Gastric tonometry in the fed or fasting state?
Explore the source record for details and available documents.
Bias↗
Biomedical subjects
A B Groeneveld
Publications and source records attributed to A B Groeneveld.
Occlusive and non-occlusive gastrointestinal ischaemia: a clinical review with special emphasis on the diagnostic value of tonometry.
BACKGROUND: To review clinical features of the occlusive splanchnic ischaemia syndromes with special emphasis on the diagnostic value of tonometry. METHODS: The English literature was reviewed with an emphasis on papers concerning anatomy and physiology of splanchnic perfusion, the clinical presentation and diagnostic procedures in occlusive splanchnic ischaemia syndromes. RESULTS: Splanchnic ischaemia can result from hypovolaemic states, resulting in splanchnic vasoconstriction and ischaemia with normal splanchnic vessels (non-occlusive ischaemia) or from vascular stenoses (occlusive ischaemia). The former is frequently encountered in critically ill patients, whereas the latter is considered rare, despite a relatively high incidence of splanchnic atherosclerosis. The main problem hindering assessment of the incidence of symptomatic chronic splanchnic ischaemia is the lack of a diagnostic procedure separating symptom-free from symptomatic splanchnic atherosclerosis. Although angiography provides precise anatomical information, the correlation with symptoms is poor. From various studies it emerges that tonometry of luminal PCO2 enables assessment of ischaemia. CONCLUSIONS: Splanchnic ischaemia may be more common than currently assumed, but a gold standard diagnostic tool is lacking. Tonometry of the gastric PCO2 may be the most promising technique for detecting and grading splanchnic ischaemia.
Arteriosclerosis↗
Radionuclide assessment of pulmonary microvascular permeability.
The literature has been reviewed to evaluate the technique and clinical value of radionuclide measurements of microvascular permeability and oedema formation in the lungs. Methodology, modelling and interpretation vary widely among studies. Nevertheless, most studies agree on the fact that the measurement of permeability via pulmonary radioactivity measurements of intravenously injected radiolabelled proteins versus that in the blood pool, the so-called pulmonary protein transport rate (PTR), can assist the clinician in discriminating between permeability oedema of the lungs associated with the adult respiratory distress syndrome (ARDS) and oedema caused by an increased filtration pressure, for instance in the course of cardiac disease, i.e. pressure-induced pulmonary oedema. Some of the techniques used to measure PTR are also able to detect subclinical forms of lung microvascular injury not yet complicated by permeability oedema. This may occur after cardiopulmonary bypass and major vascular surgery, for instance. By paralleling the clinical severity and course of the ARDS, the PTR method may also serve as a tool to evaluate new therapies for the syndrome. Taken together, the currently available radionuclide methods, which are applicable at the bedside in the intensive care unit, may provide a gold standard for detecting minor and major forms of acute microvascular lung injury, and for evaluating the severity, course and response to treatment.
Adult↗
Type of solution and PCO2 measurement errors during tonometry.
OBJECTIVE: The choice of solution for gastrointestinal tonometry influences the PCO2 measurement bias, precision and the time required for equilibration. We compared saline with buffered solutions during in vitro tonometry, with respect to systematic and accidental measurement errors and equilibration time. DESIGN: A prospective laboratory study. MEASUREMENTS: Saline, phosphate, phosphate bicarbonate and succinylated gelatin solutions were equilibrated in a specialized blood gas tonometer at PCO2s of 2.7, 3.6, 4.5, 6.2 and 9.0 kPa, using calibration gases. Accidental errors were determined: the within-syringe decline of PCO2 and the effects of handling errors (five up and down movements of the plunger). The PCO2 build up in gastrointestinal tonometers was determined in 5000 ml saline baths with fixed PCO2 levels of 2.7 and 9.0 kPa. RESULTS: The build up of PCO2 in phosphate bicarbonate and gelatin was about 4 and 2 times slower than in saline and phosphate, respectively, both for gas and gastrointestinal tonometers. The bias of the measured PCO2 at equilibrium was -15% for saline, and between -1 and 3% for phosphate, phosphate bicarbonate and gelatin. The precision was comparable among the solutions: 2 +/- 1% for saline, 2 +/- 1% for phosphate, 1 +/- 0% for phosphate bicarbonate and 1 +/- 1% for gelatin. The accidental errors were virtually absent with phosphate bicarbonate, intermediate with gelatin and largest with saline and phosphate. CONCLUSION: Phosphate bicarbonate buffer and succinylated gelatin allow accurate PCO2 measurements, but their equilibration is too slow for clinical application. The advantage of phosphate over saline solution is a smaller bias only. Thus, both saline and phosphate are currently the tonometer solutions of choice, provided that strictly anaerobic conditions are applied and the bias by the blood gas analyzer is known.
