Kirchheim Hospital

Kirchheim an der Weinstraße, Germany

Kirchheim Hospital

Kirchheim an der Weinstraße, Germany
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Swoboda S.,University of Heidelberg | Gruettner J.,University of Mannheim | Lang S.,University of Mannheim | Wendel H.-P.,University of Tübingen | And 4 more authors.
Experimental and Therapeutic Medicine | Year: 2014

Deep hypothermic circulatory arrest (DHCA) is a common technique used to protect vital organs during surgical interventions on the thoracic aorta or during surgery for complex congenital heart disease. Activated leukocytes are key mediators of inflammatory responses during ischemia. Intercellular crosstalk between leukocytes, platelets and endothelial cells is mediated by cell adhesion molecules. These molecules trigger complex cell-cell interaction mechanisms and initiate the release of proinflammatory molecules. One parameter that is known to have a significant impact on inflammatory cell activation and the production of proinflammatory markers is temperature. However, to the best of our knowledge, no data have yet been published on the effect of hypothermia on leukocyte surface markers during DHCA. Thus, the aim of the present study was to investigate the effect of hypothermia on the expression of cell adhesion molecules on monocytes under DHCA conditions in vitro. Blood samples collected from 11 healthy volunteers were incubated in a well-established model simulating circulatory arrest at 36°C and 18°C for 30 min. The expression of cluster of differentiation (CD) molecule 11B (CD11b), CD54 and CD162 on monocytes was measured as the mean fluorescence intensity (MFI) using flow cytometry. The expression level of CD11b on monocytes was significantly decreased following the incubation of the blood samples at 18°C compared with the level in blood samples incubated at 36°C (P<0.001). After 30 min of blood stasis in the circulatory arrest model, the expression level of CD162 on monocytes was significantly lower in the blood samples incubated at 18°C than in those incubated at 36°C (P<0.001). No association was identified between temperature and the surface expression of CD54 on monocytes following 30 min of stasis. These findings demonstrate that deep hypothermia decreases the expression of CD11b and CD162 on monocytes in an experimental setup simulating the conditions of DHCA. This may be the result of the inhibition of leukocyte-endothelial and leukocyte-platelet interactions, which may be a beneficial aspect of deep hypothermia that affects the inflammatory response and tissue damage during DHCA.


Swoboda S.,University of Heidelberg | Walter T.,University of Mannheim | Lang S.,University of Mannheim | Wendel H.-P.,University of Tübingen | And 4 more authors.
In Vivo | Year: 2014

Aim: The aim of the present study was to investigate the effect of GPIIb/IIIa inhibition with eptifibatide and tirofiban on the expression of cellular adhesion molecules on monocytes at different temperatures. Materials and Methods: Circulation of blood from six volunteers was performed in an extracorporal circulation model at 36°C and 18°C for 30 min. The blood of each donor was prepared either with addition of eptifibatide or tirofiban, or was left untreated as control. CD54 and CD162 on monocytes was measured using flow cytometry. Results: Expression of CD11b was lower at 18°C compared to 36°C by 51% in the eptifibatide group (p=0.0043), by 29% in the tirofiban group (p=0.095) and by 34% in the control group (p=0.038). Expression of CD54 was not significantly different at 18°C compared to 36°C, neither with eptifibatide (p=0.29) nor tirofiban (p=0.48) nor in the control group (p=0.26). Expression of CD162 was lower at 18°C compared to 36°C by 40% using eptifibatide (p=0.0010), by 94% using tirofiban (p=0.0095) and by 34% in the control group (p=0.019). At 36°C and 18°C, no significant differences were found regarding the expression of CD11b, CD54 and CD162 between the eptifibatide-treated group, the tirofiban-treated group and the control group. Conclusion: GPIIb/IIIa inhibition with eptifibatide or tirofiban seems to have no effect on the expression of CD11b, CD54 and CD162 on monocytes during normothermia or hypothermia. Our results show that the beneficial effect induced by hypothermia on the extracorporal circulation-Associated alteration of leukocyte function, with decreased expression of CD11b and CD162, seems not to be affected by additional treatment with eptifibatide or tirofiban.


