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Biomedical subjects

C Deby

Publications and source records attributed to C Deby.

At least 37 records · Page 2Linked to original sources
PubMed1998

An electron spin resonance (ESR) study on the mechanism of ascorbyl radical production by metal-binding proteins.

The mechanism of ascorbate oxidation by metal-binding proteins (ceruloplasmin, albumin and transferrin) was investigated in vitro and in isolated plasma by the measurement of the ascorbyl free radicals (AFR) by electron spin resonance (ESR). In plasma of 13 healthy volunteers, a spontaneous and variable production of AFR was detected, which was increased by a 10(-4) M ascorbate overloading; however, this increase was not correlated to the intensity of the spontaneous AFR signal. The addition of Cu2+ and ceruloplasmin to plasma increased the ESR signal, while the addition of transferrin decreased the signal intensity in a dose-dependent manner. In vitro, we demonstrated that ascorbate was oxidized by human serum albumin and by ceruloplasmin, and that this oxidase-like activity was lost by trypsin or heat treatment of these proteins. These two proteins positively interacted in the oxidation of ascorbate, since addition of crude albumin to a solution of ascorbate and ceruloplasmin increased the intensity of ESR signal in a dose-dependent manner. The treatment of albumin by a metal chelator (DDTC) abolished these positive interactions. The respective roles of copper and iron in ascorbate oxidation were studied and showed a dose-dependent effect of these ions on ascorbate oxidation. The role of iron was confirmed by the inhibiting effect of metal-free transferrin on iron-dependent ascorbate oxidation. Concerted actions between iron carrying albumin and copper carrying ceruloplasmin appear responsible for the production of AFR in vitro and in vivo.

Adult↗
PubMed1998

Possible in vivo tolerance of human polymorphonuclear neutrophil to low-grade exercise-induced endotoxaemia.

To address the question of whether translocation of bacterial lipopolysaccharide (LPS) into the blood could be involved in the process of exercise-induced polymorphonuclear neutrophil (PMN) activation, 12 healthy male subjects who took part in a sprint triathlon (1.5 km river swim, 40 km bicycle race, 10 km road race) were studied. While there was no detectable amount of endotoxin in the blood samples drawn at rest, exercise was followed by the appearance of circulating endotoxin molecules at the end of competition in four subjects, and after one and 24 h recovery in three and seven athletes, respectively. The concentrations of plasma granulocyte myeloperoxidase ([MPO]), were significantly higher immediately after exercise and one hour later-than baseline values (P<0.001). This variable returned to pre-race levels the day after exercise, despite the presence of detectable amounts of LPS, at that time, in seven athletes. The absence of significant correlation (r=0.26; P=0.383) and temporal association between [MPO] and plasma endotoxin levels led us to conclude that endotoxaemia was not involved in the process of exercise-induced PMN degranulation observed in our subjects.

Adult↗
PubMed1998

Protective activity of propofol, Diprivan and intralipid against active oxygen species.

We separately studied the antioxidant properties of propofol (PPF), Diprivan (the commercial form of PPF) and intralipid (IL) (the vehicle solution of PPF in Diprivan) on active oxygen species produced by phorbol myristate acetate (10(-6) M)-stimulated human polymorphonuclear leukocytes (PMN: 5 x 10(5) cells/assay), human endothelial cells (5 x 10(5) cells/assay) or cell-free systems (NaOCl or H2O2/peroxidase systems), using luminol (10(-4) M)-enhanced chemiluminescence (CL). We also studied the protective effects of Diprivan on endothelial cells submitted to an oxidant stress induced by H2O2/MPO system: cytotoxicity was assessed by the release of preincorporated 51Cr. Propofol inhibited the CL produced by stimulated PMN in a dose dependent manner (until 5 x 10(-5) M, a clinically relevant concentration), while Diprivan and IL were not dose-dependent inhibitors. The CL produced by endothelial cells was dose-dependently inhibited by Diprivan and PPF, and weakly by IL (not dose-dependent). In cell free systems, dose-dependent inhibitions were obtained for the three products with a lower effect for IL. Diprivan efficaciously protected endothelial cells submitted to an oxidant stress, while IL was ineffective. By HPLC, we demonstrated that PPF was not incorporated into the cells. The drug thus acted by scavenging the active oxygen species released in the extracellular medium. IL acted in the same manner, but was a less powerful antioxidant.

