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Biomedical subjects

C Pasquier

Publications and source records attributed to C Pasquier.

At least 55 records · Page 3Linked to original sources
PubMed1998

Reactive oxygen species activate focal adhesion kinase, paxillin and p130cas tyrosine phosphorylation in endothelial cells.

Reactive oxygen species (ROS), particularly hydroxyl radical (HO*), increase neutrophil adherence to hypoxanthine-xanthine oxidase (HX-XO)-treated human umbilical vein endothelial cells (HUVEC) in culture. This adherence is inhibited by the tyrosine kinase inhibitors genistein (30 microM) and herbimycin A (0.9 microM), suggesting the involvement of tyrosine kinase. Phosphorylation of several HUVEC proteins in the range of 120-130 and 70 kDa was found to depend on the XO concentration and stimulation time. This phosphorylation was inhibited by the antioxidants dimethylthiourea (DMTU, 0.75 to 7.5 mM) and pentoxifylline (Ptx, 0.1 mM), and by the iron chelators desferrioxamine (DF, 1 mM) and hydroxybenzyl ethylene diamine (HBED, 0.5 mM), suggesting the involvement of HO*. Three tyrosine-phosphorylated proteins, focal adhesion kinase (p125FAK), paxillin (PAX) and p130cas were isolated and characterized by immunoprecipitation and western blotting. Antioxidants and iron chelators reduced their phosphorylation. HUVEC treated with ROS for 15 min showed actin stress fiber formation. Cytochalasin D (5 microM) inhibited tyrosine phosphorylation and PMN-HUVEC adherence, showing the importance of cytoskeleton integrity in these two functions. In conclusion, HO*, which is involved in increased PMN-HUVEC adhesion, also increases tyrosine phosphorylation on three major cytoskeleton proteins which seem to play a role in this adhesion.

Cell Adhesion↗
PubMed1998

Effects of characterised Pseudomonas aeruginosa exopolysaccharides on adherence to human tracheal cells.

This study evaluated, in vitro, the role of different Pseudomonas aeruginosa exopolysaccharides (EPS) in mediating adherence to human respiratory epithelial cells. Two mucoid and non-mucoid isogenic pairs of P aeruginosa strains isolated from patients with cystic fibrosis (CF) and bronchiectasis were used. Adherence was tested with human tracheal epithelial cell lines from CF and normal fetuses. The CF cells bound significantly more bacteria than the normal cells. The strain from the bronchiectasis patient was significantly more adherent than that from the CF patient and this difference was consistently most marked with the non-mucoid variant and with normal epithelial cells. The differing behaviour of mucoid CF and non-mucoid bronchiectasis strains reflected the chemical composition of their EPS: mainly alginate in the former and neutral polysaccharides in the latter. Additive inhibition experiments with chemically characterised EPS indicated that neutral polysaccharides associated with alginate may act as ligands for the adherence of P. aeruginosa to CF epithelial cells.

Alginates↗
PubMed1998

Comparison of the QUANTIPLEX HIV-1 RNA 2.0 assay with the AMPLICOR HIV-1 MONITOR 1.0 assay for quantitation of levels of human immunodeficiency virus type 1 RNA in plasma of patients receiving stavudine-didanosine combination therapy.

We compared the QUANTIPLEX HIV-1 RNA 2.0 assay with the AMPLICOR HIV-1 MONITOR 1.0 assay for quantitation of human immunodeficiency virus type 1 (HIV-1) RNA in plasma in the Stadi trail, which evaluated a stavudine plus didanosine combination therapy in 52 patients. HIV-1 RNA baseline values measured with AMPLICOR HIV-1 MONITOR 1.0 were significantly higher than those measured with QUANTIPLEX HIV-1 RNA 2.0, and decreases in HIV-1 RNA levels from baseline were also found to be significantly higher when measured with the AMPLICOR HIV-1 MONITOR 1.0 assay. The frequency of HIV-1 RNA levels below the lower limit of quantitation was significantly higher with QUANTIPLEX HIV-1 RNA 2.0 than with AMPLICOR HIV-1 MONITOR 1.0. Reanalysis of these results by an ultrasensitive procedure of AMPLICOR HIV-1 MONITOR 1.0 or by a modified version of the test that included additional primers adapted for non-B HIV-1 clades yielded greater differences between the QUANTIPLEX HIV-1 RNA 2.0 assay and the AMPLICOR HIV-1 MONITOR 1.0 assay. Our results indicate that a valid comparison of the virological efficacies obtained with different antiretroviral drug regimens requires the use of the same viral load quantitation procedure; further standardization between the different HIV-1 RNA quantitation kits is therefore needed.

