Biomedical subjects

B Lachmann

Publications and source records attributed to B Lachmann.

At least 19 recordsLinked to original sources

PubMed2006

Mechanical ventilation affects alveolar fibrinolysis in LPS-induced lung injury.

The aim of the present study was to determine the effects of mechanical ventilation on alveolar fibrin turnover in lipopolysaccharide (LPS)-induced lung injury. In a randomised controlled trial, Sprague-Dawley rats (n = 61) were allocated to three ventilation groups after intratracheal LPS (Salmonella enteritidis) instillations. Group I animals were subjected to 16 cmH(2)O positive inspiratory pressure (PIP) and 5 cmH(2)O positive end-expiratory pressure (PEEP); group II animals to 26 cmH(2)O PIP and 5 cmH(2)O PEEP; and group III animals to 35 cmH(2)O PIP and 5 cmH(2)O PEEP. Control rats (not mechanically ventilated) received LPS. Healthy rats served as a reference group. Levels of thrombin-antithrombin complex (TATc), D-dimer, plasminogen activator inhibitor (PAI) activity and PAI-1 antigen in bronchoalveolar lavage fluid were measured. LPS-induced lung injury increased TATc, D-dimer and PAI activity and PAI-1 antigen levels versus healthy animals. High pressure-amplitude ventilation increased TATc concentrations. D-dimer concentrations were not significantly raised. Instead, PAI activity increased with the amplitude of the pressure, from 0.7 U.mL(-1) in group I to 3.4 U.mL(-1) in group II and 5.0 U.mL(-1) in group III. There was no change in PAI-1 antigen levels. In conclusion, mechanical ventilation creates an alveolar/pulmonary anti-fibrinolytic milieu in endotoxin-induced lung injury which, at least in part, might be due to an increase in plasminogen activator inhibitor activity.

Animals↗

PubMed2006

Small-dose perfluorocarbon reduces the recruitment pressure needed to open surfactant-deficient atelectatic lungs.

BACKGROUND: This study was undertaken to investigate the effect of a small dose of perfluorocarbon on the recruitment pressure needed to open atelectatic lung areas. METHODS: In 12 Yorkshire pigs (body weight, 9 kg), lung injury was induced by whole lung lavage. After 1 h of conventional ventilation, an open lung maneuver was performed to obtain PaO2 values equal to the pre-lavage PaO2 values (+/-10%). After 1 h of ventilation at the lowest possible airway pressure that stabilized the recruited lung volume, the animals were disconnected from the ventilator to allow the lung to collapse. Six animals received a 5 ml/kg intratracheal dose of perfluorocarbon and a second open lung maneuver was performed. Six animals served as controls and received no perfluorocarbon but also underwent a second open lung maneuver. RESULTS: In both groups, an open lung maneuver resulted in a significant increase in oxygenation. The peak pressures needed to open the lung after 1 h of mechanical ventilation in the perfluorocarbon and control groups were 43.8 +/- 8.4 cmH2O and 46.6 +/- 4 cmH2O, respectively. The addition of perfluorocarbon significantly reduced the opening pressure to 34.5 +/- 6.3 cmH2O (P < 0.01), whereas the opening pressure in the control group, 45.0 +/- 0.2 cmH2O, did not change. CONCLUSION: The instillation of a small amount of perfluorocarbon significantly reduces the opening pressures needed to recruit atelectatic lung areas.

Air Pressure↗

PubMed2006

Surfactant as a carrier: influence of immunosuppressive agents on surfactant activity.

INTRODUCTION: It has been proposed that exogenous pulmonary surfactant can be used as a drug delivery system for immunosuppressive agents to the alveolar compartment of the lung while reducing the risk of systemic toxicity. Before using this combination, however, alterations in activity of both substances should be examined. Therefore, this study investigated whether the activity of a natural derived surfactant preparation is changed after it is mixed with cyclosporine A (CsA) or rapamycin (RPM). METHODS: A surfactant suspension was mixed with CsA or RPM and minimal surface tension of these mixtures was measured in vitro. Surfactant activity was evaluated in vivo by its capacity to restore gas exchange in an established model of surfactant deficiency in rats. CsA-surfactant, RPM-surfactant or surfactant alone was instilled intratracheally and blood gases were measured under standardized ventilatory conditions. RESULTS: Minimal surface tension of surfactant-CsA was comparable with that of surfactant alone, whereas minimal surface tension of the surfactant-RPM mixture was increased. In vivo partial arterial oxygen pressure levels increased immediately to prelavage values after instillation of CsA-surfactant, RPM-surfactant and surfactant only and were comparable during the entire study period. CONCLUSION: The activity of a naturally derived surfactant was affected when mixed with RPM but not when mixed with CsA at the used concentrations.

