Biomedical subjects

S Kapiotis

Publications and source records attributed to S Kapiotis.

At least 73 records · Page 4Linked to original sources

PubMed1998

Low-dose aspirin does not lower in vivo platelet activation in healthy smokers.

Smoking causes atherosclerosis, and smokers have increased thromboxane (TXA2) formation. As aspirin inhibits TXA2 production we speculated that smokers would preferentially profit from inhibition of the TXA2 pathway by aspirin. Increased expression of P-selectin, a constituent of the alpha-granules of platelets, and increased levels of circulating (c)P-selectin in plasma are markers for platelet activation. The aim of this study was to compare P-selectin expression on platelets between smokers and nonsmokers, and to compare with placebo the effect of 2 weeks administration of 100 mg/d aspirin on platelet activation in smokers. Smokers exhibited higher P-selectin expression on platelets than non-smokers (2.7+/-1.8% v 1.6+/-0.6%, P=0.018), thus confirming increased platelet activation. Aspirin did not reduce platelet activation as demonstrated by unchanged P-selectin expression on platelets and cP-selectin plasma levels.

Adult↗

PubMed1998

Differential induction of P-selectin expression on platelets by two cell separators during plateletpheresis and the effect of gender on the release of soluble P-selectin.

BACKGROUND: Though a number of studies have elegantly characterized platelet activation during storage, less attention has been paid to the initial activation caused by different collection procedures. STUDY DESIGN AND METHODS: The effects of two blood cell separators on the initial activation of platelets were measured by flow cytometric analysis of P-selectin expression in 13 male donors on one cell separator (CS 3000 Plus) and 11 men and 9 women on the other (MCS 3P). In addition, the storage and release of soluble P-selectin (circulating P-selectin [cP-selectin]) by platelets were quantified, to determine whether the change in cP-selectin is a more sensitive marker for initial platelet activation, and the influence of gender on measured endpoints was evaluated. RESULTS: The CS 3000 Plus increased the percentage of P-selectin-positive platelets from a median of 3.4 percent before apheresis to 7.6 percent (p = 0.006) in platelet concentrates (PCs), whereas the MCS 3P did not (p = 0.002 between the two cell separators). When preapheresis cP-selectin levels were compared to those in apheresis PCs, cP-selectin increased from 51 to 101 ng per mL in plasma of CS 3000 Plus PCs, whereas cP-selectin levels increased from 53 to 78 ng per mL in MCS 3P PCs (men) and from 48 to 99 ng per mL in MSC 3P PCs (women) (p<0.005 for all). The relative increase in cP-selectin was higher in women than in men in MCS 3P PCs (p = 0.013). Concomitantly, the amount of P-selectin stored in platelets before apheresis decreased (p<0.025 for all). When donors undergoing apheresis on the MCS 3P were compared, the amount of P-selectin stored in the platelets of PCs was higher in men than women (p = 0.026). CONCLUSION: This trial shows 1) that initial activation of platelets obtained with the MCS 3P is less than that of platelets obtained with the CS 3000 Plus; 2) that the increase in cP-selectin is a more sensitive marker for initial platelet activation than the expression of P-selectin on the surface; and 3) that the relative amount of cP-selectin is higher in women than in men given the same stimulus. Differences in platelet activation by various cell separators and the sex of the donor may contribute to variability of PC quality.

Blood Platelets↗

PubMed1998

Sufentanil inhibits migration of human leukocytes through human endothelial cell monolayers.