Anti-HIV Agents↗
PubMed1998

Molecular evidence for mother-to-child transmission of multiple variants by analysis of RNA and DNA sequences of human immunodeficiency virus type 1.

We have examined the viral selection that may occur during transmission by studying the env gene sequences from four cases of mother-to-child transmission of human immunodeficiency virus type 1. The V3 region sequences were directly amplified from both plasma viral RNA and peripheral blood mononuclear cells containing proviral DNA from mothers at delivery and at the time of diagnosis for children. Transmission occurred perinatally in three cases. The similarity of the viral sequences in each infant sample contrasted with the heterogeneous viral populations in the mothers. Phylogenetic analysis indicated the transmission of one or a few closely related maternal minor virus variants. In contrast, the child virus population in the fourth case was as heterogeneous as that of his mother, and phylogenetic analysis strongly suggested the transmission of multiple maternal variants. This case of multiple transmission was confirmed by analyzing sequences obtained at three times after delivery. Strains with sequences corresponding to the syncytium-inducing phenotype were also transmitted in this fourth case, and this was associated with the rapid development of disease in the child. There was no evidence for transmission of particular viral variants from mother to infant. We have thus described a particular case of vertical human immunodeficiency virus type 1 transmission with the transmission of multiple maternal variants to the infant and a rapid, fatal outcome in the child.

Amino Acid Sequence↗
PubMed1997

Implication of neutral polysaccharides associated to alginate in inhibition of murine macrophage response to Pseudomonas aeruginosa.

There is evidence that exopolysaccharides (EPS) contribute to the persistence of Pseudomonas aeruginosa in cystic fibrosis lung. However, the relationship between the chemical composition of EPS and the modulation of phagocytic cells is poorly understood. In order to evaluate the role of the chemical composition of EPS in macrophage behavior changes, we pretreated macrophages with characterized EPS and assessed P. aeruginosa phagocytosis and reactive oxygen intermediate (ROI) production. The results showed that alginate and neutral polysaccharides are involved in phagocytic impairment of P. aeruginosa. Moreover, alginates were able to prime macrophages for increased P. aeruginosa-induced macrophage oxidative burst as determined by chemiluminescence. In contrast, neutral polysaccharides are responsible for the decrease of ROI by a scavenging effect evaluated by the xanthine-xanthine oxidase system. This study showed that the content of P. aeruginosa EPS in alginate, but also in neutral polysaccharides, influences the behavior of strains towards phagocytosis and macrophage oxidative burst.

Alginates↗
PubMed1997

Induction of interleukin-1 and subsequent tissue factor expression by anti-proteinase 3 antibodies in human umbilical vein endothelial cells.

OBJECTIVE: To assess the ability of anti-proteinase 3 (anti-PR3) classic antineutrophil cytoplasmic antibodies (cANCA) to stimulate endothelial expression of tissue factor (TF), which is the main initiator of the coagulation cascade that can lead to endothelial injury and thrombosis in patients with Wegener's granulomatosis. METHODS: Human umbilical vein endothelial cells (HUVEC) were grown to confluence and stimulated with affinity-purified anti-PR3 antibodies, Igs from healthy subjects, and endotoxin (lipopolysaccharide) as positive control. RESULTS: TF activity was generated in anti-PR3-stimulated cells, as shown by a chromogenic test. This activity was inhibited by specific anti-TF antibodies. TF messenger RNA (mRNA) was found in anti-PR3-stimulated cells, as detected by reverse transcriptase-polymerase chain reaction, but not in cells stimulated with irrelevant human Igs or Igs from normal control sera. TF expression reached maximum levels 12 hours after exposure to the anti-PR3 cANCA, and did not require complement. TF mRNA expression was inhibited by cycloheximide, suggesting a requirement for protein synthesis. When added to the incubation medium, interleukin-1 (IL-1) receptor antagonist inhibited the induced TF mRNA expression, suggesting that cANCA-stimulated cells initiate IL-1 synthesis. Moreover, cANCA induced IL-1alpha mRNA before TF mRNA. CONCLUSION: This study showed that anti-PR3 treatment of HUVEC induces sequential expression of IL-1alpha mRNA and TF mRNA, as well as their corresponding proteins. Both proteins could have pathogenic roles in the vasculitic process, since TF is the main initiator of the coagulation cascade.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1997

A new generation of serum anti-HIV antibody immunocapture assay for saliva testing.