Acute Disease↗

PubMed2006

Liver-type fatty acid binding protein in serum and broncho-alveolar lavage in a model of acute respiratory failure because of surfactant depletion--a possible marker for lung damage?

INTRODUCTION: Liver-type fatty acid binding proteins (L-FABP) have been shown to be present in alveolar macrophages and type II pneumocytes of the lung. This study determined levels of L-FABP in serum and broncho-alveolar lavage (BAL) during experimental acute respiratory failure (ARF) to evaluate whether this molecule can serve as a marker for lung damage. METHODS: Male Sprague-Dawley rats (n = 24) were ventilated and either lung lavaged or lavaged and treated with surfactant, and compared to ventilated, non-lavaged controls. Blood samples were drawn every hour for 4 h to measure L-FABP concentrations in serum. At the end of the experiment a BAL was performed to determine L-FABP levels in BAL fluid. L-FABP was measured with a sandwich enzyme-linked immunosorbent assays. RESULTS: Serum L-FABP concentrations rose significantly during the first 2 h of ventilation in all groups compared with baseline values. After 2 h L-FABP levels were significantly higher in lavaged animals compared with the ventilated controls and to animals treated with surfactant. After 4 h of ventilation, L-FABP in BAL was significantly higher in lavaged, non-surfactant treated animals compared with the ventilated controls. CONCLUSION: In the early phase of experimental ARF serum L-FABP levels correlate well with the degree of lung injury.

Acute Disease↗

PubMed2006

Lung protective ventilation in ARDS: the open lung maneuver.

This review addresses the current state of lung protective strategies and their physiological rationale. Lung protective ventilation can reduce mortality in adult respiratory distress syndrome (ARDS) patients. We review the latest knowledge on the progression of lung injury by mechanical ventilation. Results from clinical studies on mechanical ventilation are compared with results obtained in experimental studies. Furthermore, we discuss possible future improvements to mechanical ventilation; especially the open lung maneuver. The rationale behind the open lung maneuver and steps to accomplish an open lung are described, as well as data from animal and human studies. Finally, guidelines for future strategies and/or investigations are presented.

Clinical Trials as Topic↗

PubMed2005

Influence of phosphatidylglycerol on the uptake of liposomes by alveolar cells and on lung function.

The effect of phosphatidylglycerol on the uptake of surfactant-like liposomes by alveolar type II cells and alveolar macrophages as well as the effect on endogenous surfactant function was studied in vivo. Healthy ventilated rats were intratracheally instilled with fluorescent labeled liposomes with different concentrations of phosphatidylglycerol. Lung function was determined by monitoring arterial oxygenation and, at the end of the experiment, by recording static pressure-volume curves. In addition, alveolar cells were isolated, and cell-associated fluorescence was determined using flow cytometry. The results show that, in the presence of cofactors (Ca(2+), Mg(2+)), phosphatidylglycerol stimulates the uptake by alveolar macrophages but hardly affects the uptake by alveolar type II cells. High concentrations of phosphatidylglycerol reduce the number of alveolar macrophages in the alveolar space and deteriorate lung function. On the other hand, the presence of cofactors protects the lung against the negative effects of phosphatidylglycerol on endogenous surfactant and alveolar macrophages. This study indicates that the phosphatidylglycerol concentration may play a fundamental role in the surfactant function and metabolism depending on the presence of so-called cofactors like calcium and magnesium; further study is needed to clarify the mechanisms involved.

Animals↗

PubMed2005

Effect of ventilation strategy and surfactant on inflammation in experimental pneumonia.

