Lack of influence of the COX inhibitors metamizol and diclofenac on platelet GPIIb/IIIa and P-selectin expression in vitro

BACKGROUND: The effect of non-steroidal anti-inflammatory drugs (NSAIDs) for reduced platelet aggregation and thromboxane A(2 )synthesis has been well documented. However, the influence on platelet function is not fully explained. Aim of this study was to examine the influence of the COX-1 inhibiting NSAIDs, diclofenac and metamizol on platelet activation and leukocyte-platelet complexes, in vitro. Surface expression of GPIIb/IIIa and P-selectin on platelets, and the percentage of platelet-leukocyte complexes were investigated. METHODS: Whole blood was incubated with three different concentrations of diclofenac and metamizol for 5 and 30 minutes, followed by activation with TRAP-6 and ADP. Rates of GPIIb/IIIa and P-selectin expression, and the percentage of platelet-leukocyte complexes were analyzed by a flow-cytometric assay. RESULTS: There were no significant differences in the expression of GPIIb/IIIa and P-selectin, and in the formation of platelet-leukocyte complexes after activation with ADP and TRAP-6, regarding both the time of incubation and the concentrations of diclofenac and metamizol. CONCLUSIONS: Accordingly, the inhibitory effect of diclofenac and metamizol on platelet aggregation is not related to a reduced surface expression of P-selectin and GPIIb/IIIa on platelets

Carbon monoxide poisoning from waterpipe smoking: a retrospective cohort study

<p><b>Objective:</b> Waterpipe smoking may increasingly account for unintentional carbon monoxide poisoning, a serious health hazard with high morbidity and mortality. We aimed at identifying waterpipe smoking as a cause for carbon monoxide poisoning in a large critical care database of a specialty care referral center.</p> <p><b>Methods:</b> This retrospective cohort study included patients with a history of exposure to waterpipe smoking and carbon monoxide blood gas levels >10% or presence of clinical symptoms compatible with CO poisoning admitted between January 2013 and December 2016. Patients’ initial symptoms and carbon monoxide blood levels were retrieved from records and neurologic status was assessed before and after hyperbaric oxygen treatment.</p> <p><b>Results:</b> Sixty-one subjects with carbon monoxide poisoning were included [41 males, 20 females; mean age 23 (SD ± 6) years; range 13–45] with an initial mean carboxyhemoglobin of 26.93% (SD ± 9.72). Most common symptoms included syncope, dizziness, headache, and nausea; 75% had temporary syncope. Symptoms were not closely associated with blood COHb levels.</p> <p><b>Conclusion:</b> CO poisoning after waterpipe smoking may present in young adults with a wide variability of symptoms from none to unconsciousness. Therefore diagnosis should be suspected even in the absence of symptoms.</p

Unsaturated long-chain fatty acids induce the respiratory burst of human neutrophils and monocytes in whole blood

Abstract Background It is increasingly recognized that infectious complications in patients treated with total parenteral nutrition (TPN) may be caused by altered immune responses. Neutrophils and monocytes are the first line of defence against bacterial and fungal infection through superoxide anion production during the respiratory burst. To characterize the impact of three different types of lipid solutions that are applied as part of TPN formulations, we investigated the unstimulated respiratory burst activation of neutrophils and monocytes in whole blood. Methods Whole blood samples were incubated with LCT (Intralipid®), LCT/MCT (Lipofundin®) and LCT-MUFA (ClinOleic®) in three concentrations (0.06, 0.3 and 0.6 mg ml-1) for time periods up to one hour. Hydrogen peroxide production during the respiratory burst of neutrophils and monocytes was measured by flow cytometry. Results LCT and LCT-MUFA induced a hydrogen peroxide production in neutrophils and monocytes without presence of a physiological stimulus in contrast to LCT/MCT. Conclusion We concluded that parenteral nutrition containing unsaturated oleic (C18:1) and linoleic (C18:2) acid can induce respiratory burst of neutrophils and monocytes, resulting in an elevated risk of tissue damage by the uncontrolled production of reactive oxygen species. Contradictory observations reported in previous studies may in part be the result of different methods used to determine hydrogen peroxide production.</p

Unsaturated long-chain fatty acids induce the respiratory burst of human neutrophils and monocytes in whole blood-0

Atelets and bacteria. (B) Neutrophils and monocytes were identified by setting a polygonal gate in a forward scatter/sideward scatter dot plot. The negative control sample (C) was used to define a marker for rhodamine 123 (FL 1) where less than 5% of the cells would be positive. The percentage of neutrophils having produced hydrogen peroxide following lipid incubation was determined by counting the number of rhodamine positive cells above this marker position and by dividing it by the whole number of events observed (D).<p><b>Copyright information:</b></p><p>Taken from "Unsaturated long-chain fatty acids induce the respiratory burst of human neutrophils and monocytes in whole blood"</p><p>http://www.nutritionandmetabolism.com/content/5/1/19</p><p>Nutrition & Metabolism 2008;5():19-19.</p><p>Published online 14 Jul 2008</p><p>PMCID:PMC2483276.</p><p></p

Unsaturated long-chain fatty acids induce the respiratory burst of human neutrophils and monocytes in whole blood-1

Atelets and bacteria. (B) Neutrophils and monocytes were identified by setting a polygonal gate in a forward scatter/sideward scatter dot plot. The negative control sample (C) was used to define a marker for rhodamine 123 (FL 1) where less than 5% of the cells would be positive. The percentage of neutrophils having produced hydrogen peroxide following lipid incubation was determined by counting the number of rhodamine positive cells above this marker position and by dividing it by the whole number of events observed (D).<p><b>Copyright information:</b></p><p>Taken from "Unsaturated long-chain fatty acids induce the respiratory burst of human neutrophils and monocytes in whole blood"</p><p>http://www.nutritionandmetabolism.com/content/5/1/19</p><p>Nutrition & Metabolism 2008;5():19-19.</p><p>Published online 14 Jul 2008</p><p>PMCID:PMC2483276.</p><p></p

Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro

BACKGROUND: Endothelial adhesion molecules ICAM-1 (CD54) and VCAM-1 (CD106) mediate cellular adhesion and transcellular migration. Cell adhesion and diapedesis have a key role in the course of shock and sepsis. During severe sepsis, adrenoceptor agonist levels may be increased due to endogenous production or due to intensive care treatment. As yet, the influence of β1 or β2 agonists on adhesion molecule formation on endothelial cells has remained unclear. METHODS: Cultured human umbilical vein endothelial cells were stimulated with E. coli. Following bacterial stimulation the cells were incubated with either β2 receptor agonist terbutaline or β1 agonist norepinephrine. ICAM-1 and VCAM-1 expression were examined using flow cytometry. RESULTS: Administration of norepinephrine did not cause increases of both CD54 and CD106 in stimulated HUVEC. Compared to negative controls the bacterial stimulation itself led to an increase of adhesion molecules. Following administration of terbutaline no significant increase in CD54 expression was found. CONCLUSIONS: Bacterial stimulation led to an increase of adhesion molecule expression. Adrenoceptor stimulation of activated endothelial cells did not cause significant increases of cellular adhesion molecules