Volume-targeted modes of modern neonatal ventilators: how stable is the delivered tidal volume?

Objective: Volume-targeted modes are designed to deliver aconstant tidal volume (Vt) at lowest possible pressure independently of changes in compliance, resistance, and leak of the respiratory system. We examined whether these volume-targeted modes respond rapidly enough to sudden changes in respiratory mechanics (e.g., selective intubation, surfactant administration, endotracheal tube kinking, de-kinking, obstruction), resulting in insufficient or excessive Vt delivery. Design and setting: Bench study of six neonatal ventilators in the volume-targeted mode simulating preterm and full-term infant settings on atest lung. Measurements and results: Breath-to-breath expiratory Vt were measured after rapid compliance, resistance, and leak changes. Under our test settings all ventilators showed important volume overshooting following rapid increase in compliance or decrease in resistance. Between one and 16 inflations were required to return to the set Vt. Some ventilators delivered inaccurate Vt under steady state condition while others showed considerable breath-to-breath Vt variability. Conclusions: We observed inaccurate Vt delivery under specific conditions as well as immediate and sometimes prolonged volume overshooting after arapid respiratory system compliance increase or resistance decrease in volume-targeted modes of modern neonatal ventilators. Similar discrepancies between the set Vt and the delivered inflations can be harmful in clinical situations, especially in newborns. Their clinical relevance needs to be clarified with safety studies in the neonatal population and we encourage manufacturers to further improve the ventilators algorithm

Role of Sex Peptide in Drosophila Males

Drosophila male sex peptide ACP70A is a small peptide mainly produced in the accessory glands. It elicits a high number of post-mating responses in mated females; yet its function in male physiology is not well known. Here, we explore its role in male sex behavior and pheromone biosynthesis, using males either mutant or RNAi knocked-down for Acp70A. Courtship was severely affected in both Acp70A mutants and Acp70A knocked-down males, with only 2% of the males succeeding copulation. Cuticular hydrocarbon amounts were moderately affected with 25% decrease in sp0 mutant (without Acp70A expression) and 10–22% increase in flies overexpressing Acp70A. Acp70A knock-down either ubiquitously or in the testes surprisingly resulted in an overproduction of hydrocarbons, whose amounts were double of the controls. We tested eight putative “off-target” genes but none of these led to an increase in hydrocarbon amounts. These results show that male courtship behavior is largely dependent on the presence of Acp70A and independent of cuticular hydrocarbons. The presence of potential “off-target” genes explaining the hydrocarbon phenotype is discussed

Assessing the two-dimensional behaviour of drystone retaining walls by full-scale experiments and yield design simulation

International audienceDrystone walling is a widespread form of construction that utilises local materials. It has received growing interest over the past few years, owing to the recognition of its rich heritage in the framework of sustainable development. However, the growth of dry masonry has been slowed by the lack of scientific evidence proving its reliability. The authors have previously established a model based on yield design to assess drystone wall stability. This theoretical approach has been supplemented by field experiments on full-scale drystone retaining walls that were backfilled until failure with a cohesionless soil. These field experiments followed a first set of experiments in 2002-2003 in which the walls were loaded using hydrostatic pressure. The aim of these experimental programmes was to achieve better understanding of drystone masonry behaviour under loading, and of its failure mode. The present paper consists of a comparative analysis of these theoretical and experimental results, and provides a richer understanding of drystone retaining wall phenomenology. Further perspectives on this work are presented in the conclusion

Yield design modelling of dry joint retaining structures

International audienceThis study presents an analysis of dry masonry retaining structures based on yield design theory: the structure stability is assessed using rigid block and shear failure mechanisms in the wall and its backfill. An application of this simulation on 2D scale-down brick and wood models is then addressed, showing close agreement between theoretical predictions and experimental results. Finally, the possibility of widespreading the study to periodic dry joint and dry-stone retaining structures is discussed

Componentising a scientific application for the grid

CoreGRID is a Network of Excellence funded by the European Commission under the Sixth Framework Programm

Time course of lung injury in rat acute pancreatitis

Objective: Lung injury is asevere complication of acute pancreatitis that increases the mortality rate of the disease. The pathophysiology of acute pancreatitis has been studied in several experimental models, but the kinetics of pulmonary complications in relation to the pancreatic disease is not completely understood. We then studied the severity of acute pancreatitis-associated lung injury over 18 h in rats that had taurocholic acid injection in the pancreatic duct and determined whether blood collected from rats with pancreatitis is toxic enough to induce injury in normal lungs. Design and setting: Prospective, randomized, and controlled animal study in an animal research laboratory in auniversity hospital. Interventions: We isolated lungs from rats with acute pancreatitis 2, 6, and 18 h after taurocholic acid injection in the biliopancreatic duct and perfused them with blood collected from the same rats. Additionally, blood collected from rats with acute pancreatitis (time-points: 2 and 6 h) was perfused in normal lungs. Measurements and results: Taurocholic acid injection induced asevere pancreatic injury that started as early as 2 h after the injection and persisted without recovery over the 18-h study period. In contrast, the pulmonary injury was transient, appearing at the 6-h time point with recovery by the end of the study. Pulmonary injury was moderate and evidenced mostly during lung reperfusion. Interestingly, blood collected at the 2-h time point in pancreatic rats induced pulmonary injury in normal lungs while blood collected at the 6-h time-point was not toxic. Conclusions: While pancreatic injury persists over the full experimental period, pulmonary injury is transient in our experimental model. The recovery of lung injury by 18 h might be explained by adecrease in the overall toxicity of pancreatic blood over tim