This study explored, the inflammatory response during experimental pneumonia in surfactant-depleted animals as a function of ventilation strategies and surfactant treatment. Following intratracheal instillation of Group B streptococci (GBS), surfactant-depleted piglets were treated with conventional (positive-end expiratory pressure (PEEP) of 5 cmH2O, tidal volume 7 mL x kg(-1)) or open lung ventilation. During the latter, collapsed alveoli were recruited by applying high peak inspiratory pressures for a short period of time, combined with high levels of PEEP and the smallest possible pressure amplitude. Subgroups in both ventilation arms also received exogenous surfactant. Conventionally ventilated healthy animals receiving GBS and surfactant-depleted animals receiving saline served as controls. In contrast with both control groups, surfactant-depleted animals challenged with GBS and conventional ventilation showed high levels of interleukin (IL)-8, tumour necrosis factor (TNF)-alpha and myeloperoxidase in bronchoalveolar lavage fluid after 5 h of ventilation. Open lung ventilation attenuated this inflammatory response, but exogenous surfactant did not. Systemic dissemination of the inflammatory response was minimal, as indicated by low serum levels of IL-8 and TNF-alpha. In conclusion, the current study indicates that the ventilation strategy, but not exogenous surfactant, is an important modulator of the inflammation during Group B streptococci pneumonia in mechanically ventilated surfactant-depleted animals.

Animals↗

PubMed2004

Distinct effects of SP-B and SP-C on the uptake of surfactant-like liposomes by alveolar cells in vivo and in vitro.

The effects of surfactant protein B (SP-B) and SP-C on the uptake of surfactant-like liposomes by alveolar type II cells and alveolar macrophages were studied both in vivo and in vitro. In vivo, mechanically ventilated rats were intratracheally instilled with fluorescently labeled liposomes that had SP-B and/or SP-C incorporated in different concentrations. Consequently, the alveolar cells were isolated, and cell-associated fluorescence was determined using flow cytometry. The results show that the incorporation of SP-B does not influence the uptake, and it also does not in the presence of essential cofactors. The inclusion of SP-C in the liposomes enhanced the alveolar type II cells at a SP-C to lipid ratio of 2:100. If divalent cations (calcium and magnesium) were present at physiological concentrations in the liposome suspension, uptake of liposomes by alveolar macrophages was also enhanced. In vitro, the incorporation of SP-B affected uptake only at a protein-to-lipid ratio of 8:100, whereas the inclusion of SP-C in the liposomes leads to an increased uptake at a protein-to-lipid ratio of 1:100. From these results, it can be concluded that SP-B is unlikely to affect uptake of surfactant, whereas SP-C in combination with divalent cations and other solutes are capable of increasing the uptake.

Animals↗

PubMed2004

The open lung concept: effects on right ventricular afterload after cardiac surgery.

BACKGROUND: The open lung concept (OLC) is a method of ventilation intended to maintain end-expiratory lung volume by increased airway pressure. Since this could increase right ventricular afterload, we studied the effect of this method on right ventricular afterload in patients after cardiac surgery. METHODS: We studied 24 stable patients after coronary artery surgery and/or valve surgery with cardiopulmonary bypass. Patients were randomly assigned to OLC or conventional mechanical ventilation (CMV). In the OLC group, recruitment manoeuvres were applied until Pa(o(2))/FI(O(2)) was greater than 50 kPa (reflecting an open lung). This value was maintained by sufficient positive airway pressure. In the CMV group, volume-controlled ventilation was used with a PEEP of 5 cm H(2)O. Cardiac index, right ventricular preload, contractility and afterload were measured with a pulmonary artery thermodilution catheter during the 3-h observation period. Blood gases were monitored continuously. RESULTS: To achieve Pa(O(2))/Fl(O(2)) > 50 kPa, 5.3 (3) (mean, SD) recruitment attempts were performed with a peak pressure of 45.5 (2) cm H(2)O. To keep the lung open, PEEP of 17.0 (3) cm H(2)O was required. Compared with baseline, pulmonary vascular resistance and right ventricular ejection fraction did not change significantly during the observation period in either group. CONCLUSION: No evidence was found that ventilation according to the OLC affects right ventricular afterload.

Aged↗

PubMed2004

Immunoglobulin M-enriched intravenous polyclonal immunoglobulins reduce bacteremia following Klebsiella pneumoniae infection in an acute respiratory distress syndrome rat model.

Mechanical ventilation is known to induce bacterial translocation from the lung into the systemic circulation. This study determined the effect of immunoglobulin M (IgM)-enriched polyclonal immunoglobulins on bacteremia due to ventilation-induced translocation in an acute respiratory distress syndrome (ARDS) rat model with Klebsiella-induced pneumonia. After whole lung lavage, Sprague-Dawley rats intravenously received either a high dose or a low dose of an immunoglobulin preparation, or an albumin solution as control, followed by an intratracheal injection of a Klebsiella pneumoniae solution. Blood colony-forming units (CFUs) in the treatment groups were significantly lower during the 3-hour ventilation period compared to the control group. The authors conclude that IgM-enriched polyclonal immunoglobulins lead to a reduction of bacteria in blood of surfactant-deficient, ventilated rats infected with Klebsiella pneumoniae.