BACKGROUND: Epidemiological studies need easier tools to evaluate HIV prevalence, particularly in high-risk groups under difficult field conditions. Testing saliva antibody with accurate immunoassay could serve as an alternative to serum testing. OBJECTIVES: To evaluate performances on saliva of a novel commercially available assay for anti-HIV antibody. STUDY DESIGN: Samples of saliva from 530 patients were tested for the presence of HIV antibodies with a third generation commercially available serum-screening kit and the use of a sample diluent adapted to saliva. RESULTS: Compared with serum sampling the sensitivity and specificity of oral sampling were respectively, 100 and 99.8%. CONCLUSION: The ICE HIV-1.0.2 assay used on saliva could be an efficient and non-invasive epidemiological tool for HIV testing.

Adult↗
PubMed1997

Thiol-mediated inhibition of FAS and CD2 apoptotic signaling in activated human peripheral T cells.

Fas and CD2 receptors can transduce apoptotic signals through two independent biochemical pathways. In this study, we first evaluated the role of intracellular GSH in these signaling pathways by inducing variations in the GSH pool of activated peripheral T lymphocytes. Increasing the concentration of intracellular GSH by means of N-acetyl-L-cysteine (NAC) and GSH ethyl ester (OEt) resulted in total protection against cell death, while inhibiting GSH synthesis with buthionine sulfoximine (BSO) greatly enhanced cell sensitivity to Fas and CD2 apoptotic signaling. The protection exerted by NAC and GSH OEt was essentially based on their capacity to establish an intracellular reducing environment as it still occurred in BSO-treated cells. Thiol-containing compounds (cysteine, captopril, D-penicillamine and 2-mercaptoethanol) inhibited apoptosis while a series of non-thiol antioxidants (including catalase and vitamin E) failed to do so, suggesting that protection was secondary to thiols/disulfides exchange reactions at the level of cysteine residues in proteins and not to detoxification of reactive oxygen intermediates. This conclusion was further supported by the finding that no enhanced generation of O.-2 and H2O2 could be detected in cells experiencing early stages of apoptosis such as a decreased concentration of intracellular GSH and cell shrinkage. Also, protection occurred in the presence of protein synthesis inhibitors, indicating that it was due to post-translational sulfhydryl redox regulation of critical molecules involved in the apoptotic cascade. These data suggest that GSH, the most abundant intracellular thiol antioxidant, may be important in counteracting Fas- and CD2-mediated apoptosis of T lymphocytes.

Acetylcysteine↗
PubMed1997

Antibodies to proteinase-3 mediate expression of intercellular adhesion molecule-1 (ICAM-1, CD 54).

We investigated the role of intercellular adhesion molecule-1 (ICAM-1) in the adhesion of polymorphonuclear neutrophils (PMN) to classic antineutrophil cytoplasmic antibody (C-ANCA)-treated endothelial cells, independently of cytokines. Human umbilical vein endothelial cells (HUVEC) grown to confluence in cytokine-free conditions were stimulated with C-ANCA sera and affinity-purified anti-proteinase 3 antibodies (PR3) from Wegener's granulomatosis (WG) patients. Non-activated PMN were added to treated HUVEC and adhesion was measured. In parallel experiments, treated HUVEC were fixed and ICAM-1 and E-selectin were assayed by cyto-ELISA; in other experiments anti-ELAM-1 and anti-ICAM-1 antibodies were assessed. In this in vitro model, adhesion of non-activated PMN to anti-PR3-stimulated HUVEC was enhanced. Adhesion was greater with anti-PR3 antibodies than with control and normal immunoglobulins, and correlated with the level of anti-PR3 antibodies. Neutralization of anti-PR3 antibodies by neutrophil azurophilic granule proteins abolished adhesion. This adhesion increased at the fourth hour after simulation, peaked at the twelfth hour and then decreased. This phenomenon occurred mainly through endothelial expression of ICAM-1 (the main counter-receptor for integrins, involved in firm PMN adhesion and migration) and E-selectin on HUVEC membranes. Anti-adhesion molecule antibodies inhibited this adhesion. This work supports the hypothesis of a direct effect of C-ANCA in endothelial stimulation, namely, on endothelium-PMN adhesion, and strengthens the major role of ICAM-1, directly involved in firm sticking of PMN to HUVEC, besides E-selectin. C-ANCA upregulate endothelial adhesiveness and thus participate in inflammatory reactions by providing endothelial adhesive structures for neutrophils. This might be one of the first steps leading to clinical expression of the disease. These results provide new insights into the pathogenesis of C-ANCA-related diseases.

