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C Chopin

Publications and source records attributed to C Chopin.

At least 37 records · Page 2Linked to original sources

Recognition of an extensive range of IgE-reactive proteins in cod extract.

Allergy to fish is one of the most common food allergies. Gad c 1 is the only fish allergen which has been purified and characterized. Other allergens have been detected by Western blot in cod extracts. We have now improved the Western-blot procedure in order to characterize fish IgE-reactive proteins from extracts prepared under different conditions: pre-rigor mortis and post-rigor mortis, EDTA addition or not, and DEAE ion-exchange chromatography. Several IgE-reactive protein bands have been identified over a wide molecular-weight range. In particular, the 104- and 130-kDa IgE-reactive protein bands were detected. These new bands may correspond to aggregates, as EDTA increased the relative amount of the 60-, 67-, 104-, and 130-kDa IgE-reactive protein bands in Western blot. All these bands were also detected by antiparvalbumin monoclonal antibody, specific to the first calcium-binding site. The longer period of storage increased the relative amounts of the 41-, 80-, 104-, and 130-kDa IgE-reactive protein bands. The 18-kDa band was detected only in fish stored for several days. In conclusion, we have described IgE-reactive protein bands over a wide molecular-weight range (12-130 kDa) in Western blot of cod extract, and shown that EDTA and storage conditions may influence the relative distribution of IgE-reactive protein bands.

Adolescent↗

Effects of N omega-nitro-L-arginine methyl ester on the endotoxin-induced disseminated intravascular coagulation in porcine septic shock.

OBJECTIVES: Nitric oxide is known to prevent platelet aggregation and clot formation. Inhibitors of nitric oxide synthase might promote or enhance endotoxin disseminated intravascular coagulation. The present study was designed to evaluate the effects of the arginine analog, N omega-nitro-L-arginine methyl ester (L-NAME), on the endotoxin-induced disseminated intravascular coagulation in a porcine model of septic shock. DESIGN: Prospective, comparative, experimental study. SETTING: Laboratory at a large university hospital. SUBJECTS: Sixteen female piglets, weighing 20 to 28 kg. INTERVENTIONS: Three groups of animals were studied: a control group (n = 6); a lipopolysaccharide (LPS)-treated group (n = 5) receiving Escherichia coli endotoxin (5 micrograms/kg/min over 30 mins); and an LPS + L-NAME group (n = 5) receiving endotoxin and, 1 hr after, a bolus of L-NAME (25 mg/kg). MEASUREMENTS AND MAIN RESULTS: Hemodynamic changes, usual coagulation parameters, and plasma concentrations of thrombin-antithrombin complexes, antithrombin III activity (At III), tissue plasminogen activator, plasminogen activator inhibitor type 1, and von Willebrand factor were measured at baseline, and at 30, 60, 90, 120, 180, 240, and 300 mins. After euthanasia or death, lungs and kidneys were withdrawn for histologic study. The extent of microvascular thrombosis was assessed by a semiquantitative disseminated intravascular coagulation score. In both septic endotoxin group, administration of LPS resulted in hemodynamic changes typical of severe septic shock, with disseminated intravascular coagulation and histologic changes characterized by adult respiratory distress syndrome and kidney microthrombosis. L-NAME administration normalized mean arterial pressure with a dramatic increase in systemic vascular resistances and a marked decrease in cardiac index. The changes in usual coagulation parameters, AT III, tissue plasminogen activator, and plasminogen-activator inhibitor type 1 concentrations were not different between both septic groups. However, in the LPS + L-NAME group, thrombin-antithrombin complexes and von Willebrand factor were higher and associated with a higher histologic disseminated intravascular coagulation score. CONCLUSION: In this model of endotoxin septic shock, L-NAME administration resulted in histologic and coagulation changes consistent with an increased activation of intravascular coagulation.

Animals↗

Effects of inter-alpha-inhibitor in experimental endotoxic shock and disseminated intravascular coagulation.