Analysis of Variance↗
Low- and high-blood flow regions in the normal pig heart are equally vulnerable to ischaemia during partial coronary stenosis.
Myocardial perfusion is heterogeneous, even in the normal heart. It is unknown whether the resting normal blood flow level predicts the severity of mismatch between local blood flow and metabolism during acute ischaemia. In the present study local blood flow (measured with radioactively labelled microspheres) and metabolic indicators of ischaemia [tissue contents of lactate and inosine (INO), a breakdown product of adenosine triphosphate (ATP)] were determined in 84-102 simultaneously frozen samples (approximately 0.9 g) of normal (n = 7) and partially ischaemic (n = 4) porcine left ventricles. Ischaemia was induced for 20 min by partially occluding the left anterior descending artery to reduce perfusion pressure from 107 +/- 17 mm Hg to 39 +/- 10 mm Hg (mean +/- SD). Flow reduction in the ischaemic region was strongly variable, both within the subepicardium (range 6-66%, average 34%) and the subendocardium (range 33-84%, average 57%), indicating redistribution of blood flow inside transmural layers in addition to the well-known preferential decrease in subendocardial perfusion. The relative flow reduction during stenosis was not dependent on normal local perfusion level (Spearman rank correlation coefficient -0.002, P = 0.99). Samples with low or high myocardial blood flows before stenosis showed similar increases in lactate content and INO/ATP content ratio, as long as the percentage blood flow reduction was the same. It is concluded that regions with low and high resting flows in the normally perfused heart are equally susceptible to metabolism-perfusion mismatch resulting from coronary stenosis.
Adenosine Triphosphate↗
The inflammatory response to vascular surgery-associated ischaemia and reperfusion in man: effect on postoperative pulmonary function.
OBJECTIVES: To characterise the inflammatory response to vascular surgery and ischaemia/reperfusion (I/R) in man, regarding release of inflammatory mediators, recruitment and activation of neutrophils, and their relation to postoperative pulmonary function. DESIGN: Prospective cohort study. MATERIALS AND METHODS: Circulating neutrophil counts and plasma levels of elastase-alpha 1-antitrypsin (AT), a neutrophil degranulation product, were measured before and approx. 2.5 h (group 1, n = 19) after elective abdominal aortic surgery, and approx. 2.9 h after elective peripheral vascular surgery (group 2, n = 6), together with concentrations of neutrophil agonists, including activated complement (C3a), secretory phospholipase A2 (sPLA2), tumor necrosis factor (TNF-alpha), interleukin (IL)-6, IL-8 and granulocyte colony-stimulating factor (G-CSF). At the time of blood sampling, respiratory variables allowing computation of the lung injury score (LIS) were obtained in patients admitted after surgery in the intensive care unit (ICU), i.e. all group 1 patients and one group 2 patient. RESULTS: Median (range) neutrophil counts rose by 80% (-28-208) and 90% (10-147) in groups 1 and 2, respectively (n.s. between groups). The increase (p < 0.05) in elastase-alpha 1-AT level was 121% (-5-439) in group 1 and 82% (18-792) in group 2 (n.s. between groups). There was a rise (p < 0.05) in C3a level by 93% (-42-751) and of sPLA2 level by 68% (-40-1400) after surgery for the groups together (n.s. between groups), and the rise of the elastase-alpha 1-AT related to that of the C3a levels. IL-6 and G-CSF concentrations increased more in group 1 than 2. The IL-8 concentration increased in group 1 only, and TNF-alpha was unchanged in all groups. In ICU patients, the LIS related to the postoperative rise in IL-6 level only, even though the rise in plasma concentrations of cytokines interrelated. No patient developed ARDS and all survived. CONCLUSIONS: Vascular surgery and I/R in man activates complement, releases cytokines (except for TNF-alpha), and induces neutrophil recruitment and degranulation, which may primarily depend on complement activation. In contrast to the latter, the release of cytokines may depend on the extent of I/R and may contribute to transient pulmonary dysfunction after extensive I/R.
Adult↗
In vitro evaluation of intragastric PCO2 measurement by air tonometry.
