Biomedical subjects

L W de Rossi

Publications and source records attributed to L W de Rossi.

3 recordsLinked to original sources

PubMed2004

Xenon modulates neutrophil adhesion molecule expression in vitro.

BACKGROUND AND OBJECTIVE: Xenon reduces the infarct size after regional ischaemia in the rabbit heart in vivo, but the underlying mechanisms are unknown. Since adhesion molecules on neutrophils are closely involved in the pathophysiology of ischaemia/reperfusion injury and modulation of neutrophil function, we investigated the effect of xenon on neutrophil adhesion molecule expression in vitro. METHODS: Freshly isolated neutrophils were incubated with 30% or 60% xenon for 60 min. In unstimulated and after stimulation with either N-formyl-methionyl-leucyl-phenylalanine or phorbol-12-myristate-13-acetate neutrophil surface expression of PSGL-1, L-selectin, CD11a and CD11b were measured by flow cytometry. RESULTS: At both concentrations, xenon reduced the surface expression of PSGL-1 by 10% (P < 0.05), and of L-selectin by 15% (P < 0.05) in the 60% xenon group. Furthermore, N-formyl-methionyl-leucyl-phenylalanine activated neutrophils showed an increased removal of L-selectin from the neutrophil surface following incubation with xenon (30% compared to controls, P < 0.05). Neutrophil beta2-integrin expression was not altered by xenon. CONCLUSIONS: Xenon increases the removal of the selectins PSGL-1 and L-selectin from the neutrophil surface in vitro. Since both selectins are involved in the initial contact between neutrophils and endothelial cells, xenon may affect neutrophil adhesion to endothelium during ischaemia/reperfusion injury. However, because the beta2-integrin expression was unaffected by xenon, further investigations are required to clarify whether xenon may modulate neutrophil transmigration through endothelial cells in vivo.

Anesthetics, Inhalation↗

PubMed2003

Effect of isoflurane on monocyte adhesion molecule expression in human whole blood.

BACKGROUND: Recruitment of monocytes to inflamed tissue is a crucial step in the acute inflammatory reaction. Adherence of monocytes to endothelial cells followed by transmigration depends on monocyte surface adhesion molecules, inflammatory cytokines and chemoattractant chemokines. In the present study, we determined the effect of isoflurane on monocyte adhesion receptor expression in vitro. METHODS: Citrated whole blood was incubated for 60 min with either 0.5 or 1 MAC isoflurane. In unstimulated blood samples and after stimulation with N-formyl-methionyl-leucyl-phenylalanine (FMLP) monocyte cell-surface expression of the selectins PSGL-1 and L-selectin, and the beta2-integrins CD11a and CD11b were evaluated by flow cytometry. RESULTS: Isoflurane reduced significantly the expression of PSGL-1 on unstimulated monocytes, whereas the remaining selectins and beta2-integrins were not affected. At both concentrations, the FMLP-induced removal of PSGL-1 from the monocyte surface was increased. Furthermore, at 1 MAC isoflurane the FMLP-induced increase in CD11a expression was significantly inhibited. The surface expression of L-selectin and CD11b was not affected following exposure to isoflurane. CONCLUSION: Isoflurane increases the removal of the selectin PSGL-1 from the monocyte surface. Since PSGL-1 is important during the initial step of monocyte adhesion to endothelial P-selectin, the decrease in monocyte surface PSGL-1 may have profound effects on monocyte-endothelial interactions. Furthermore, the effects of isoflurane on monocyte adhesion molecule expression are different from those reported for neutrophils.

Anesthetics, Inhalation↗

PubMed2001

Xenon does not affect human platelet function in vitro.

We sought to determine whether xenon affects platelet glycoprotein expression and platelet-related hemostasis in vitro at a clinically relevant concentration. Human whole blood was stimulated with either adenosine diphosphate or the thrombin receptor agonist peptide (TRAP)-6 after incubation with 65% xenon. Halothane at 2 minimum alveolar anesthetic concentration was used as a positive control. Platelet function and activation were evaluated with two-color flow cytometry. The expression of the platelet glycoproteins GPIIb/IIIa, GPIb, and P selectin were detected with fluorochrome-conjugated monoclonal antibodies. In vitro measurement of platelet-related hemostasis under conditions of high shear stress was performed in citrated whole blood with a platelet function analyzer (PFA-100((R))) by using collagen/epinephrine and collagen/adenosine diphosphate cartridges. Xenon did not affect basal or agonist-induced expression of platelet membrane glycoproteins, activation-dependent conformational changes of the GPIIb/IIIa receptor, expression of P selectin, or PFA closure times. In contrast, halothane reduced TRAP-6-induced activation of the GPIIb/IIIa complex. Furthermore, collagen/epinephrine-induced PFA closure time was significantly prolonged. These results demonstrate that xenon does not affect the unstimulated or agonist-induced platelet glycoprotein expression, activation of GPIIb/IIIa, or platelet-related hemostasis.

Anesthetics, Inhalation↗