We investigated the effects of human inter-alpha-inhibitor (I alpha I) on hemodynamics, oxygenation, and coagulation parameters in a porcine model of endotoxic shock. Four groups of six animals were studied: (1) control, (2) I alpha I group receiving 30 mg/kg I alpha I over 30 min, (3) LPS group receiving 5 micrograms.kg/min Escherichia coli endotoxin over 30 min, and (4) LPS + I alpha I group receiving 30 min after endotoxin 30 mg/kg/30 min I alpha I. We measured hemodynamic and oxygenation parameters, usual coagulation markers and plasma levels of thrombin-antithrombin complexes, antithrombin III activity, plasminogen activator tissue type, plasminogen activator inhibitor type 1, von Willebrand factor, tumor necrosis factor-alpha, and I alpha I at baseline and at 30, 60, 90, 120, 180, 240, and 300 min. In the I alpha I group, plasma I alpha I levels reached 447 +/- 23 mg/L just after injection and 287 +/- 39 mg/L at 300 min. I alpha I half-life was 7.3 +/- 1.9 h. In the IPS + I alpha I group, I alpha I plasma levels decreased more rapidly, reaching 260 mg/L at 300 min. Compared with the LPS group, administration of I alpha I normalized the mean arterial pressure and cardiac index, improved the LPS-induced pulmonary hypertension, and resulted in the blunted increase in blood lactate and oxygen extraction ratio. A significant decrease in thrombin-antithrombin complexes and plasminogen activator inhibitor type 1 levels were observed. There was no significant difference in plasma tumor necrosis factor-alpha levels. We concluded that in this hypodynamic model of endotoxin shock, I alpha I administration resulted in a marked improvement in the hemodynamic, oxygenation, and coagulation parameters.

Alpha-Globulins↗

Increased initial flow rate reduces inspiratory work of breathing during pressure support ventilation in patients with exacerbation of chronic obstructive pulmonary disease.

OBJECTIVE: To investigate whether the level of initial flow rate alters the work of breathing in chronic obstructive pulmonary disease (COPD) patients ventilated in pressure support ventilation (PSV). DESIGN: Prospective study. SETTINGS: Medical ICU in University hospital. PATIENTS: Eleven intubated COPD patients. METHODS: We modulated the initial flow rate in order to achieve seven different sequences. In each sequence, the plateau pressure was reached within a predetermined time: 0.1, 0.25, 0.50, 0.75, 1, 1.25 or 1.50 s. The more rapidly the pressure plateau was achieved, the higher was the initial flow rate. In each patient, the pressure support level was an invariable parameter. The order of the seven sequences for each patient was determined randomly. MEASUREMENTS AND RESULTS: Ten minutes after application of each initial flow rate, we measured the following parameters: inspiratory work of breathing, electromyogram (EMG) of the diaphragm (EMGdi), breathing pattern, and intrinsic positive end-expiratory pressure (PEEPi). Comparison between the means for each sequence and each variable measured was performed by two-way analysis of variance with internal comparisons between sequences by Duncan's test. The reduction of the initial flow rate induced a progressive increase in the values of the work of breathing, EMGdi, and mouth occlusion pressure (P 0.1). In contrast, the reduction of the initial flow rate did not induce any significant change in tidal volume, respiratory frequency or PEEPi. CONCLUSIONS: As the objective of PSV is to reduce the work of breathing, it seems logical to use the highest initial flow rate to induce the lowest possible work of breathing in COPD ventilated patients.

Aged↗

Introduction of knowledge bases in patient's data management system: role of the user interface.

As the number of signals and data to be handled grows in intensive care unit, it is necessary to design more powerful computing systems that integrate and summarize all this information. The manual input of data as e.g. clinical signs and drug prescription and the synthetic representation of these data requires an ever more sophisticated user interface. The introduction of knowledge bases in the data management allows to conceive contextual interfaces. The objective of this paper is to show the importance of the design of the user interface, in the daily use of clinical information system. Then we describe a methodology that uses the man-machine interaction to capture the clinician knowledge during the clinical practice. The different steps are the audit of the user's actions, the elaboration of statistic models allowing the definition of new knowledge, and the validation that is performed before complete integration. A part of this knowledge can be used to improve the user interface. Finally, we describe the implementation of these concepts on a UNIX platform using OSF/MOTIF graphical interface.