The effects of β1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise

At exercise steady state, the lower the arterial oxygen saturation (SaO2), the lower the O2 return (\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2}). A linear relationship between these variables was demonstrated. Our conjecture is that this relationship describes a condition of predominant sympathetic activation, from which it is hypothesized that selective β1-adrenergic blockade (BB) would reduce O2 delivery (\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} ) and \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} . To test this hypothesis, we studied the effects of BB on \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} and \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} in exercising humans in normoxia and hypoxia. O2 consumption (\ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} ), cardiac output (\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}, CO_{2}\; \hbox{rebreathing}), heart rate, SaO2 and haemoglobin concentration were measured on six subjects (age 25.5±2.4years, mass 78.1±9.0kg) in normoxia and hypoxia (inspired O2 fraction of 0.11) at rest and steady-state exercises of 50, 100, and 150W without (C) and with BB with metoprolol. Arterial O2 concentration (CaO2), \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2}, and \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} were then computed. Heart rate, higher in hypoxia than in normoxia, decreased with BB. At each \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} , \ifmmode\expandafter\dot\else\expandafter\.\fi{Q} was higher in hypoxia than in normoxia. With BB, it decreased during intense exercise in normoxia, at rest, and during light exercise in hypoxia. SaO2 and CaO2 were unaffected by BB. The \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} changes under BB were parallel to those in \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}. \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} was unaffected by exercise in normoxia. In hypoxia the slope of the relationship between \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} and \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} was lower than 1, indicating a reduction of \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} with increasing workload. \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} was a linear function of SaO2 both in C and in BB. The line for BB was flatter than and below that for C. The resting \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} in normoxia, lower than the corresponding exercise values, lied on the BB line. These results agree with the tested hypothesis. The two observed relationships between \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} and SaO2 apply to conditions of predominant sympathetic or vagal activation, respectively. Moving from one line to the other implies resetting of the cardiovascular regulatio

Respiratory change in ECG-wave amplitude is a reliable parameter to estimate intravascular volume status

Electrocardiogram (ECG) is a standard type of monitoring in intensive care medicine. Several studies suggest that changes in ECG morphology may reflect changes in volume status. The "Brody effect”, a theoretical analysis of left ventricular (LV) chamber size influence on QRS-wave amplitude, is the key element of this phenomenon. It is characterised by an increase in QRS-wave amplitude that is induced by an increase in ventricular preload. This study investigated the influence of changes in intravascular volume status on respiratory variations of QRS-wave amplitudes (ΔECG) compared with respiratory pulse pressure variations (ΔPP), considered as a reference standard. In 17 pigs, ECG and arterial pressure were recorded. QRS-wave amplitude was measured from the Biopac recording to ensure that in all animals ECG electrodes were always at the same location. Maximal QRS amplitude (ECGmax) and minimal QRS amplitude (ECGmin) were determined over one respiratory cycle. ΔECG was calculated as 100×[(ECGmax−ECGmin)/(ECGmax+ECGmin)/2]. ΔECG and ΔPP were simultaneously recorded. Measurements were performed at different time points: during normovolemic conditions, after haemorrhage (25mL/kg), and following re-transfusion (25mL/kg) with constant tidal volume (10mL/kg) and respiration rate (15 breath/min). At baseline, ΔPP and ΔECG were both <12%. ΔPP were significantly correlated with ΔECG (r2=0.89, p<0.001). Volume loss induced by haemorrhage increased significantly ΔPP and ΔECG. Moreover, during this state, ΔPP were significantly correlated with ΔECG (r2=0.86, p<0.001). Re-transfusion significantly decreased ΔPP and ΔECG, and ΔPP were significantly correlated with ΔECG (r2=0.90, p<0.001). The observed correlations between ΔPP and ΔECG at each time point of the study suggest that ΔECG is a reliable parameter to estimate the changes in intravascular volume status and provide experimental confirmation of the "Brody effect.

An improved method for isolation of microvascular endothelial cells from normal and inflamed human lung

Summary: Microvascular endothelial cells (MVEC), which differ from large vessel endothelial cells, have been isolated successfully from lungs of various species, including man. However, contamination by nonendothelial cells remains a major problem in spite of several technical improvements. In view of the organ specificity of MVEC, endothelial cells should be derived from the tissue involved in the diseases one wishes to study. Therefore, to investigate some of the immunopathological mechanisms leading to acute respiratory distress syndrome (ARDS), we have attempted to isolate lung MVEC from patients undergoing thoracic surgery for lung carcinoma and patients dying of ARDS. The method described here includes four main steps: (1) full digestion of pulmonary tissue with trypsin and collagenase, (2) aggregation of MVEC induced by human plasma, (3) Percoll density centrifugation, and (4) selection and transfer of MVEC after local digestion with trypsin/EDTA under light microscopy. Normal and ARDS-derived lung MVEC purified by this technique presented contact inhibition (i.e., grew in monolayer), and expressed classical endothelial markers, including von Willebrand factor (vWF), platelet endothelial cell adhesion molecule 1(PECAM-1, CD31), and transcripts for the angiogensin converting enzyme (ACE). The cells also formed capillarylike structures, took up high levels of acetylated low-density lipoprotein (Ac-LDL), and exhibited ELAM-1 inducibility in response to TNF. Contaminant cells, such as fibroblasts, smooth muscle cells, or pericytes, were easily recognized on the basis of morphology and were eliminated by selection of plasma-aggregated cells under light microscopy. The technique presented here allows one to study the specific involvement and contribution of pulmonary endothelium in various lung disease