UNLABELLED: The interactions between blood and vascular wall cells are essential for understanding pathophysiological processes, e.g., during inflammation. The influence of anesthetics on leukocyte function is well documented. An inhibitory effect of thiopental, midazolam, and ketamine on leukocyte chemotaxis in a Boyden chamber chemotaxis assay (i.e., endothelial cells were not included) has been demonstrated. Little is known, however, about the influence of sufentanil on the inflammatory processes. To reach their targets in the tissue in vivo, leukocytes must interact with endothelial cell monolayers (ECMs). The aim of the current study was to investigate the influence of sufentanil on the migration of leukocytes through an ECM. Human umbilical vein endothelial cells were cultured to achieve a monolayer. Isolated polymorphonuclear leukocytes and ECM were preincubated with different concentrations of sufentanil. The rate of leukocyte migration against the chemotactic protein formyl-methyl-leucyl-phenylalanine was measured (n = 7). Sufentanil significantly reduced the amount of leukocyte migration through ECM to 77%+/-7.8% (P < 0.05 compared with control). Endothelial cells as well as leukocytes contributed to this effect: treatment of both cell types showed an additive effect. Although lower concentrations showed no effect, high concentrations reduced leukocyte migration through ECM to 61%+/-7.1%. IMPLICATIONS: Leukocytes play an important role during inflammation, and anesthetics influence leukocyte functions, e.g., respiratory burst or chemotaxis. The effect of sufentanil on transendothelial leukocyte migration has not been investigated. Therefore, we used a migration assay including endothelial cell monolayers. Sufentanil showed a reducing effect on transendothelial leukocyte migration.

Adult↗

PubMed1998

Ketamine significantly reduces the migration of leukocytes through endothelial cell monolayers.

OBJECTIVE: To study the role of neutrophils in host defense, using human endothelial cells in migration studies in the presence of ketamine (0.3, 3, and 30 microg/mL). DESIGN: Prospective, controlled study. SETTING: University research laboratories. SUBJECTS: Seven independent experiments from different donors were done, investigating the influence of ketamine (0.3, 3, and 30 microg/mL) to the migration of human leukocytes through human endothelial cell monolayers. INTERVENTIONS: Human endothelial cell monolayers and/or human leukocytes were preincubated with clinically relevant (3 microg/mL), higher (30 microg/mL), and lower (0.3 microg/mL) concentrations of ketamine. The amount of leukocyte migration after 3 hrs was measured in a fluorometer. MEASUREMENTS AND MAIN RESULTS: Human endothelial cells isolated from umbilical veins were cultured on microporous membranes (polyethylene-terephthalat membranes) until they formed an endothelial cell monolayer. Leukocytes were separated by standard procedures. The migration of leukocytes through monolayers of endothelial cells under the clinically relevant concentration of ketamine was reduced to 59+/-9.8% (SD) (p< .05) when leukocytes but not the endothelial cell monolayers were preincubated with ketamine. Leukocyte migration was reduced to 92+/-7.3% (p > .05) when only monolayers of endothelial cells were treated with ketamine, and to 52+/-8.8% (p< .05) when both leukocytes and monolayers of endothelial cells were treated with ketamine. The higher and lower concentrations showed a dose-dependent effect. CONCLUSIONS: We investigated the cellular interaction between both cell systems, leukocytes and endothelial cells, simultaneously in the presence of ketamine. Ketamine is able to reduce significantly the migration of leukocytes through endothelial cell monolayers. The use of different dosages revealed a dose-dependent effect. The current model allowed treatment of one cell type, either leukocyte or endothelial cell. Ketamine inhibits the function of leukocytes more than the function of endothelial cells.

Anesthetics, Dissociative↗

PubMed1998

Kinetics of circulating selectin levels during bone marrow aplasia.

We have studied the kinetics of plasma levels of circulating (c)selectins in 8 patients undergoing bone marrow or stem cell transplantation to gain estimates for the distribution and half-life of (c)selectins and to potentially identify an endothelial source of cP-selectin in patients who are deprived of platelets and megakaryocytes. Blood was sampled just before conditioning treatment and immediately after, at 2 occasions under bone marrow aplasia (1 and 2 wk after BMT), on 2 separate days (3-8 d apart) before and at 60 min after platelet transfusion, and 30-72 d after BMT. All (c)selectins showed a strikingly parallel decrease during bone marrow aplasia: cP-selectin decreased by a median of 70% (range: 59-95%), cE-selectin by 63% (range: 27-78%), and cL-selectin by 75% (range: 66-90%) compared to baseline (p=0.012 for all comparisons). Estimates for plasma half-lives of all (c)selectins were obtained from individual time vs. concentration profiles of the maximal decreases and ranged from 2 to 4 d. cP-selectin increased by 23% (p=0.003), cE-selectin by 5% (p=0.041) and cL-selectin by 19% (p=0.009) 1 h after the platelet transfusions. Based on these results the calculated volume of distribution (Vd) of transfused (c)selectins was 2.5-fold higher than the plasma volume, which supports the concept of the in-vivo expression of binding sites, i.e. ligands, for cE-selectin and cL-selectin. In summary, while our study cannot provide any evidence for endothelial cells as a source of cP-selectin, we have found for the first time evidence for the existence of ligands for soluble cE-selectin and cL-selectin in humans.