Algorithms↗

Coagulation inhibitor substitution during sepsis.

This review presents the rationale for and main results of coagulation inhibitor substitution during experimental and human sepsis. Activation of the contact system induces activation of the classical complement pathway with generation of anaphylatoxins, of the kinins pathway and of fibrinolysis. Physiologic inhibition depends on the C1-inhibitor (C1-Inh.). Septic patients exhibit a relative deficiency of biologically active C1-Inh. Substitution with concentrations of C1-Inh has been safely performed and preliminary results are consistent with a possible beneficial effect on hypotension and vasopressor requirement in septic shock. The extrinsic pathway is the main initial coagulation process involved in sepsis-induced DIC. Endothelial and monocyte generation of tissue factor (TF) is activated by bacterial products and endotoxin. Activation of TF is counteracted by a specific tissue factor pathway inhibitor (TFPI). The potential for TFPI substitution to inhibit the activation of the coagulation cascade in sepsis requires further study. Thrombin generation is inhibited by antithrombin III (AT III) and the protein C-protein S system. During sepsis, AT III is consumed and degraded by elastase. Animal studies have shown that DIC and death were prevented by high doses of AT III concentrates. Although a significant reduction in the duration of biological symptoms of DIC has been reported in most human studies, the usefulness of AT III substitution in human sepsis is still debated. None of the studies was able to document a statistically significant reduction in mortality. Protein C is activated by thrombomodulin and, with its cofactor protein S, inhibits factors Va and VIIIa. The free level of protein S depends on the level of the C4b binding protein (C4bBP), an acute-phase complement regulatory protein. During sepsis, protein C activity is significantly reduced, either by acute consumption or by thrombomodulin down-regulation, and increased levels of plasma C4bBP inhibit protein S. Infusion of activated protein C and protein S substitution both protect animals from the lethal effects of bacteria. Combining these different coagulation inhibitors should be carefully studied before its use in septic patients is recommended.

Animals↗

ATP-sensitive K+ channel blockade impairs O2 extraction during progressive ischemia in pig hindlimb.

Tissues maintain O2 consumption (VO2) when blood flow and O2 delivery (DO2) are decreased by better matching of blood flow to meet local cellular O2 demand, a process that increases extraction of available O2. This study tested the hypothesis that ATP-sensitive K+ channels play a significant role in the response of pig hindlimb to ischemia. We pump perfused the vascularly isolated but innervated right hindlimb of 14 anesthetized pigs with normoxic blood while measuring hindlimb DO2, VO2, perfusion pressure, and cytochrome aa3 redox state. In one-half of the pigs, the pump-perfused hindlimb was also infused with 10 micrograms.min-1.kg-1 of glibenclamide, a potent blocker of ATP-sensitive K+ channels. Control animals were infused with 5% glucose solution alone. Blood flow was then progressively reduced in both groups in 10 steps at 10-min intervals. Glibenclamide had no effect on any preischemic hindlimb or systemic measurements. Hindlimb VO2 and cytochrome aa3 redox state began to decrease at a significantly higher DO2 in glibenclamide-treated compared with control pigs. At this critical DO2, the O2 extraction ratio (VO2/DO2) was 53 +/- 4% in the glibenclamide group and 73 +/- 5% in the control group (P < 0.05). Hindlimb vascular resistance increased significantly with ischemia in the glibenclamide group but did not change in the control group. We conclude that ATP-sensitive K+ channels may be importantly involved in the vascular recruitment response that tried to meet tissue O2 needs as blood flow was progressively reduced in the pig hindlimb.

Adenosine Triphosphate↗

[Acute liver failure and pregnancy. A case report].

Acute liver failure occurred in a 33 WA pregnant 4th parity woman. Transfer to intensive care was required and liver transplantation was discussed. Search for the causal mechanism revealed viral hepatitis A. On the basis of this observation, the different hypotheses concerning this clinical situation are presented in addition to different aspects of an association with viral hepatitis (particularly hepatitis A).

Acute Disease↗

Sex steroid hormones in circulatory shock, sepsis syndrome, and septic shock.