Animals↗

PubMed2004

Brain glucose and lactate levels during ventilator-induced hypo- and hypercapnia.

OBJECTIVE: Levels of glucose and lactate were measured in the brain by means of microdialysis in order to evaluate the effects of ventilator-induced hypocapnia and hypercapnia on brain metabolism in healthy non-brain-traumatized animals. DESIGN AND SETTING: Prospective animal study in a university laboratory. SUBJECTS: Eight adult Landrace/Yorkshire pigs. INTERVENTIONS: The microdialysis probe was inserted in the brain along with a multiparameter sensor and intracranial pressure (ICP) probe. The animals were ventilated in a pressure-controlled mode according to the open lung concept with an inspired oxygen fraction of 0.4/1.0. Starting at normoventilation (PaCO(2) +/-40 mmHg) two steps of both hypercapnia (PCO(2) +/- 70 and 100 mmHg) and hypocapnia (PaCO(2) +/- 20 and 30 mmHg) were performed. Under these conditions, brain glucose and lactate levels as well as brain oxygen (PbrO(2)), brain carbon dioxide (PbrCO(2)), brain pH (brpH), brain temperature and ICP were measured. RESULTS: At hypercapnia (PaCO(2) = 102.7 mmHg) there were no significant changes in brain glucose and lactate but there was a significant increase in PbrCO(2), PbrO(2) and ICP. In contrast, at hypocapnia (PCO(2) = 19.8 mmHg) there was a significant increase in brain lactate and a significant decrease in both brain glucose and PbrCO(2). CONCLUSIONS: Hypocapnia decreases brain glucose and increases brain lactate concentration, indicating anaerobic metabolism, whereas hypercapnia has no influence on levels of brain glucose and brain lactate.

Animals↗

PubMed2004

Mechanical ventilation of healthy rats suppresses peripheral immune function.

This study was designed to investigate the possible effect of injurious mechanical ventilation on peripheral immune function of healthy rats. Three ventilation strategies were compared: 1) low peak inspiratory pressure (PIP)/positive end-expiratory pressure (PEEP); 2) high PIP/PEEP; and 3) high PIP/zero PEEP (ZEEP). As a reference group, healthy, nonventilated, sham-operated, anaesthetised rats were used. After 4 h, rats were sacrificed and macrophage inflammatory protein (MIP)-2 levels in lung and plasma were determined. Peripheral immune function was determined by measurement of splenic natural killer (NK) activity, mitogen-induced splenocyte proliferation and in vitro cytokine production. All immune measurements in the low PIP/PEEP group did not differ from the immune measurements in the reference group. High PIP strategies, irrespective of applied PEEP, enhanced MIP-2 levels in lung and plasma. NK cell activity, mitogen-induced splenocyte proliferation and MIP-2 and interleukin (IL)-10 production significantly decreased after high PIP/PEEP ventilation. In the high PIP/ZEEP-ventilated group, the decrease in splenocyte proliferation, MIP-2 and IL-10 production and NK cell activity was more pronounced and interferon-gamma production was also significantly lower than in the low PIP/PEEP group. These data show that high positive inspiratory pressure ventilation induces an inflammatory response in the lung, whereas at the same time the peripheral immune response is downregulated. Ventilator-induced peripheral immune suppression may contribute to poor outcome in acute respiratory distress syndrome patients.

Animals↗

PubMed2003

Effects of cerebral air embolism on brain metabolism in pigs.

OBJECTIVES: Cerebral air embolism was induced in pigs and changes in intracranial pressure (ICP), brain oxygen (PbrO2), brain carbon dioxide (PbrCO2), brain pH (brpH) and glucose, lactate and pyruvate levels were used to characterize this model. METHODS: In seven anesthetized pigs, ICP, PbrO2, PbrCO2 and brpH were measured continuously with multiparameter sensors and brain glucose metabolism by microdialysis. After injection of air into the internal carotid artery, these parameters were recorded for 2 h. RESULTS: ICP increased (433%) from 12 +/- 1 to 52 +/- 8 mmHg (P < 0.05). PbrO2 decreased from 25.7 +/- 6.2 to 11.9 +/- 5.2 mmHg. PbrCO2 increased (109%) from 57.7 +/- 2.7 to 120.4 +/- 21.5 mmHg (P < 0.05). Brain glucose decreased (38%) from 3.05 +/- 0.91 to 1.91 +/- 0.55 mmol, while brain lactate increased (384%) from 1.36 +/- 0.15 to 5.22 +/- 0.53 mmol/l (P < 0.05). CONCLUSIONS: Cerebral air embolism has a deleterious effect on ICP and brain metabolism. Therefore, this model may be suitable for testing therapeutic regimens in cerebral air embolism.