Swoboda S.,University of Heidelberg | Gruettner J.,University of Mannheim | Lang S.,University of Mannheim | Wendel H.-P.,University of Tübingen | And 4 more authors.
In Vivo | Year: 2013

Aim: The aim of the present study was to investigate the effect of different hypothermic temperatures on the expression of cellular adhesion molecules on leukocytes. Materials and Methods: Circulation of blood from six volunteers was performed in an extracorporeal circulation model at 36°C, 28°C and 18°C for 30 minutes. Expression of CD11b, CD54 and CD162 on monocytes was measured using flow cytometry. Results: Expression of CD11b significantly decreased at 18°C and at 28°C compared to 36°C. A significant reduction of CD162 expression was found at 18°C compared to 28°C and 36°C and at 28°C compared to 36°C. No association was found between temperature and expression of CD54. Conclusion: Expression of CD11b and CD162 on monocytes has a temperature-dependent regulation, with decreased expression during hypothermia, which may result in an inhibition of leukocyte-endothelial and leukocyte-platelet interaction. This beneficial effect may influence the extracorporeal circulation-related inflammatory response and tissue damage.


PubMed | University of Tübingen, Kirchheim Hospital, University of Mannheim, Solingen Hospital and University of Heidelberg
Type: Journal Article | Journal: Experimental and therapeutic medicine | Year: 2014

Deep hypothermic circulatory arrest (DHCA) is a common technique used to protect vital organs during surgical interventions on the thoracic aorta or during surgery for complex congenital heart disease. Activated leukocytes are key mediators of inflammatory responses during ischemia. Intercellular crosstalk between leukocytes, platelets and endothelial cells is mediated by cell adhesion molecules. These molecules trigger complex cell-cell interaction mechanisms and initiate the release of proinflammatory molecules. One parameter that is known to have a significant impact on inflammatory cell activation and the production of proinflammatory markers is temperature. However, to the best of our knowledge, no data have yet been published on the effect of hypothermia on leukocyte surface markers during DHCA. Thus, the aim of the present study was to investigate the effect of hypothermia on the expression of cell adhesion molecules on monocytes under DHCA conditions


PubMed | University of Tübingen, Kirchheim Hospital, University of Mannheim, Solingen Hospital and University of Heidelberg
Type: Journal Article | Journal: In vivo (Athens, Greece) | Year: 2014

The aim of the present study was to investigate the effect of GPIIb/IIIa inhibition with eptifibatide and tirofiban on the expression of cellular adhesion molecules on monocytes at different temperatures.Circulation of blood from six volunteers was performed in an extracorporal circulation model at 36C and 18C for 30 min. The blood of each donor was prepared either with addition of eptifibatide or tirofiban, or was left untreated as control. CD54 and CD162 on monocytes was measured using flow cytometry.Expression of CD11b was lower at 18C compared to 36C by 51% in the eptifibatide group (p=0.0043), by 29% in the tirofiban group (p=0.095) and by 34% in the control group (p=0.038). Expression of CD54 was not significantly different at 18C compared to 36C, neither with eptifibatide (p=0.29) nor tirofiban (p=0.48) nor in the control group (p=0.26). Expression of CD162 was lower at 18C compared to 36C by 40% using eptifibatide (p=0.0010), by 94% using tirofiban (p=0.0095) and by 34% in the control group (p=0.019). At 36C and 18C, no significant differences were found regarding the expression of CD11b, CD54 and CD162 between the eptifibatide-treated group, the tirofiban-treated group and the control group.GPIIb/IIIa inhibition with eptifibatide or tirofiban seems to have no effect on the expression of CD11b, CD54 and CD162 on monocytes during normothermia or hypothermia. Our results show that the beneficial effect induced by hypothermia on the extracorporal circulation-associated alteration of leukocyte function, with decreased expression of CD11b and CD162, seems not to be affected by additional treatment with eptifibatide or tirofiban.

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