OBJECTIVE: To assess the in vitro performance of a new device, the Tonocap, for semi-continuous air tonometry of regional PCO2 in the gastrointestinal tract. METHODS: The tonometer consists of an air filled balloon-tipped catheter, connected to a prototype Tonocap system. The tonometer was placed in saline baths at steady-state PCO2's ranging from 0 to 105 torr, to evaluate bias, precision and reproducibility to PCO2 measurements. The response time was defined as the time needed to detect 95% of an instantaneous change in bath PCO2. RESULTS: The bias of the PCO2 measurement (mean +/- SD) was -2 +/- 2% and reproducibility (coefficient of variation) was 2 +/- 1%. The response time was 19 +/- 2 min. CONCLUSIONS: Tonocap air tonometry is simple and eliminates most sources of error associated with conventional saline tonometry. The bias, precision, reproducibility and response time in vitro are consistent with a clinically reliable device.
Carbon Dioxide↗
Gastric PCO2 tonometry is independent of carbonic anhydrase inhibition.
Tonometric measurement of an elevated intragastric Pco2 and a decreased calculated gastric intramucosal pH can be used to detect gastric mucosal ischemia, provided that intraluminal production of CO2 through acid buffering by bicarbonate is avoided by adequate acid secretion suppression. If the diffusion rate is known, steady state Pco2 can be calculated when measurement intervals are used that are shorter than needed for complete equilibration. The CO2 diffusion might be influenced by the choice of acid-suppressive drugs, since some of them inhibit gastric carbonic anhydrase (CA) and CA facilitates diffusion of CO2/bicarbonate over the gastrointestinal mucosa. We therefore performed gastric Pco2 tonometry, using acid-suppressive regimens with and without CA inhibition. The diffusion rate of CO2 in a gastric tonometer was studied in healthy volunteers, following intravenously administered ranitidine (group I, N = 8) or ranitidine plus pirenzepine (group II, N = 12), a muscarinic antagonist with CA inhibiting capacities. Measurement intervals were 10, 20, 30 and 60 min. Neither the diffusion rate of CO2 (k = 0.13 +/- 0.02/min in group I and 0.11 +/- 0.02/min in group II), nor the steady-state Pco2 (38 +/- 3 mm Hg in group I and 40 +/- 4 mm Hg in group II), nor the gastric-blood differences in Pco2 and pH differed between groups. These results indicate that diffusion of CO2 into the tonometer balloon is independent of CA and thus of the type of gastric acid secretion inhibition.
Adult↗
The 67gallium-transferrin pulmonary leak index in pneumonia and associated adult respiratory distress syndrome.
1. The aim of the study was to determine the role of increased microvascular protein permeability, as measured by the 67gallium (Ga)-transferrin pulmonary leak index, in pneumonia and associated adult respiratory distress syndrome (ARDS). 2. Eighteen consecutive patients with microbiologically confirmed pneumonia (radiographic infiltrates, purulent sputum) and needing respiratory monitoring (n = 2) or mechanical ventilation (n = 16) in the intensive care unit were studied prospectively. The pulmonary leak index using 67Ga-transferrin and 99mTc red blood cells was measured with a mobile probe system over both lung apices (normal value below 14.1 x 10(-3) min-1) within 72 h of intensive care unit admission, and the lung injury score was calculated from radiographic, ventilatory and lung mechanical data. 3. Patients with pneumonia (lung injury score < 2.5, n = 10) had a lower (P < 0.01) pulmonary leak index, averaged for both lungs, with a median of 23.9 [range (7.0-47.0) x 10(-3) min-1] than patients with pneumonia-associated ARDS (lung injury score > or = 2.5, n = 8), and an average pulmonary leak index of 37.5 [(23.4-144.2) x 10(-3) min-1], so that, for all patients, the pulmonary leak index, averaged for both lungs, directly related to the lung injury score (r2 = 0.61, P < 0.01). A normal average pulmonary leak index excluded pneumonia-associated ARDS. Patients with unilateral pneumonia had a greater inter-lung difference (P < 0.01) in the pulmonary leak index between affected and unaffected lung than patients with bilateral pneumonia. The index did not have prognostic significance. 4. The 67Ga-transferrin pulmonary leak index parallels the degree of radiographic, ventilatory and lung mechanical abnormalities of pneumonia and evolving ARDS. The data support the idea that the clinical manifestations of pneumonia culminating in ARDS directly relate to the degree of microvascular injury. Conversely, the pulmonary leak index may be used to monitor the effect of anti-inflammatory drugs in the adjunctive treatment for severe pneumonia aimed at circumventing mechanical ventilation in future studies.