Antibodies↗
PubMed1996

Inhibition of human neutrophil binding to hydrogen peroxide-treated endothelial cells by cAMP and hydroxyl radical scavengers.

Hydrogen peroxide (H2O2) increases adherence of human polymorphonuclear neutrophils (PMN) to cultured human umbilical vein endothelial cells (HUVEC). Catalase and HO. scavengers did not affect the increased PMN adherence to HUVEC stimulated by other compounds such as phorbol myristate acetate (PMA) and thrombin, showing that the observed effect was H2O2- and HO.-specific. This effect was inhibited by hydroxyl radicals (HO.) scavengers and not by iron-chelators that do not penetrate the cells, suggesting the involvement of intracellular HO. in the increased adherence mechanism. An increase in cAMP inhibited H2O2-induced adherence, as observed with isoproterenol, isobutylmethylxanthine, and dibutyryl-cAMP. Similarly, pentoxifylline (Ptx), an HO. scavenger that also increases cAMP, inhibited H2O2-mediated adherence but had no effect on that induced by PMA or thrombin. PKA inhibitors cancelled the Ptx-induced inhibition of H2O2-mediated adherence. However, PKA inhibitors or atrial natriuretic peptide that decreases cAMP did not increase adherence, showing that decrease in cAMP is not responsible for increased adherence. HO. scavengers did not alter the H2O2-induced reduction in cAMP levels, but did inhibit the effect of H2O2 on adherence. We conclude that HO. mediates the H2O2-induced increased in PMN adherence to HUVEC, and that the increase in cAMP that mediates PKA activation downregulates this effect.

1-Methyl-3-isobutylxanthine↗
PubMed1995

Effects of pentoxifylline on the adherence of polymorphonuclear neutrophils to oxidant-stimulated human endothelial cells: involvement of cyclic AMP.

Cultured human umbilical vein endothelial cells (HUVECs) treated with reactive oxygen species (ROS) show increased adherence of polymorphonuclear leukocytes (PMNs). Because pentoxifylline (PTX) is known to inhibit cell interactions, we studied PMN adherence to ROS-stimulated HUVECs pretreated with PTX. ROS were generated by the oxidation of hypoxanthine by xanthine oxidase, giving rise to superoxide anion and hydrogen peroxide. Human PMNs were then added to HUVEC monolayers. After various times, the cultures were washed and the number of adherent PMNs was estimated by measuring myeloperoxidase in the total cell homogenate. PTX inhibited adherence in a concentration-dependent manner. Moreover, the increase in intracellular cAMP content varied with the PTX concentration. Isobutylmethylxanthine (IBMX) and isoproterenol (ISO) which increase intracellular cAMP content, also inhibited the adherence of PMNs to ROS-stimulated HUVECs. We conclude that cAMP is probably involved in the intracellular regulation of ROS-mediated PMN adherence to endothelial cells.

1-Methyl-3-isobutylxanthine↗
PubMed1995

Neutrophil degranulation related to the reperfusion of ischemic human heart during cardiopulmonary bypass.

Activation of polymorphonuclear neutrophils (PMNs) during cardiopulmonary bypass (CPB) is a wellknown phenomenon. This study aimed to determine if activated PMNs are sequestered and degranulated within the myocardium at reperfusion in patients undergoing coronary artery bypass grafting (CABG). Nineteen patients undergoing elective CABG were included in a prospective randomized study. Blood samples were obtained simultaneously from the radial artery (RA) and the coronary sinus (CS) at the following times: T0 (5 min after onset of CPB), T1 (2 min after aortic unclamping), and T2 (10 min after aortic unclamping). Neutrophil function was evaluated by PMN count and by elastase and lactoferrin concentrations. All patients survived. Neutrophils increased significantly from T0 to T1 and T2 in both RA and CS (p < 0.001 between T0 and T1 or T2). Pre-ischemia and reperfusion were associated with a significantly lower neutrophil count in CS compared with RA blood (p < 0.001), suggesting that PMNs were trapped within the myocardium at the onset of the CPB. Elastase and lactoferrin concentrations increased significantly from T0 to T1 and from T1 to T2 for each site, with greater concentrations (p < 0.001) in the CS compared with the RA, suggesting that activated neutrophils released their granular content into the plasma milieu only after reperfusion of the ischemic heart. This study establishes that neutrophil sequestration seems to be secondary to PMN activation by CPB but that the ischemia-reperfusion sequence induces specific degranulation of the PMNs trapped within the ischemic myocardium.