Animals↗

PubMed2002

Impact of carbon dioxide and helium insufflation on cardiorespiratory function during prolonged pneumoperitoneum in an experimental rat model.

BACKGROUND: Experimental studies on laparoscopic surgery are often performed in rats. However, the hemodynamic and respiratory responses related to the pneumoperitoneum have not been studied extensively in rats. Therefore, the aim of this study was to investigate in spontaneously breathing rats the effects of CO2 and helium, insufflation pressure, and duration of pneumoperitoneum on blood pressure, arterial pH, pCO2, pO2, HCO3-, base excess, and respiratory rate. METHODS: Five groups of 9 Brown Norway rats were anesthetized and underwent CO2 insufflation (6 or 12 mmHg), helium insufflation (6 or 12 mmHg), or abdominal wall lifting (gasless control) for 120 min. Blood pressure was monitored by an indwelling carotid artery catheter. Baseline measurements of mean arterial pressure (MAP), respiratory rate, arterial blood pH, pCO2, pO2, HCO3-, and base excess were recorded. Blood gases were analyzed at 5, 30, 60, 90, and 120 min during pneumoperitoneum, and MAP and respiratory rate were recorded at 5 and 15 min and at 15-min intervals thereafter for 2 h. RESULTS: CO2 insufflation (at both 6 and 12 mmHg) caused a significant decrease in blood pH and increase in arterial pCO2. Respiratory compensation was evident since pCO2 returned to preinsufflation levels during CO2 insufflation at 12 mmHg. There was no significant change in blood pH and pCO2 in rats undergoing either helium insufflation or gasless procedures. Neither insufflation pressure nor the type of insufflation gas had a significant effect on MAP over time. CONCLUSION: The cardiorespiratory changes during prolonged pneumoperitoneum in spontaneously breathing rats are similar to those seen in clinical practice. Therefore, studies conducted in this animal model can provide valuable physiological data relevant to the study of laparoscopic surgery.

Animals↗

PubMed2002

In vivo and in vitro uptake of surfactant lipids by alveolar type II cells and macrophages.

The uptake of fluorescent-labeled liposomes (with a surfactant-like composition) by alveolar macrophages and alveolar type II cells was studied using flow cytometry, in vivo by instillation of the labeled liposomes in the trachea of ventilated rats followed by isolation of the alveolar cells and determination of the cell-associated fluorescence, and in vitro by incubation of isolated alveolar cells with the fluorescent liposomes. The results show that the uptake of liposomes by the alveolar cells is time and concentration dependent. In vivo alveolar macrophages internalize more than three times as many liposomes as alveolar type II cells, whereas in vitro, the amount of internalized liposomes by these cells is approximately the same. In vitro, practically all the cells (70-75%) internalize liposomes, whereas in vivo only 30% of the alveolar type II cells ingest liposomes vs. 70% of the alveolar macrophages. These results indicate that in vivo, only a small subpopulation of alveolar type II cells is able to internalize surfactant liposomes.

Animals↗

PubMed2002

Lodixanol inhibits exogenous surfactant therapy in rats with acute respiratory distress syndrome.

Optimal alveolar distribution of exogenous surfactant is an important determinant of its beneficial effect. This distribution can be determined by suspending surfactant in a radiological contrast medium before intratracheal instillation, followed by radiological imaging. Iodixanol is reported to be a safe contrast medium that causes no lung injury when instilled intratracheally. In this study, the effects of surfactant suspended in saline were compared with surfactant suspended either in 4:1 saline-iodixanol (64 mg iodine x mL(-1)) or in 1:1 saline-iodixanol (160 mg iodine x mL(-1)), on oxygenation and lung mechanics in a rat model of adult respiratory distress syndrome (ARDS) induced by lung lavage. After the induction of ARDS, surfactant instillation improved oxygenation, total lung volume at inflation with a distending pressure of 35 cmH2O, lung volume at transpulmonary pressure of 5 cmH2O and Gruenwald index. The effects of surfactant suspended in 4:1 saline-iodixanol were similar to those of surfactant alone. However, instillation of surfactant suspended in 1:1 saline-iodixanol resulted in significantly lower values in all measured parameters. Surface tension was the lowest in surfactant suspended in saline alone and addition of iodixanol led to an increase in surface tension in a dose-dependent manner. In conclusion, iodixanol at the higher dose caused an inhibition of the exogenous surfactant effect, characterized as a lack of improvement in oxygen tension in arterial blood, low total lung compliance, volume at 5 cmH2O end-expiration and Gruenwald index. This effect of iodixanol was probably due to its high surface tension, especially if a high concentration was used. Surfactant suspended in a lower concentration of iodixanol seems a better alternative, allowing for radiological imaging of the distribution of surfactant when intratracheally instilled.