Antioxidants↗
PubMed1998

Purification of myeloperoxidase from equine polymorphonuclear leucocytes.

Increases of plasma concentrations of neutrophil myeloperoxidase (MPO) can be used as markers of polymorphonuclear leucocytes (PMN) activation in pathological situations (sepsis, acute lung injury, acute inflammation). To develop an assay for measurement of plasma MPO in horses during the above-mentioned infectious and inflammatory conditions, MPO was purified from equine PMN isolated from blood anticoagulated with citrate. PMN were extracted in a saline milieu (0.2 M Na acetate, 1 M NaCl, pH 4.7) to eliminate most of cellular proteins. Pellets were then extracted in the same buffer containing cationic detergent (1% cetyltrimethyl ammonium bromide). The supernatant was further purified by ion exchange chromatography (Hiload S Sepharose HP column 0.5 x 26 cm, equilibrated with 25 mM Na acetate, 0.2 M NaCl, pH 4.7) with a NaCl gradient (until 1 M). Most of the peroxidase activity of MPO (spectrophotometrically measured by the oxidation of orthodianisidine by hydrogen peroxide) was eluted at 0.65 M NaCl. MPO was further purified by gel filtration chromatography (Sephacryl S 200 column 2.6 x 42 cm with 25 mM Na acetate, 0.2 M NaCl, pH 4.7). MPO (specific activity: 74.3 U/mg) was obtained with a yield of 30% from the detergent extraction supernatant. Electrophoresis (non-reducing conditions) showed 3 bands identified, by comparison with human MPO, (i) the mature tetrameric enzyme (150 kDa) with 2 light and 2 heavy subunits, (ii) the precursor form (88 kDa) and (iii) a form of the heavy subunit without the prosthetic heme group (40 kDa). The mature enzyme and its precursor were glycosylated and possessed peroxidase activity. Equine MPO showed strong similarities with human and bovine MPO, with an absorption peak at 430 nm (Soret peak) characteristic of ferrimyeloperoxidase. Enzymatic activity was pH dependent (optimal value at pH 5.5).

Animals↗
PubMed1997

Failure of lipopolysaccharides to directly trigger the chemiluminescence response of isolated equine polymorphonuclear leukocytes.

Divergent results have been reported on the effects of lipopolysaccharides (LPS) on the activation of equine polymorphonuclear leukocytes (PMN). We therefore attempted to determine whether LPS alone can stimulate equine PMN or whether plasma factors are necessary. PMN were isolated from citrated blood on a discontinuous density gradient of Percoll. The luminol (10(-3) mol/L)-enhanced chemiluminescence (CL) of 1.25 x 10(6) cells was measured after addition of Escherichia coli LPS (0.001-10 micrograms/ml) alone or after incubation in autologous plasma (1 h, 37 degrees C). After direct stimulation with LPS, there were random variations of CL in 16 horses that were not reproducible from one sample to the next for the same horse. LPS which had been incubated in plasma gave a dose-dependent stimulation of the CL of the PMN, which did not occur if the plasma had been heat inactivated (1 h, 56 degrees C). These results indicated a role for plasma factors, which were unlikely to be cytokines, as there were no monocytes or lymphocytes in the plasma incubated with LPS, but might have been complement fragments or LPS ligands, such as LPS binding protein. Studies using specific antibodies against these factors are needed to clarify this question.

Animals↗
PubMed1997

Mild endotoxaemia and the inflammatory response induced by a marathon race.