Adult↗

PubMed1998

Glucocorticoids dose-dependently increase plasma levels of granulocyte colony stimulating factor in man.

Glucocorticoids increase neutrophil counts by decreasing the margination of neutrophils and mobilizing neutrophils from the bone marrow pool. The mechanisms for these effects however are not fully elucidated, but it has been demonstrated that dexamethasone enhances release of colony stimulating factor (G-CSF) in-vitro. We therefore hypothesized, that dexamethasone may increase plasma levels of G-CSF. A double blind, randomized, placebo-controlled, three-way cross-over trial was conducted in nine healthy men. Every subject received four identical infusions of saline, 0.04 mg/kg or 1.0 mg/kg dexamethasone during three observation periods of 48 hours each. The low dose of dexamethasone increased G-CSF levels from a baseline of 15.5 ng/L (CI: 10.6-20.4) by 240% (CI: 115-366%) at 24 hours. The high dexamethasone dose increased G-CSF levels from a baseline of 12.3 ng/L (CI: 9.7-14.9) by 871% (CI: 592-1149%) at 24 hours (p=0.008 for all comparisons). No further increase was observed at 48 hours but the effect was less pronounced (p<0.008 and p=0.08 for the high and the low dose of dexamethasone, respectively). Granulocyte-macrophage-CSF (GM-CSF) levels were below the assay's detection limit of 0.36 ng/L in all subjects. In conclusion, dexamethasone dose dependently increases G-CSF levels in healthy men, an effect which may account for some of its effects on neutrophils.

Adult↗

PubMed1998

Plasma levels of activated factor VII decrease during the menstrual cycle.

Men have an increased cardiovascular risk as compared to women, which is largely ascribed to the cardioprotective effects of female sex steroids. We hypothesised that this may be reflected by differences in the activation status of the coagulation system. Hence the aim of this study was to compare plasma levels of activated factor VII (FVIIa) in men and women, and to study the influence of the menstrual cycle on FVIIa levels. In a prospective study we investigated 20 healthy young women and 20 men. Men had significantly higher levels of activated factor VII (60 mU/ml, CI: 52 to 67) than women during all phases of the menstrual cycle. In women FVIIa was higher during the follicular phase (41 mU/ml, CI: 33 to 50) than during midcycle (34 mU/ml, CI: 24 to 45; p = 0.022 vs. follicular phase) and during the luteal phase (33 mU/ml, CI: 24 to 42; p = 0.006 vs. follicular phase). Prothrombin fragment (F1 + 2) levels decreased from 0.86 nmol/l (CI: 0.51-1.21) by -23% (-39% to -8%; p = 0.011) during midcycle and by -25% (CI: -51% to 1%; p = 0.023) during the luteal phase. These data support the contention that plasma levels of FVIIa, a key enzyme of the coagulation cascade, may be down-regulated by endogenously produced female sex hormones during the menstrual cycle. This may at least partially explain the marked gender differences found in FVIIa.

Adult↗

PubMed1997

Enhanced blood coagulation and enhanced fibrinolysis during hemodialysis with prostacyclin.