Animals↗

PubMed2002

Ventilation-induced activation of the mitogen-activated protein kinase pathway.

Mechanical ventilation of patients can be a life-saving treatment, but also imposes additional stress on the lung. Mitogen-activated protein kinases (MAPK) represent a family of protein kinases that become phosphorylated and activated by many different forms of stress. Using Western blot analysis, the present study analysed the effects of high distending pressure ventilation on the activation of the MAPK extracellular signal-related kinases (ERK)-1/2, c-Jun amino-terminal kinases (JNK) and p38 kinase, and on the MAPK-activated transcription factors c-Jun, ETS-like protein (Elk)-1 and activating transcription factor (ATF)-2. In adult rats, ventilation with high pressure (45/10 peak inspiratory pressure/positive end-expiratory pressure in cmH2O) for 30 or 60 min did not affect arterial oxygenation, but resulted in enhanced phosphorylation of ERK-1/2, JNK, c-Jun, Elk-1 and ATF-2 compared to normally ventilated (13/3) rats. The activation of ERK-1/2 and JNK was located to cells resembling alveolar type II cells. In addition, high pressure ventilation enhanced phosphorylation of the inhibitor of nuclear factor (NF)-kappaB and nuclear translocation of the transcription factor NF-kappaB. In isolated perfused mouse lungs, the MAPK/ERK kinase inhibitor U0126 prevented ventilation-induced activation of ERK-1/2 and Elk-1, but had no effect on ventilation-induced cytokine release. The present authors conclude that mechanical ventilation triggers specific signalling pathways, such as the mitogen-activated protein kinase and the nuclear factor-kappaB pathways, which may contribute to pulmonary inflammation and proliferation.

Analysis of Variance↗

PubMed2002

[Experimental results of using the "open lung concept"].

Several elements of the "open lung concept", like ventilation with small tidal volumes, were incorporated into various ventilatory strategies. Our study demonstrates how the whole concept can be applied in an animal model using a standardized protocol with the following possible results. Eighteen pigs weighing between 30 and 45 kg were anaesthetized, tracheotomized and ventilated. Acute lung injury was induced by surfactant washout. Blood gases were monitored via a continuous arterial sensor system (Trendcare system). After washout, the ventilatory pattern of the American "ARDS Network study" was applied (PEEP = 9 cmH2O, volume controlled mode with a tidal volume of 6 ml/kg body weight and a respiratory rate of 25 breaths per minute). Afterwards, the opening pressure and the pressure at which the lung collapses were titrated. Both levels were used as the basis for adjusting the recruitment pressure and PEEP, which was necessary to keep the lung open. The respiratory rate was chosen in such a way that at a low intrapulmonary pressure difference between inspiration and expiration as well as normocapnia was reached. After induction of an acute lung injury by surfactant washout, the oxygenation index (OI) dropped from 556 +/- 54 to 176 +/- 89 mmHg. In the "ARDS Network" mode, OI increased to 285 +/- 49 mmHg. After alveolar recruitment with a peak pressure of 53 +/- 7 cmH2O and application of a median PEEP of 17 +/- 3 cmH2O, oxygenation returned close to baseline. A pCO2 of 33 +/- 4 mmHg resulted after using a respiratory rate of 39 breaths per minute. The median tidal volume was 8 ml/kg body weight. Despite a short arterial systolic blood pressure drop of 23 +/- 11 mmHg during recruitment, no significant difference was detectable afterwards compared to the baseline. Using low tidal volumes alone, complete reopening was not achieved in an experimentally induced acute lung injury. After recruitment manoeuvres, it was possible to reopen the lung and keep it open by application of a sufficient PEEP.

Air Pressure↗