as the ratio of RV Pes to SV [Ea(PV) ϭ Pes/SV]. In both groups, although the correlation between Ea(PV) and Ea(WK) was excellent over a broad range of altered conditions, Ea(PV) systematically overestimated Ea(WK). This offset disappeared when left atrial pressure (Pla) was incorporated into Ea [Ea ‫ء‬ (PV) ϭ (Pes Ϫ Pla)/SV]. Thus Ea ‫ء‬ (PV), defined as the ratio of RV Pes minus Pla to SV, provides a convenient, useful, and simple method to assess the pulmonary arterial load and its impact on the RV function.hemodynamics; pulmonary hypertension; right ventricle; ventriculoarterial coupling IN CURRENT CLINICAL practice, pulmonary arterial load [or right ventricular (RV) afterload] is usually expressed as the mean pulmonary vascular resistance, computed as the ratio of the pressure drop through the pulmonary circulation [difference between mean pulmonary arterial pressure (PAP mean ) and left atrial pressure (Pla)] to the mean pulmonary blood flow [cardiac output (CO)]. Such an evaluation ignores the pulsatile nature of both pressure and flow. Although oscillatory components of the pulmonary arterial load are low, and mean resistance may be a valuable index of the pulmonary vascular load, the pulsatile nature of the load may be prominent in numerous pathological situations. Wave reflections play an important role and should be taken into account in pulmonary hypertension resulting from several pathological conditions, like pulmonary embolism and septic shock (1,2,5,14). In this way, the pulmonary arterial impedance spectrum, which is defined in the frequency domain, provides a more precise and complete description of the pulmonary vascular load (12, 17). However, be...

Hemodynamic improvement in patients suffering from both septic shock and renal failure who received hemofiltration suggested that an extrarenal epuration technique could be of interest in patients with septic shock alone. However, most of the studies using continuous venovenous hemofiltration (CVVH) in this setting evidenced neither cytokine clearance nor significant reduction in their plasma level. Lack of significant clearance was explained in part by the small size of the membrane pores. Therefore, we investigated the effects of large-pore membrane hemofiltration (LPHF) during endotoxic shock in pigs on interleukin 6 (IL-6) and interleukin 10 (IL-10) clearances, and on right ventricular (RV)-vascular coupling. Thirteen anesthetized healthy pigs weighing 20-30 kg were divided into two groups. In the Endo group (n = 6), the pigs received a 0.5-mg/kg endotoxin infusion over a period of 30 mins from T0 to T30. In the EndoHF group (n = 7), LPHF (cutoff = 80 kDa) and an ultrafiltration rate of 45 mL/kg/h were started 30 mins after the end of the endotoxin infusion, from T60 to T240. In this model of porcine endotoxic shock, LPHF was responsible for a significant clearance of IL-6 (20 mL/min) and Il-10 (14 mL/min), and for an improvement in RV-vascular coupling.

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