In the present study the effect of unfractionated heparin (UFH) (Liquemin, 750-1000 IU/h), low molecular weight heparin (LMWH) (Fragmin, 3000-7250 IU bolus), and prostacyclin (Flolan, 5 ng/kg body weight/min) on the activation of blood coagulation and fibrinolysis, induced by polysulfone membrane dialyzers during hemodialysis, was compared. Plasma levels of thrombin-antithrombin III complex (TAT), fibrin split product D-dimer, and plasmin-plasmin inhibitor-complex (PPI) were measured in the arterial and venous line of the dialyzer at the beginning and at 10, 60, 120, and 180 minutes of hemodialysis. Five patients on chronic hemodialysis treatment were investigated in a cross over study. Clinically all three anticoagulation regimen were sufficient for hemodialysis treatment. Using UFH or LMWH TAT, PPI, and D-dimer levels were similar in the venous and the arterial line of the dialyzer. However, during prostacyclin treatment the levels of these activation markers were significantly higher in the venous line. Based on these data the dialyzer membrane can be considered as a site of activation of blood coagulation and of fibrinolysis during anticoagulation with prostacyclin in hemodialysis.

Adult↗

PubMed1997

Evaluation of a new screening assay ProC Global for identification of defects in the protein C/protein S anticoagulant pathway.

In the present study a new assay, ProC Global, globally estimating the activity of the main plasma components of anticoagulant protein C/protein S pathway, was evaluated with respect to test characteristics and its sensitivity in the detection of deficiency states of protein C and protein S and of increased aPCR. In the ProC Global assay procedure protein C is activated in patient's plasma by an activator reagent (venom from agkistrodon contortrix). The extent of the prolongation of a sample's aPTT, caused by the activation of protein C, is taken as a measure for its anticoagulant capacity. Ninety-eight patients with one of the above mentioned defects were investigated. Decreased plasma protein C activity and increased aPCR were detected with a sensitivity of 1.0, while only 11 of 14 patients with decreased levels of free protein S antigen showed abnormal results in the ProC Global assay (sensitivity = 0.79). The test can be used in heparinized samples up to 1.0 anti Xa U/ml heparin (UFH and LMWH). When samples from patients on oral anticoagulant treatment are prediluted with factor V deficient plasma the test is sensitive for increased aPCR.

Administration, Oral↗

PubMed1997

Evaluation of bedside prothrombin time and activated partial thromboplastin time measurement by coagulation analyzer CoaguCheck Plus in various clinical settings.

In the present study CoaguCheck Plus (CCP), a coagulation test system using whole blood, was evaluated with respect to its comparability with widely distributed conventional routine coagulation assays. A correlation of r = 0.997 (p < 0.0001) was found between INR of CCP-prothrombin time (CCP-PT) and Thrombotest (KC-1 analyzer) in patients on oral anticoagulant therapy. A correlation of r = 0.899 (p < 0.001) between CCP-aPTT and Actin ES aPTT (STA analyzer) was found in heparinized patients. Impaired hepatic hepatic coagulation factor synthesis in liver cirrhosis patients was detected by CCP-PT with a sensitivity of 0.75 and by Normotest (STA analyzer) with a sensitivity of 0.92. Those patients with normal CCP-PT values and liver disease had, only mild reductions (> 30% of normals) in coagulation factors II, V, VII or X. CCP-aPTT was also performed in patients with a deficiency in the so called endogenous coagulation factors VIII, IX, XI and XII. CCP-aPTT showed a sensitivity similar to that of Actin FS aPTT in the detection even of mild deficiencies in factors VIII, IX and XII; factor XI deficiency was however detected only in patients with severe (< 12% of normals) disease; lupus anticoagulants were detected with a high sensitivity.

Blood Coagulation Tests↗

PubMed1997

Morning hypercoagulability and hypofibrinolysis. Diurnal variations in circulating activated factor VII, prothrombin fragment F1+2, and plasmin-plasmin inhibitor complex.