1. To address the question of whether endotoxaemia could be involved in the inflammatory response induced by long-term strenuous exercise, 18 male marathon runners [mean age 41 +/- 2 (SEM) years] were studied. Their performance in the marathon ranged from 2 h 46 min to 4 h 42 min. 2. Four venous blood samples were drawn: at rest, just before the race (baseline); within 15 min following the completion of the marathon; after 1 h of recovery; and the morning after the race. 3. The following humoral markers of the inflammatory response to exercise were measured: polymorphonuclear myeloperoxidase (MPO), anaphylatoxin C5a (C5a), tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Plasma endotoxin was measured by a sensitive and rapid chromogenic Limulus assay. All inflammatory markers were significantly increased (P < 0.001) after the race, reaching in most cases peak values in the first blood sample drawn following the completion of the marathon [MPO, 298 +/- 19 ng/ml (SEM); C5a, 1.45 +/- 0.32 ng/ml; TNF-alpha, 20 +/- 3 pg/ml; IL-6, 88 +/- 13 pg/ml] when compared with baseline [MPO, 146 +/- 16 ng/ml (SEM); C5a, 0.27 +/- 0.2 ng/ml; TNF-alpha, 12 +/- 1.5 pg/ml: IL-6, 1.0 +/- 0.5 pg/ml]. Traces of plasma endotoxin (ranging from 5 to 13 pg/ml, with one exceptionally high value of 72 pg/ml measured in one runner) were detected in seven subjects within the first hour of recovery. An ELISA method was used to determine the endogenous IgG antibodies toward a range of Gram-negative bacterial lipopolysaccharides (LPSs) of different sizes and structures. A transient decrease in certain anti-LPS activities, mainly against rough LPS, occurred in most cases in the first blood sample drawn after the race. There was no correlation between the magnitude of the inflammatory response to exercise, as assessed by the increase in blood levels of humoral markers of inflammation, and the changes in circulating endotoxin levels of anti-LPS IgG activity following the race. 4. From these results, we conclude that the mild, transient endotoxaemia detected in some of our subjects does not play a major role in the observed inflammatory response to a marathon competition.

Adult↗
PubMed1997

Increase in antioxidant capacity of plasma during propofol anesthesia.

We have examined the effect of total intravenous anesthesia (TIVA) using a continuous propofol infusion on the antioxidant capacity of plasma in 18 neurosurgical patients who required cerebrospinal fluid shunting. Patients were premedicated with hydroxyzine, alprazolam, and atropine. Anesthesia was induced intravenously with propofol 1.5 mg kg-1 and sufentanil 0.15-0.3 microgram kg-1. Tracheal intubation was facilitated with atracurium 0.5 mg kg-1. Anesthesia was maintained with a continuous propofol infusion at an increasing rate from 6 to 12 mg kg-1 h-1 under controlled ventilation (FiO2 = 0.4 in air). In all patients, arterial blood samples were drawn before induction of anesthesia and during surgery for measurement of blood propofol concentration and plasma antioxidant capacity, which was assessed as the ability to inhibit lipid peroxidation. Lipid peroxidation was induced in vitro by exposing a linoleic acid microemulsion to hemoglobin-generated oxoferryl radicals, and assessed by ultraweak chemiluminescence in the absence (control) and the presence of the plasma samples. The antioxidant capacity of plasma, measured by the inhibition of light emission and expressed as a percentage of control, increased significantly from 39.8 +/- 2% (mean +/- SEM) to 44.7 +/- 2.4% during anesthesia (Wilcoxon test, p < 0.001). No correlation was observed between this increased resistance to lipid peroxidation and blood propofol concentrations (Spearman test, r = 0.07, NS). We conclude that the capacity of plasma to inhibit lipid peroxidation increases in patients during TIVA maintained with a continuous propofol infusion.

Anesthesia, Intravenous↗
PubMed1997

Effects of perfluorocarbon emulsions on cultured human endothelial cells.

Perfluorocarbons (PFCs) and their emulsions (PFCEs) were used in organ preservation before transplantation, but not in organ perfusion. Our purpose was to achieve organ perfusion with a PFCE at room temperature or at 37 degrees C, i. e. with oxygenation, to prevent damages related to reoxygenation after hypoxia. Therefore, we first investigated the effect of such emulsions on endothelial cells, the first cells to be in contact with the emulsion. A stem emulsion was prepared from perfluorooctyl bromide (90% w/v), emulsified with egg yolk phospholipids (2% w/v) and stabilized with a mixed fluorocarbon-hydrocarbon "molecular dowel" (1.4% w/v) (droplets of ca 0.2 micron in diameter). This emulsion was found to be stable when diluted with cell culture media or organ preservation fluids. Endothelial cells from human umbilical vein (HUVECs) were cultured in multiwell plates in M199 medium (with growth factors, 10% foetal calf serum and 5% human serum). Confluent cells were incubated overnight with 51Cr, washed and overlayed with M199 (control) or the above PFCE diluted 2x or 4x with M199 (test). After incubation, the cytotoxicity of the PFCEs was estimated by measuring 51Cr release and observing cell morphology by electron and light microscopy. The percentages of released 51Cr were identical to those of the control cells for the 2x, 3x or 4x diluted PFCEs at 4, 25 or 37 degrees C. After return to the M199 medium, the cells grew and multiplied normally. We conclude that the diluted PFCEs were devoid of cytotoxicity. The 2x diluted PFCE was however partially taken up by the cells: by microscopy, we observed intracellular PFC droplets and by density gradient analysis we found a slight increase in cellular density. The diluted PFCEs were compared to classical organ preservation solutions : HUVECs were incubated with UW (University of Wisconsin) or EC (EuroCollins) solutions at +4 and 37 degrees C (3, 17 or 24 h of incubation). The solutions were observed to be toxic to the cells under these conditions, with cell mortality after return to the M199 medium. This cytotoxicity may be attributed to the high K+ concentration of UW and EC, since similar assays performed on HUVECs with Hank's solution adjusted to 100 mM K+ showed a similar % of 51Cr release. UW and EC are therefore not acceptable as dilution media for PFCEs.