Adult↗
Acute lung injury after aortic surgery: the relation between lung and leg microvascular permeability to 111indium-labelled transferrin and circulating mediators.
BACKGROUND: Aortic surgery is a risk factor for acute lung injury and this may relate to ischaemia/reperfusion (I/R) of the lower body and release of inflammatory mediators. The aim of this study was to define the changes in microvascular protein permeability and circulating inflammatory mediators after aortic surgery. METHODS: In 11 consecutive patients who underwent elective aortic surgery microvascular permeability in lung and leg was measured before and a median of 2.8 hours after completion of surgery using 111indium (In)-labelled transferrin and 99mtechnetium (Tc)-labelled red blood cells, yielding a protein leak index (PLI) that is specific for protein permeability. Circulating leucocyte counts and levels of inflammatory mediators were determined. RESULTS: In the lung the PLI rose from a median of 0.6 (range -0.5 to 2.2) x 10(-3)/min before surgery to 5.4 (-2.3 to 33.5) x 10(-3)/min after surgery, and in the leg from 0.3 (-1.6 to 1.7) x 10(-3)/min to 5.0 (1.0 to 27.8) x 10(-3)/min. The increase in PLI in the lung was related to that in the leg. Levels of activated complement C3a and tumour necrosis factor-alpha did not change, but levels of interleukin (IL)-6, IL-8 and elastase-alpha 1-antitrypsin increased. After surgery there was slight neutrophilia and the leucocyte counts were inversely related to the IL-8 level. The rise in lung but not in leg PLI was greatest in patients with the highest IL-8 levels and the lowest leucocyte counts. CONCLUSIONS: Early after aortic surgery microvascular protein permeability increases in the leg and lung. Leg I/R injury may result in neutrophil activation and release of IL-8, which may induce neutrophil sequestration and subsequently increased pulmonary microvascular permeability. These findings may help to explain the occurrence of acute lung injury after I/R in man.
Adult↗
Effect of nasogastric suction and ranitidine on the calculated gastric intramucosal pH.
Explore the source record for details and available documents.
Gastric Acid↗
Heterogeneity of DMIPP uptake and its relationship with heterogeneous myocardial blood flow.
UNLABELLED: To assess its potential role as a new metabolic probe, the relationship between regional uptake of the 15-(p-[125I]-iodophenyl)-3,3-dimethylpentadecanoic acid (DMIPP) fatty acid analog and myocardial blood flow was studied. METHODS: In 14 open-chest dogs, the left anterior descending coronary artery was cannulated and extracorporal bypass-perfused at normal (control group; n = 4) and reduced flow (intervention group; n = 10). Myocardial blood flow (MBF) was assessed with 46Sc-labeled microspheres. Forty minutes after intravenous injection of DMIPP, the heart was excised and cut into 120 samples. In each sample, MBF ml x g(-1) x min(-1) and DMIPP uptake (percentage of the injected dose per gram, %ID/g) were assessed. RESULTS: In normal myocardium, MBF and DMIPP uptake were 1.10 +/- 0.18 ml x g(-1) x min(-1) and 1.18 +/- 0.42 x 10(-2) %ID/g, respectively. In the extracorporal bypass area, flow was reduced to 0.49 +/- 0.20 ml x g(-1) x min(-1) (p < 0.0001 compared to normal), and DMIPP uptake was decreased to 0.75 +/- 0.26 x 10(-2) %ID/g (p < 0.0001 compared to normal). DMIPP uptake and MBF positively correlated in normal (DMIPP uptake = 0.77 +/- 0.23 x MBF; r = 0.41; p < 0.0001) and hypoperfused (DMIPP uptake = 0.35 +/- 0.70 x MBF; r = 0.63; p < 0.0001) myocardium. The heterogeneity, indicated by the coefficient of variation, in normal myocardium was 0.23 +/- 0.05 for MBF and was lower (p < 0.0001) for DMIPP uptake: 0.13 +/- 0.05. During flow reduction, heterogeneity increased significantly (p < 0.0001) for both MBF (0.59 +/- 0.22) and DMIPP uptake (0.37 +/- 0.23). Also heterogeneity of the DMIPP uptake to MBF ratio, as an indicator of agreement, increased from 0.23 +/- 0.07 in normal to 0.46 +/- 0.19 in hypoperfused myocardium (p < 0.0001). CONCLUSION: DMIPP detects regionally hypoperfused myocardium, in which agreement between MBF and fatty acid uptake deteriorates. DMIPP uptake shows a different relationship with MBF in hypoperfused compared to normal myocardium. These observations suggest that DMIPP uptake may provide additional, unique information on regional myocardial ischemia.