BACKGROUND: Diurnal fluctuations of blood coagulation and fibrinolysis activity are thought to play a role in the observed circadian variation in the frequency of onset of acute cardiovascular events. In the present study, the diurnal variations in blood coagulation and fibrinolysis activity were investigated in 10 young, healthy control subjects by use of specific molecular activation markers. METHODS AND RESULTS: The plasma levels of activated factor FVII (FVIIa), the active portion of the main coagulation activator, decreased during the day (8 AM: 2.03 ng/mL, CI 1.16 to 2.88 ng/mL; 8 PM: 1.16 ng/mL, CI 0.81 to 1.5 ng/mL; P = .005), whereas FVII antigen did not change significantly. In parallel with the diurnal variations of FVIIa, we found a decrease of prothrombin fragment F1+2 (8 AM: 0.97 nmol/L, CI 0.79 to 1.15 nmol/L; 8 PM: 0.78 nmol/L, CI 0.64 to 0.93 nmol/L; P = .005), a molecular marker of intravasal thrombin generation. Evidence for a possible functional relevance of circulating FVIIa was found because this parameter was significantly correlated with prothrombin fragment F1+2 in 72 fasting healthy individuals (r = .29, P = .011). Plasminogen activator inhibitor-1 levels decreased (8 AM: 9.9 ng/mL, CI 7.7 to 12.1 ng/mL; 8 PM: 5.4 ng/mL, CI 3.8 to 6.9 ng/mL; P < .005), whereas plasmin-plasmin inhibitor complex levels, representing the degree of intravascular plasmin generation, concomitantly increased (8 AM: 235 micrograms/L, CI 198 to 272 micrograms/L; 8 PM: 449 micrograms/L, CI 391 to 507 micrograms/L; P = .008). CONCLUSIONS: Our data suggest that the diurnal changes in the plasma levels of activators and inhibitors of coagulation and fibrinolysis lead to corresponding changes in the activity state of these systems, leading to morning hypercoagulability and hypofibrinolysis.

Adult↗

PubMed1997

Tyrosine: an inhibitor of LDL oxidation and endothelial cell cytotoxicity initiated by superoxide/nitric oxide radicals.

Tyrosyl radicals can catalyze LDL oxidation. In addition to their LDL oxidizing ability, superoxide (O2.-)/nitric oxide (NO.) generate phenoxyl radicals when reacting with tyrosine. Therefore we tested if tyrosine can act as a pro-oxidant in O2.-/NO.-initiated LDL oxidation. When LDL was exposed to O2.-/NO., tyrosine exerted a strong inhibitory effect on O2.-/ NO.-initiated LDL oxidation as measured by TBARS formation and alteration in electrophoretic mobility of LDL. Tyrosine was also able to protect human endothelial cells from the cytotoxic effect of O2.-/NO.. Because O2.-/NO. can occur in vivo, the results may indicate that serum-free tyrosine could act as an efficacious physiological antioxidant in case of O2.-/NO.-initiated LDL oxidation and endothelial cell cytotoxicity.

Endothelium, Vascular↗

PubMed1997

Menstrual cycle-associated changes in blood levels of interleukin-6, alpha1 acid glycoprotein, and C-reactive protein.

Based on previous studies we hypothesized that interleukin-6 (IL-6) plasma levels would increase during the menstrual cycle, in analogy to the increase in IL-1 levels seen during the luteal phase. Thus we have investigated menstrual cycle-associated changes in IL-6, alpha1 acid glycoprotein (AGP), and C-reactive protein (CRP). The study design was cross-sectional and was conducted in 18 healthy premenopausal women with regular menstrual cycles and in 15 age-matched men. The women had blood drawings in the follicular phase, at midcycle, and in the luteal phase of the menstrual cycle. A single blood sample was obtained from men to compare IL-6 levels between sexes. The median IL-6 level was 0.68 pg/ml (95% confidence interval (CI): 0.60 to 1.05) in the follicular phase and did not change significantly during the menstrual cycle. IL-6 levels did not differ between women and men (0.79 pg/ml; CI: 0.66 to 1.05; p > 0.05). Median AGP levels decreased by 6% (CI: -14% to 1%) during the luteal phase (p = 0.005), and a significant correlation between mean AGP and IL-6 levels was found (r = 0.60; p = 0.01). Median CRP levels increased by 44% (CI: 27% to 59%; p < 0.001) at midcycle and by 31% (CI: 17% to 68%; p = 0.002) in the luteal phase, and there was a significant correlation between the relative increase in CRP at midcycle and the relative increase in progesterone levels during midcycle (r = 0.60; p = 0.01) and the luteal phase (r = 0.71; p = 0.001). In conclusion, we found no sustained menstrual cycle-dependent changes in systemic IL-6 plasma levels. AGP and CRP levels may be differentially regulated during the menstrual cycle of healthy women: AGP levels correlated with IL-6 levels, and AGP levels decreased during the menstrual cycle, whereas CRP levels increased during the menstrual cycle and correlated with the increase in progesterone levels. The reason for the observed changes in CRP levels remains to be elucidated.