Cell Survival↗
PubMed1996

Bactericidal activity against Pseudomonas aeruginosa is acquired by cultured human monocyte-derived macrophages after uptake of myeloperoxidase.

Myeloperoxidase (MPO) is an enzyme located within polymorphonuclear neutrophils capable of producing cytotoxic oxidant species that are particularly active against bacteria with polysaccharide capsules. Pseudomonas aeruginosa (10(6) bacteria per 1ml) are killed within 1 h in vitro by a MPO/H2O2/C1- system (48mU=132ng of MPO). The question arose as to whether human macrophages would acquire cytotoxic activity when loaded with this enzyme. Monocytes were therefore isolated from human blood and cultured for up to ten days to induce maturation to macrophages. These cells lost endogenous MPO within five days while H2O2 production in response to stimulation by phorbol myristate acetate (10(-6)M) decreased to 23% within ten days. On the other hand, their capacity to take up exogenous MPO increased fourfold from day three to day ten. Human macrophages cultured from eight days (when both H2O2 production and MPO uptake were sufficient) were therefore used to study the effects of MPO uptake on cytocidal activity against Pseudomonas aeruginosa. After a 1 h MPO loading period, macrophages (5X10(5) cells per ml) were incubated in the presence of bacteria (0.5 to 2X10(6) bacteria per ml) for 2 h at 37 degrees C. At a bacteria/macrophage ratio of 1, only 34.8+/-7.0% of bacteria survived (compared to killing by non-loaded macrophages), while 74.4+/-9.3% survived at a ratio of 4. From these results, we conclude that loading macrophages with exogenous MPO could enhance their microbicidal activity, suggesting a potentially useful therapeutic application.

Blood Bactericidal Activity↗
PubMed1996

Experimental model for the study by chemiluminescence of the activation of isolated equine leucocytes.

The activation of human polymorphonuclear leucocytes (the respiratory burst) can be studied by measuring their chemiluminescent response. This technique was adapted to equine leucocytes to investigate the effects of cell number, activator concentration, enhancers of chemiluminescence, pH, temperature and inhibitors. Leucocytes were isolated from citrated blood from healthy horses and chemiluminescence was measured with a Bio-Orbit luminometer sensitive to 900 nm light. The optimal cell density for the maximal chemiluminescent response ranged from 10(6) to 10(7) leucocytes 600 microliters-1. Chemiluminescence increased as a function of temperature, and the concentrations of luminol, lucigenin and phorbol myristate acetate (PMA), and was pH related (optimal pH value = 8.0 for lucigenin and 8.5 for luminol). The inhibition of chemiluminescence by 5 x 10(-5) M azide was 88 per cent for luminol and 37 per cent for lucigenin. Superoxide dismutase (100 IU) totally inhibited the chemiluminescence response. Approximately 30 per cent variability in chemiluminescence was observed under the same assay conditions, depending on the origin of the leucocytes. Based on these results, the conditions selected for the measurement of equine leucocyte chemiluminescence were: 10(6) to 10(7) leucocytes 600 microliters-1, 1 x 10(-6)M PMA, 1 mM luminol or 0.4 mM lucigenin, physiological pH (7.4) and physiological temperature (37.8 degrees C). These conditions were similar to those used for measuring the chemiluminescent response of human leucocytes.