METHODS: Estrone (E1), estradiol (E2), testosterone (T), FSH, and LH levels were daily measured during a ten day period in 50 critically ill patients (38 men, 12 post-menopausal women). Patients were separated into four groups: A) no circulatory failure, no sepsis, B) sepsis syndrome without circulatory failure, C) circulatory failure without sepsis syndrome, D) septic shock. Results of hormonal measurements were compared 1) among the 4 groups, 2) between male and female patients, 3) between septic and nonseptic patients. The potential for the infusion of the vasoactive drug dobutamine to induce sex hormonal changes was documented in ten additional septic shock patients by measuring cortisol, E1, and T at base-line and after dobutamine infusion. Changes in active renin and plasma renin activity (PRA) were used as indirect witness of the dobutamine-induced beta 2-stimulation. RESULTS: A dramatic increase in E1 and E2 levels was observed in women of groups B and D, and only in male patients of group D. In the septic patients, estrogen levels peaked at days 1 and 2 and trended to normal from day 6 after the onset of sepsis, while FSH and LH decreased. No difference was found between survivors and non-survivors. Whatever the group, male patients had low T levels throughout the study. Dobutamine induced a significant increase in active renin levels and a decrease in the regression slope between renin and PRA. Cortisol levels remained normal. No significant change in E1 and T was observed after dobutamine. CONCLUSIONS: High estrogen levels were specifically observed in patients with sepsis and septic shock, either males or females. Decreased LH and FSH levels were consistent with the negative feed-back effect of high estrogen levels on pituitary secretion. Circulating T levels were decreased in all male patients. We found no correlation between sequential estrogen levels and outcome. These levels were not modified by a dobutamine-induced beta-2 stimulation.

Adult↗

Prognostic value of the dobutamine test in patients with sepsis syndrome and normal lactate values: a prospective, multicenter study.

OBJECTIVES: To determine the oxygen supply (DO2) and uptake (VO2) responses to a 60-min dobutamine infusion in critically ill septic patients without circulatory shock and with normal blood lactate concentrations. Also, to determine whether these responses would predict outcome. DESIGN: Prospective, cohort study. SETTING: Five intensive care units in university-affiliated, city hospitals. PATIENTS: Fifty critically ill patients with sepsis syndrome were studied from April 1990 to August 1991. INTERVENTIONS: Pulmonary artery catheterization; fluid loading if pulmonary artery occlusion pressure was < 10 mm Hg; and 10 micrograms/min/kg dobutamine infusion for 60 mins. MEASUREMENTS AND MAIN RESULTS: Cardiac index, DO2, VO2, and oxygen extraction ratio were determined immediately before and 1 hr after the onset of the dobutamine test. Using receiver operating characteristic curves, responders to the dobutamine infusion were identified by a > 15% increase in VO2 from the time immediately before to 1 hr after the onset of the dobutamine test. We identified 23 responders and 27 nonresponders. Groups differed significantly in age (responders 46 yrs vs. nonresponders 55 yrs) and associated chronic disease (responders one cancer vs. nonresponders six cancers). Significant changes in responders were: a) cardiac index increased 42.9%; b) systemic vascular resistance decreased 20.7%; and c) DO2 increased 39.1% while VO2 increased 40.8%, with no changes in oxygen extraction or blood lactate concentration. Significant changes in nonresponders were: a) cardiac index increased 14.2%; b) DO2 increased 13.2% and c) oxygen extraction decreased from 0.26 to 0.22. Lactate concentration increased significantly by 25.1% in nonresponders. The mortality rate in responders (8.7%) was significantly less than that rate in nonresponders (44.4%). CONCLUSIONS: Most of these septic patients without shock or hyperlactatemia responded to dobutamine infusion in one of two ways: with little increase in DO2 and no increase in VO2, or with significant increases in both DO2 and VO2. The latter response is typical of healthy volunteers given dobutamine. Because of the calorigenic effect of dobutamine, our results imply nothing about the presence or absence of oxygen supply limitation. Still, patients who had increases in DO2 and VO2 had a much higher survival rate than patients who did not. We speculate that the inability of some patients to respond to dobutamine and the associated higher mortality rate may be related to beta-adrenoreceptor dysfunction.