Adult↗

PubMed1997

Effects of angiotensin-II infusion at pressor and subpressor doses on endothelin-1 plasma levels in healthy men.

Several lines of evidence suggest that effects of angiotensin-II (A-II) could be mediated in part by endothelin-1 (ET-1): A-II enhances production and secretion of ET-1 which in turn may contribute to the pressor effects and mitogenic actions of A-II. We have conducted a randomized controlled cross-over study to investigate whether A-II increases ET-1 plasma levels in humans at pressor doses. Each of the eight healthy male volunteers received a subpressor and pressor dose of A-II which were assessed by titration of the individual dose dependent blood pressure responses to A-II-infusion. The mean subpressor dose of A-II was 0.62 ng/kg/min. (range: 0.31-1.25); the mean pressor dose of A-II was 8.44 ng/kg/min. (range 2.5-20), yielding an average increase in mean arterial pressure by 35% (95% confidence interval [CI]: 24-45%). Plasma ET-1 concentrations increased significantly only in response to pressor doses of A-II (Friedman ANOVA p=0.022): ET-1 increased by 89 % (CI: 24-154%) over baseline (1.7 pmol/L; CI: 1.4-2.0) 60 min. after starting the pressor infusion of A-II and remained elevated throughout the 4-hours observation period. In conclusion, A-II at pressor doses but not at subpressor doses induced an increase in plasma levels of ET- 1 in healthy subjects. This finding may be of relevance for various diseases associated with increased production of A-II and could potentially have therapeutic implications.

Adult↗

PubMed1997

Transfer of erythropoietin across the placenta perfused in vitro.

OBJECTIVE: The purpose of this study was to investigate the placental passage of erythropoietin in a placental perfusion model ex vivo. METHODS: In an open system 18 placentas were perfused on both the maternal and the fetal side. Erythropoietin and a reference substance were added to either the maternal or fetal perfusion medium. In the first series of experiments, radiolabeled erythropoietin was added to the perfusion medium in four different concentrations to help determine the transfer rate of erythropoietin. Based on the results of these experiments unlabeled erythropoietin was added to the perfusate in three different concentrations. Radiolabeled erythropoietin was used in addition to erythropoietin because measuring radioactivity in a gamma counter is less expensive than measuring by immunoassay. RESULTS: Accumulation of radioactivity in the venous portion of the fetal circuit was only 3.21% of the activity added to the maternal circuit. No evidence of transfer of erythropoietin to the contralateral compartment was noted, regardless of whether the test substance was added maternally or fetally. These results were independent of the concentration used. The reference compound antipyrine showed a mean transfer rate of 27.9%, which is in keeping with previous results. CONCLUSION: There is no transport of erythropoietin across fetal membranes. This finding is particularly remarkable in view of results published recently indicating the placenta as a site of erythropoietin production. The lack of its transport across the human placenta is most likely due to its high molecular weight.

Biological Transport↗

PubMed1997

Natural latex, grass pollen, and weed pollen share IgE epitopes.

BACKGROUND: Because of the frequent use of natural latex products, IgE-mediated reactions to latex proteins represent an important health threat in industrialized countries. Although several latex allergens have been characterized and IgE cross-reactivities with allergens present in plant-derived food have been described, limited information is available regarding the presence of common IgE-binding components in latex and plant pollen. METHODS: By using serum IgE from 56 individuals with latex allergy, the IgE-binding components in ammoniated latex milk and latex glove extracts were characterized by immunoblotting. The presence of cross-reactive IgE-binding components in the different latex extracts, extracts from mugwort, ragweed, timothy grass pollen, and recombinant birch pollen allergens (Bet v 1 and Bet v 2 [birch profilin]) was studied by immunoblot inhibitions and quantitative competition experiments. The involvement of carbohydrates in the constitution of cross-reactive IgE epitopes was studied by periodate treatment of extracts. RESULTS: Although sera from certain individuals with latex allergy showed IgE reactivity with protein bands of different molecular weights in Western-blotted latex milk and glove extracts, both extracts contained common IgE epitopes. Although preincubation with recombinant Bet v 1 and Bet v 2 did not significantly inhibit IgE binding to latex proteins, weed and, in particular, timothy grass pollen extract strongly inhibited IgE binding to latex allergens. The cross-reactive IgE epitopes were sensitive to periodate treatment. CONCLUSIONS: Mugwort, ragweed, and timothy grass pollen share IgE epitopes with glycoprotein latex allergens. The presence of common epitopes might in part explain clinical symptoms in patients allergic to pollen on contact with latex.