Acridines↗
PubMed1996

Myocellular enzyme leakage, polymorphonuclear neutrophil activation and delayed onset muscle soreness induced by isokinetic eccentric exercise.

To address the question of whether delayed onset muscular soreness (DOMS) following intense eccentric muscle contraction could be due to increased production of the arachidonic acid derived product prostaglandin E2 (PGE2). 10 healthy male subjects were submitted to eccentric and concentric isokinetic exercises on a Kin Trex device at 60 degrees/s angular velocity. Exercise consisted of 8 stages of 5 maximal contractions of the knee extensor and flexor muscle groups of both legs separated by 1 min rest phases. There was an interval of at least 30 days between eccentric and concentric testing, and the order of the two exercise sessions was randomly assigned. The subjective presence and intensity of DOMS was evaluated using a visual analogue scale, immediately, following 24 h and 48 h after each test. Five blood samples were drawn from an antecubital vein: at rest before exercise, immediately after, after 30 min recovery, 24 h and 48 h after the tests. The magnitude of the acute inflammatory response to exercise was assessed by measuring plasma levels of polymorphonuclear elastase ([EL]), myeloperoxidase ([MPO]) and PGE2 ([PGE2]). Using two way analysis of variance, it appeared that only eccentric exercise significantly increased [EL] and DOMS, especially of the hamstring muscles. Furthermore, a significant decrease in eccentric peak torque of this muscle group only was observed on day 2 after eccentric work (- 21%; P < 0.002). Serum activity of creatine kinase and serum concentration of myoglobin increased significantly 24 and 48 h after both exercise tests. However, these variables reached significantly higher values following eccentric contractions 48 h after exercise. Mean [PGE2] in the two exercise modes remained unchanged over time and were practically equal at each time point. On the basis of these findings, we conclude that the magnitude of polymorphonuclear (PMN) activation, muscle damage, and DOMS are greater after eccentric than after concentric muscle contractions. However, the hypothesized interplay between muscle damage, increased PGE2 production, DOMS sensations, and reduced isokinetic muscle performance was not substantiated by the present results.

Adult↗
PubMed1996

Effect of propofol on in vitro lipid peroxidation induced by different free radical generating systems: a comparison with vitamin E.

Propofol has been reported to have antioxidant properties and to inhibit lipid peroxidation. In this study, we examined the ability of propofol to inhibit lipid peroxidation induced by three free radical systems (hydroxyl, ferryl, and oxo-ferryl radicals), and we compared the effect of propofol with that of vitamin E, an endogenous antioxidant. Lipid peroxidation was induced by exposing a linoleic acid emulsion to either water gamma radiation, a ferrous iron-ascorbate solution, or human hemoglobin, generating the hydroxyl, ferryl, and oxo-ferryl radicals, respectively. Each experiment was performed in triplicate with and without propofol or vitamin E at concentrations between 10(-5) and 10(-4) M. Lipid peroxidation was quantified by gas chromatography measurement of the pentane released (nmoles) from lipid decomposition. In each condition, a significant dose-response relationship was found between the release of pentane and the concentration of either propofol or vitamin E. The antioxidant activities of both agents were similar but significantly higher against the hydroxyl than the ferryl and oxo-ferryl radicals. The study suggests that propofol could be beneficial as an anesthetic or sedative drug in patients presenting pathologies associated with free radical reactions.

Anesthetics, Intravenous↗
PubMed1995

Diaspirin crosslinked hemoglobin (DCLHb): absence of increased free radical generation following administration in a rabbit model of renal ischemia and reperfusion.