Animals↗
Systemic coagulation and fibrinolysis in patients with or at risk for the adult respiratory distress syndrome.
The authors sought to evaluate the pathogenetic and prognostic role of a procoagulant and hypofibrinolytic state in the adult respiratory distress syndrome (ARDS). Twenty-two consecutive patients admitted to the intensive care unit (ICU) for respiratory monitoring (n = 2) or mechanical ventilation (n = 20) were studied, of whom 13 had ARDS and 9 were at risk for the syndrome. Plasma levels of thrombin-antithrombin III complexes (TAT), the plasmin-alpha2-antiplasmin complexes (PAP), tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor type 1 (PAI-1) were measured within 48 h after admission, together with respiratory variables allowing computation of the lung injury score (LIS), and pulmonary microvascular permeability [67Gallium-transferrin pulmonary leak index (PLI)], as measures of pulmonary dysfunction. Blood was also sampled 6-hourly until 2 days after admission. The LIS and PLI were higher in ARDS than at risk patients, in the presence of similar systemic morbidity and mortality. TAT complexes were elevated in a minority of patients of both groups, whereas the PAP, tPA and PAI levels were elevated above normal in the majority of ARDS and at risk patients, but groups did not differ. Neither circulating coagulation nor fibrinolysis variables correlated to either LIS or PLI. Furthermore, the course of haemostatic variables did not relate to outcome. These data indicate that systemic activation of coagulation and impaired fibrinolysis do not play a major role in ARDS development and outcome in patients with acute lung injury.
Adult↗
Multiple organ failure in septic shock.
Explore the source record for details and available documents.
Animals↗
What is the cause of pulmonary oedema after acute myocardial infarction? A case study.
A patient is described with an acute myocardial infarction (AMI) and pulmonary oedema, necessitating mechanical ventilation, at a mean pulmonary capillary wedge pressure (PCWP) below 13 mmHg. The 67Ga-transferrin pulmonary leak index (PLI), a measure of microvascular permeability, was normal. A study of the course of the PCWP revealed intermittent elevations up to 22 mmHg, owing to intermittent mitral regurgitation. Pulmonary oedema after an AMI can thus be caused by pressure factors, even at sporadic elevations of PCWP, following intermittent, ischaemia-induced dysfunction of the posterior papillary muscle. Conversely, the measurement of a normal 67Ga-PLI may help to diagnose hydrostatic as opposed to permeability pulmonary oedema, if sporadic elevations of the PCWP are not recognised.
Humans↗
The 67gallium pulmonary leak index in assessing the severity and course of the adult respiratory distress syndrome.
OBJECTIVE: To establish the value of the 67Gallium (Ga) pulmonary leak index, a marker of increased permeability edema of the lungs, in assessing the severity and course of the adult respiratory distress syndrome (ARDS). DESIGN: Prospective observational study. SETTING: Medical intensive care unit of a university hospital. PATIENTS: Seventeen consecutive, mechanically-ventilated ARDS patients. Eleven patients (recovering from ARDS) improved, as defined by the ability to taper the level of positive end-expiratory pressure (PEEP) to 0 cm H2O at a median of 7 days after admission. Ten patients survived. Six patients did not recover and died a median of 3.5 days after admission. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The pulmonary leak index (i.e., upper limit of normal 14.1 x 10(-3)/min) was measured within 72 hrs after admission, and repeated within 48 hrs at the time of recovery in recovering patients. At admission and recovery, respiratory variables were recorded and a lung injury score was calculated. At admission, the pulmonary leak index was increased in each patient to 32.3 (range 15.6 to 52.4) and 28.7 (range 26.0 to 40.8) x 10(-3)/min in recovering and nonrecovering patients, respectively (NS). Groups did not differ with respect to the oxygenation ratio, the level of PEEP, radiographic abnormalities, and the lung injury score. At recovery, the pulmonary leak index in recovering patients had decreased in each patient and had normalized in four patients, averaging 15.2 (range 5.6 to 25.9) x 10(-3)/min, concomitantly with an increased oxygenation ratio, less radiographic abnormalities, and a decreased lung injury score (p < .01 vs. admission). For pooled recovering and nonrecovering patient data, the pulmonary leak index directly related to the lung injury score (p < .005). CONCLUSIONS: The 67Ga pulmonary leak index may be a clinically useful tool to quantify the severity and course of ARDS, since clinical recovery from the syndrome may be characterized by amelioration of increased microvascular permeability.