Adult↗

Double-blind, placebo-controlled trial of antithrombin III concentrates in septic shock with disseminated intravascular coagulation.

BACKGROUND: Septic shock is frequently complicated by a syndrome of disseminated intravascular coagulation (DIC). Numerous uncontrolled clinical studies have reported that antithrombin III (ATIII) substitution might prevent DIC and death in septic shock. METHODS: We conducted a randomized double-blind placebo-controlled trial in patients with a documented septic shock and DIC. The patients received either a placebo or ATIII (90 to 120 IU/kg in loading dose, then 90 to 120 IU/kg/d during 4 days). Administration of fresh frozen plasma, platelets, and fibrinogen concentrates was restricted to patients with hemorrhages and severe decreases in prothrombin time, platelet count, and fibrinogen levels. RESULTS: Thirty-five patients entered the study (18 placebo, 17 ATIII). Both groups were well balanced for all demographic, hemodynamic, and biologic data. Three patients were excluded before the treatment allocation code was broken. In the ATIII group, ATIII levels were rapidly corrected and remained over normal levels until day 10; sequential protein C and protein S levels were not modified. The duration of DIC was significantly reduced: in the ATIII group, 64 percent of patients were cured of DIC at day 2, and 71 percent were cured at the end of treatment vs in the placebo group, 11 percent (p < 0.01) and 33 percent (p < 0.05), respectively. In the 32 included patients, the mortality in ICU was reduced by 44 percent in the ATIII group (p = 0.22, NS). Care loads and transfusion requirements were not different. No side effect was observed. CONCLUSIONS: Mortality was reduced by 44 percent in this trial, but the difference did not reach the statistical significance. Circulating protein C and protein S levels were not modified by ATIII supplementation. High doses of ATIII concentrates significantly improved sepsis-induced DIC during septic shock. The trend toward improved survival suggests further randomized studies.

Antithrombin III↗

Myasthenia gravis and steroid-induced myopathy of the respiratory muscles.

OBJECTIVE: We report a case of corticosteroid-induced myopathy with involvement of respiratory muscles observed in a myasthenic patient. PATIENT: A 37-years-old woman, under corticosteroid treatment for two years for typical myasthenia gravis was admitted to ICU for acute myasthenic respiratory failure. Weaning from mechanical ventilation remained impossible despite 4 plasma exchanges and azathioprine. The patient exhibited a progressive 12 kg weight loss with muscular weakness and atrophy. MEASUREMENTS AND RESULTS: Peripheral and diaphragmatic electromyography as well as histological study were consistent with a steroid-induced myopathy. Discontinuation of corticosteroid treatment was followed by a rapid weight gain with general improvement and allowed weaning from mechanical ventilation with a complete recovery. CONCLUSION: This case provides evidence that corticosteroid-induced myopathy may be observed in myasthenia gravis and may involve the respiratory muscles as well as the peripheral musculature.

Adrenal Cortex Hormones↗

Long-term prognosis of near-fatal asthma. A 6-year follow-up study of 145 asthmatic patients who underwent mechanical ventilation for a near-fatal attack of asthma.

The objective of the present study was to investigate the long-term prognosis of near-fatal asthma. A retrospective cohort study design was used. Cases were defined as any asthmatic individual requiring mechanical ventilation for the first time for an asthma exacerbation between January 1, 1983 and December 31, 1988. The consecutive sample of patients was drawn from four study sites, specifically four intensive care units (ICU), based in a large urban area (1 million inhabitants). These four ICU total approximately 5,000 admissions per year and are the referral centers for more than 95% of patients requiring respiratory intensive care in the area. Data collection was obtained by questionnaires addressed to the patients and to their attending physicians and was completed by telephone calls if necessary. A total of 147 patients entered the study. The long-term outcome could be evaluated in all but two patients. The follow-up period ranged from 1 to 75 months. In-hospital mortality was 16.5%. Among the 121 patients discharged from the ICU, 18 subsequently died, 17 of whom died from a new attack of asthma. Post-hospitalization mortality was 10.1% (95% CI, 5.9 to 16.8%) after 1 yr, 14.4% (CI, 9 to 22.3%) after 3 yr, and 22.6% (CI, 12.7 to 36.8%) after 6 yr. Nearly two-thirds (61.5%) of these secondary deaths occurred within the year following discharge from the ICU. Smoking was associated with a higher in-hospital mortality, as well as with a higher posthospitalization mortality. Age was also independently associated with a higher posthospitalization mortality. It is noteworthy that the secondary deaths were mostly observed in patients over 40 yr of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Septic shock, multiple organ failure, and disseminated intravascular coagulation. Compared patterns of antithrombin III, protein C, and protein S deficiencies.