In control rabbits, a renal ischemia of 60 min followed by 10 min of reperfusion resulted in an enhanced free radical production in cortical tissue, as assessed by a significant decrease of free glutathione (42%), protein-bound GSH (17%), and vitamin E (49%). In contrast, catalase or glutathione peroxidase activities were not affected by these experimental conditions. Free radical production in this model was also measured directly using electron spin resonance (ESR) spectroscopy associated with a PBN (alpha-phenyl N-tert-butyl-nitrone) spin trap agent in the venous blood arising from the ischemic kidney. The signal consisted of a triplet of doublets. In contrast, no signal could be detected in control blood samples taken prior to inducing ischemia. The burst of free radical production occurred in the early phase after restoration of flow in the kidneys rendered ischemic, as evidenced by a signal of weak intensity which generally appeared within the third minute after reperfusion and progressively increased to form a well-defined asymmetric signal following 10 min of reperfusion. The precise nature of free radicals trapped by the PBN agent remains, however, to be elucidated, but analysis of the coupling constants (aN = 14.5-15 G; a beta H = 2.5-3 G) and asymmetry of the central doublets suggests that the ESR signal may arise from a nitorxy-radical adduct resulting from the spin trapping by PBN of both oxygen- or carbon-centered radicals of lipid origin. As evidenced by both direct and indirect measurements, exchange of rabbit blood immediately after inducing renal ischemia with 30 ml/kg of Diaspirin Crosslinked Hemoglobin (7.5 g/dl in lactated electrolyte) or human serum albumin (7.5 g/dl in lactated electrolyte) did not exacerbate free radical production mediated by an ischemia reperfusion phenomenon, a typical situation found in a resuscitation setting.

Animals↗
PubMed1995

Anti-inflammatory properties of copper, gold and silver, individually and as mixtures.

It has been previously demonstrated that the mixture of Cu, Au and Ag impaired significantly the clinical and biochemical disorders induced by adjuvant arthritis in the rat. The efficiency of this mixture and of each component was tested on the same animal model. Treated rats were injected daily with either 22.8 micrograms of copper gluconate, 0.2 micrograms of gold thioglucose, 6.8 micrograms of silver proteinate or the blended solution over a period of 29 d. The treatment with the one component solutions was found to have a little or no effect on the plasma levels of fibrinogen, haptoglobin, ceruloplasmin, prostaglandin E2, thromboxane B2, total proteins, Zn, Cu, Mn, Se, Co and Ni, and no significant decrease was observed in the paw oedema resulting from the Freund's adjuvant injection. The treatment with the mixture had a significant preventive effect. Therefore it seems that the administration of low doses of each of the three trace elements have no anti-rheumatic property in the rat. The results indicate an enhanced effect of the metal mixture in the model studied.

Animals↗
PubMed1994

Are similar inflammatory factors involved in strenuous exercise and sepsis?

An increasing body of data suggest that strenuous exercise triggers an inflammatory response having some similarity with those occurring in sepsis. Indices of this inflammatory response to exercise (IRE) especially include leukocytosis, release of inflammatory mediators and acute phase reactants, tissue damage, priming of various white blood cell lines, production of free radicals; activation of complement, coagulation and fibrinolytic cascades. Inflammatory responses to strenuous exercise and sepsis could in part be due to the release of endotoxin in blood as common triggering factor, but it seems that tissue damage and/or contact system activation are more important triggering mechanisms in exercising subjects. While the magnitude and duration of cellular and humoral changes associated with IRE are quite different from those observed in sepsis, recent human studies suggested that chronic and/or excessive IRE could have adverse effects. Among the possible consequences of acute and chronic IRE are delayed onset muscular soreness and loss of force, cardiovascular complications, intravascular hemolysis, hypoferraemia and increased susceptibility to infection.

Blood Coagulation↗
PubMed1994

Anaphylatoxin C5a production during short-term submaximal dynamic exercise in man.

We studied the effects of short-term submaximal exercise on the plasma levels of myeloperoxidase ([MPO]) and C5a anaphylatoxin ([C5a]), taken as specific markers of polymorphonuclear neutrophil (PMN) and complement activation, respectively. Eleven young, healthy male volunteers were subjected to a constant-load concentric exercise on a cycle ergometer (20 min at 80% maximal oxygen uptake). Mean resting MPO and C5a concentrations were 437 +/- 113 and 0.47 +/- 0.21 ng/ml, respectively. During exercise, [MPO] and [C5a] increased significantly (p < 0.001) towards respective peak values of 649 +/- 131 and 1.3 +/- 0.6 ng/ml. A rapid decrease of both [MPO] and [C5a] was observed during recovery. The similar time course of [MPO] and [C5a] changes and the highly significant relationship between these two variables (r = 0.651; p < 0.001) argues for the possible involvement of the complement anaphylatoxin C5a in the process of PMN degranulation. During exercise, the number of circulating PMN increased (+80%; p < 0.001) and remained practically unchanged up to 20 minutes of recovery. As [MPO] and PMN count were not significantly related (r = 0.2; p < 0.1), we concluded that the activation of PMN was independent of their mobilization.

Adult↗