Adult↗
PubMed1995

[Relationship between perceived health status and career choice in a sample of wage-earners].

Many factors were related with subjective health status (SHS), but few studies have focused on identifying some intrinsic personal factors like the choice of job and perceived working situations. The present paper examines the relationships among such factors in a large French sample. Data were collected from 21,378 subjects who were randomly selected from the lists of male and female wage earners who were followed up by 380 occupational physicians and who were born in 1938, 1943, 1948 or 1953. SHS was evaluated using the French version of the Nottingham Health Profile (NHP). Socio-demographic and job characteristics were assessed by means of closed questions during the annual medical examination. Results showed that low subjective health status was related to sex, age and perceived working situation: for each of the six areas of the NHP (pain, physical mobility, energy, sleep, social isolation, emotional reactions) there was a lower SHS for women and a decrease with age for both sexes. The poorer the perceived working situations the worse was the SHS. Using general linear models it appeared that independently of these factors and the socio-economical category dichotomized in upper classes versus lower classes, those who had claimed to have not chosen their job had a lower SHS, whatever the area of SHS. Awaiting the second survey in 1995, it is difficult to explain these results from this cross sectional analysis: is the choice of job a possible risk factor or an artefact due to some unmeasured confounding factors like motivation or job satisfaction.

Adult↗
PubMed1995

Anti-vascular endothelial cell antibodies (AECA): comparison of two assay methods and clinical applications.

Vascular endothelial cells may be a target for autoantibodies (AECAs) against membrane antigens that are constitutively expressed, induced or bound to their surface. To test this hypothesis, we used an enzyme-linked immunosorbent assay (ELISA) with two types of human endothelial cells as the substrate, i.e., human umbilical cord vein endothelial cells (HUVECs) or the hybrid cell line EAhy-926 obtained by fusion of HUVECs with the bronchial carcinoma cell line A549. A comparative functional study of these two cell types demonstrated that EAhy-926 cells produced only small amounts of VIII von Willebrand factor and tissular factor, did not contain Weibel Palade bodies visible under the electron microscope, and expressed ICAM-1 and selectin E in levels of no more than 15% of those expressed by human umbilical cord vein endothelial cells both after stimulation by bacterial lipopolysaccharide and under basal conditions. However, the two assay methods yielded similar IgG AECA titers when used on sera from patients with rheumatoid vasculitis or antiphospholipid syndrome. These antibodies did not exhibit cytotoxicity for cord vein or EAhy-926 cells. They were not specific for endothelium, since their activity decreased by a mean of 40% after incubation of sera with the epithelial cell line A549. A cross-sectional study of 565 sera demonstrated that anti-vascular IgG and IgM AECAs reactive with EAhy-926 cells occurred mainly in patients with dermatomyositis (IgG, 58%; IgM, 22%), systemic scleroderma (IgG, 48%; IgM, 18%), primary Sjögren's syndrome (IgG, 44%; IgM, 12%) and secondary and primary systemic vasculitides (IgG, 38%; IgM, 18%) including Wegener's granulomatosis. A longitudinal study in patients with Wegener's granulomatosis showed that AECAS were predictive of disease activity.

Antibodies↗
PubMed1994

Reactive oxygen species rapidly increase endothelial ICAM-1 ability to bind neutrophils without detectable upregulation.