STUDY OBJECTIVE: Our aim was to document the following in patients with septic shock and disseminated intravascular coagulation (DIC): (1) the influence of DIC in the mortality rate and the occurrence of organ failure; (2) the comparative prognostic value of initial antithrombin III (ATIII), protein C (PC), and protein S (PS) levels; and (3) the compared pattern of sequential ATIII, PC, and PS levels according to clinical outcome. DESIGN: Demographic data, criteria of severity, mortality in ICU, frequency of organ failure, hemodynamic and oxygenation parameters, and laboratory findings were compared in patients with septic shock according to the occurrence of DIC. Initial and sequential levels of ATIII (activity), PC (antigen and activity), PS (total and free), and C4b binding protein (C4bBP) were compared according to the outcome in patients with DIC. PATIENTS: Sixty patients with septic shock were studied. Forty-four entered the group DIC+; 16 entered the group DIC-. RESULTS: Simplified acute physiologic score (SAPS), frequency of acquired organ failure, blood lactate, and transaminase values were significantly higher in the group DIC+. The mortality rate reached 77 percent in group DIC+ vs 32 percent in DIC- (p less than 0.001). In patients with DIC, a fatal outcome was associated with higher bilirubin and transaminase levels, lower PaO2/FIo2 ratio, Vo2, Do2 and O2 extraction. In the group DIC+, all patients but two had severe deficiencies in ATIII and PC levels. Significant correlations were found between initial ATIII and PC levels, PC and free PS levels, and free PS and C4bBP levels. Initial ATIII levels had the best prognostic value for prediction of subsequent death. Serial measurements were consistent with a prolonged ATIII and PC deficiency with significantly different levels between survivors and nonsurvivors. CONCLUSIONS: DIC is a strong predictor of death and multiple organ failure in patients with septic shock. Sequential ATIII, PC, and PS measurements were consistent with prolonged consumption or inhibition that might account for a sustained procoagulant state and inhibition of fibrinolysis. The initial ATIII level was the best laboratory predictor of death in these patients.

Antithrombin III Deficiency↗

[Relation between oxygen delivery and consumption during septic states. Value of an early dobutamine test].

From previous studies it has been hypothesized that multiple organ failure and high level of mortality, seen in critically ill septic patients, may be due to defective oxygen extraction and tissue hypoxia occurring early in the course of sepsis. Oxygen flux test has been proposed as a method of revealing an occult oxygen debt. We used a one hour dobutamine infusion test, in septic patients, without increase in blood lactate. Fifty patients with sepsis syndrome entered a multicentric prospective study. After fluid loading to increase pulmonary artery occlusion pressure (Paop) to a minimum value of 10 mmHg, all the patients were given 10 mcg/kg.min of dobutamine for one hour. Hemodynamic and metabolic variables were recorded before, HO, and after the test, H1 (cardiac index, Paop, oxygen deliver, DO2, and consumption, VO2, oxygen extraction ratio, (OER), blood lactate). The dobutamine test allowed to identify responders (R) who increased VO2 by more than 15% and non-responders. R and NR differed significantly in mortality (8.5% vs 44.4%). The test has a good predictive value for surviving. Without respect of the result of the test, the patients were randomized in two groups. The group D+ was given conventional therapy and dobutamine at the same rate of infusion for 9 consecutive days and the D- group received only conventional therapy. The RD+ patients improved more rapidly when compared with RD-, NRD+, NRD-. We concluded that a one hour dobutamine test is able to identify R and NR critically ill septic patients. The response is associated with significant difference in outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Infections↗