Adolescent↗

PubMed1997

Effects of exercise on circulating vascular adhesion molecules in healthy men.

Based on previous studies showing an increase in circulating soluble intercellular adhesion molecule-1 (sICAM-1) after exercise, we hypothesized that exercise may also increase serum levels of the vascular cell adhesion molecule-1 (sVCAM-1) and sE-selection. In a prospective controlled clinical trial, serum levels of sE-selectin, sICAM-1 and sVAM-1 were measured before and after two different exercise protocols in healthy untrained men. Lactate levels increased up to 12.7 mmol/L (95% confidence interval: 10.1-15.9) and 3.6 mmol/L (CI: 2.4-4.7) after ergometry and after an one hour endurance exercise at 60% of the maximal work intensity, respectively (p = 0.028 vs baseline and controls). The maximal increase in lymphocyte counts of 106% (CI: 63-146), which was only of short duration, was higher immediately after ergometry as compared to that observed after endurance exercise (p = 0.028). However, the maximal increase in neutrophil counts of 178% (CI: 120-298) which was seen at 2 hours after endurance exercise was higher than that seen after ergometry (p = 0.028). In contrast, only small changes of circulating adhesion molecules were seen immediately after ergometry: sICAM-1 increased by 11% (CI: 4-25; p = 0.028), and similar tendencies were also observed for sVCAM-1 and sE-selectin. No other consistent and time-dependent changes of circulating adhesion molecules were observed and all differences and changes were < or = 11%. In sum our study provides evidence that recreational sporting activities in untrained healthy subjects at normal altitude have little influence on serum levels of the circulating vascular adhesion molecules sE-selectin, sVCAM-1 or sICAM-1.

Adult↗

PubMed1997

Effects of endothelin-1 on circulating adhesion molecules in man.

Several studies point to a role for endothelin-1 (ET-1) in enhancing adhesion molecule expression and leucocyte adhesion. We thus hypothesized that ET-1 would induce expression of adhesion molecules by endothelial cells and by leucocytes in humans, and hence compared with placebo the effect of a continuous 6-h ET-1 infusion on plasma levels of circulating (c)E-selectin, cP-selectin, intercellular and vascular cell adhesion molecule 1. In addition, we investigated the effects of ET-1 on expression of the leucocyte adhesion molecules CD11b/CD18 and L-selectin on monocytes and neutrophils. After an open pilot study to evaluate the safety of a 6-h ET-1 infusion of 0.4 pmol kg-1 min-1 (n = 4), the main study was conducted as a randomized, double-blind, two-way, cross-over trial in 12 additional young healthy male volunteers, who received the same treatment and were observed over a period of 24 h. ET-1 infusion decreased renal plasma flow by 43% (CI 35-51%; P < 0.001) and increased the filtration fraction by 80% (CI 20-110%; P < 0.001). Heart rate decreased by -10% (CI -4% to -15%) at 6 h under ET-1 infusion in the cross-over trial (P = 0.012 between periods). Although ET-1 infusions increased plasma levels of ET-1 by about 300%, ET-1 elicited no relevant changes in any circulating adhesion molecules or leucocyte adhesion molecules measured. In the placebo period small diurnal changes were observed for cP-selectin (-8%, CI -14 to -3%, P = 0.008) and cE-selectin (-6%, CI -10 to -3%, P = 0.003) at 12 h (20.45 h). In sum, ET-1 does not regulate circulating adhesion molecules in healthy men. Circadian variations may exist for plasma levels of cP-selectin and cE-selectin.

Adult↗