We compared the effects of phorbol 12-myristate 13-acetate (PMA) and thrombin with those of nonlytic concentrations of reactive oxygen species (ROS) generated by hypoxanthine (HX)-xanthine oxidase (XO) on the adhesion properties of human umbilical cord vein endothelial cells (HUVEC) to resting polymorphonuclear neutrophils (PMN). PMN adherence to HX-XO-treated HUVEC was increased approximately twofold to 2.5-fold relative to untreated HUVEC, both immediately and after 2 hours. It was not additive to that induced by PMA or thrombin stimulation of HUVEC. ROS-induced adherence was not due to platelet-activating factor (PAF) or P-selectin expression, as it was neither antagonized by BN52021 (PAF receptor antagonist) nor inhibited by anti-P-selectin monoclonal antibody (MoAb), contrary to the increased adhesion of PMA- and thrombin-stimulated HUVEC. PMN preincubated with mannose-6-P or N-acetylneuraminic acid (sialic acid), but not mannose or galactose-6-P, showed reduced adherence to ROS-treated HUVEC, suggesting that carbohydrate molecules were expressed on the latter and served as the ligand for the PMN L-selectin. Intercellular adhesion molecule (ICAM-1), constitutively present on the surface of resting HUVEC, was involved in the PMN adherence to ROS-treated HUVEC, since this adherence was inhibited by anti-ICAM-1, anti-CD11a, anti-CD11b, and anti-CD18 MoAbs. A non-CD18, non-ICAM-1-dependent mechanism is also involved in this adherence, since effects of these MoAbs were not additive; moreover, combinations of anti-CD18 and anti-ICAM-1 MoAbs with mannose-6-P and sialic acid completely inhibited PMN adherence. The increased binding of PMN to HX-XO-exposed HUVEC observed here involved IC-AM-1, but was independent of its upregulation, and another non-ICAM-1-dependent mechanism, in which carbohydrates expressed on HUVEC recognize L-selectin on PMN.

Antibodies, Monoclonal↗
PubMed1994

Comparative sugar degradation by (OH). produced by the iron-driven Fenton reaction and gamma radiolysis.

We compared the attack of deoxyribose and mannitol by (OH). produced by gamma radiolysis or the iron-driven Fenton reaction. Deoxyribose (DR) oxidation by gamma radiolysis gave rise to thiobarbituric reactive substances (TBARS) with a yield of 17 mol (OH). per mole of TBARS. (OH). scavengers (benzoate, formate, and pentoxifylline) protected DR from oxidation. Mannitol was similarly oxidized by (OH). produced by gamma radiolysis, with a yield of 14 mol (OH). per mole of TBARS produced. A mixture containing both DR and mannitol gave rise to TBARS production with a yield of 9 mol (OH). per mole of TBARS superior to that of each product separately, suggesting the formation of secondary radicals responsible for the degradation of DR or mannitol. When (OH). was produced by the iron-driven Fenton reaction, DR gave rise to TBARS whereas mannitol did not. Furthermore, mannitol protected DR against degradation, apparently in the same way as desferrioxamine and diethylenetriaminepentaacetic acid, suggesting that it acts as an iron chelator. It can thus be assumed that, according to the site of (OH). production, sugar molecules are degraded as a function of their rate constant with (OH). or their iron chelating capacity.

Benzoates↗
PubMed1994

Myocardial neutrophil sequestration and activation related to the reperfusion of human heart during coronary artery surgery.

OBJECTIVE: The aim was to determine if neutrophils are activated and sequestered as they pass through postischaemic human myocardium. METHODS: The occurrence of neutrophil activation during the reperfusion of the ischaemic myocardium was investigated in 16 selected patients undergoing coronary artery bypass surgery. Neutrophils were counted and elastase and lactoferrin released into the plasma were measured simultaneously in myocardial venous blood and in peripheral venous blood, before aortic cross clamping (T0), and two (T1), 10 (T2), and 20 (T3) min after unclamping. RESULTS: At T0, no statistically significant difference was noted between peripheral and myocardial blood with respect to the three variables studied. Reperfusion was associated with a significantly lower neutrophil count in myocardial blood compared to peripheral blood (p < 0.001), suggesting that neutrophils were trapped within the myocardium during reperfusion. In addition, levels of elastase (T1, T2, and T3), and lactoferrin (T1) were significantly higher in myocardial blood as compared to peripheral blood (p < 0.001), suggesting that activated neutrophils released their granular content into the plasma milieu. CONCLUSION: We provide evidence consistent with local neutrophil activation during myocardial reperfusion in patients undergoing coronary artery bypass surgery, in addition to the well described systemic activation related to cardiopulmonary bypass.

Adult↗