Adult↗
Diagnostic value of the gallium-67 pulmonary leak index in pulmonary edema.
UNLABELLED: We studied the value of a noninvasive, bedside, dual-radionuclide method (67Ga-circulating transferrin and 99mTc-red blood cells) to measure pulmonary microvascular permeability in efforts to discriminate between pulmonary edema due to adult respiratory distress syndrome (ARDS) and hydrostatic pulmonary edema (HPE). METHODS: Patients had respiratory insufficiency and bilateral alveolar pulmonary edema on chest radiographs. All patients, except one, were mechanically ventilated. Patients, were divided into groups according to various sets of etiologic, hemodynamic and ventilatory factors. Group 1 (n = 8) had risk factors for HPE only. Group 2 (n = 5) had risk factors for both ARDS and HPE, such as a pulmonary capillary wedge pressure (PCWP) above 18 torr. Group 3 (n = 13) had risk factors for ARDS only and a PCWP below 18 torr. Patients were also classified on the basis of a lung injury score, using radiographic and ventilatory variables. Group 4 (n = 12) had a score below 2.5 and Group 5 (n = 14) above 2.5, arbitrarily defined as ARDS. Any radioactivity measurements over the lungs and in blood within 72 hr after admission were used to calculate the 1 hr pulmonary leak index as a measure of microvascular permeability (upper limit of normal 14.1 x 10(-3).min-1). RESULTS: The PLI ( x 10(-3).min-1) was median 10.2 (range 4.4-16.2) in Group 1, 26.8 (14.2-31.9) in Group 2 and 32.3 (23.0-52.4) in Group 3 (p < 0.001). It was 13.3 (4.4-39.9) in Group 4 and 31.1 (14.2-52.4) in Group 5 (p < 0.01). Using the various definitions, the sensitivity of a supranormal pulmonary leak index for ARDS was 100% and the specificity varied between 46% and 75%. In receiver operating characteristic curves, the pulmonary leak index performed best when ARDS and HPE were defined on the basis of risk factors only, and performed better than hemodynamic and equally well as ventilatory variables in discriminating between edema types, if definitions of the latter were mainly based on hemodynamic and ventilatory variables, respectively. CONCLUSION: The 67Ga pulmonary leak index is a useful tool to differentiate ARDS from HPE.
Aged↗
Interleukin 8-related neutrophil elastase and the severity of the adult respiratory distress syndrome.
The interaction between activated neutrophils and pulmonary endothelium is thought to contribute to the pathogenesis of the adult respiratory distress syndrome (ARDS), but its relation to ARDS severity, which may support a pathogenetic role, is unclear. Therefore, circulating inflammatory mediators, including the neutrophil chemoattractant and activator interleukin 8 (IL-8), the acute phase cytokine IL-6, and the neutrophil product elastase complexed to alpha 1-antitrypsin (alpha 1-AT), were measured prospectively, together with gas exchange, ventilatory and radiographic variables, in 13 mechanically ventilated patients with ARDS, mostly owing to sepsis, at admission into the intensive care unit. Measurements were repeated in the eight improving patients at the time that positive end-expiratory pressure could be reduced to 0 cm H2O. From the gas exchange, ventilatory and radiographic abnormalities, a lung injury score (LIS) was calculated. For pooled data, the LIS and the arterial PO2/inspiratory O2 fraction, the oxygenation ratio, correlated with plasma levels of IL-8 (rs = 0.60, P < 0.01 and rs = -0.65, P < 0.005, respectively), with levels of IL-6 (rs = 0.60, P < 0.01, and rs = -0.68, P < 0.005, respectively), and the oxygenation ratio related to elastase-alpha 1-AT (rs = -0.70, P < 0.005). Levels of IL-8 and IL-6 interrelated (rs = 0.61, P < 0.01) and related to the elastase complexes (rs = 0.45, P < 0.05). Hence, our data support a role of cytokine-induced activation of neutrophils in the clinical severity of ARDS.
Adult↗