Thromb Haemost 2004; 91(04): 761-770
DOI: 10.1160/TH03-11-0685
Platelets and Blood Cells
Schattauer GmbH

Platelet-endothelial cell interaction in pulmonary microcirculation: the role of PARS

Rainer Kiefmann
1   Department of Anesthesiology, Ludwig-Maximilians-University, Munich, Germany
,
Kai Heckel
1   Department of Anesthesiology, Ludwig-Maximilians-University, Munich, Germany
,
Sonja Schenkat
2   Institute for Surgical Research, Ludwig-Maximilians-University, Munich, Germany
,
Martina Dörger
2   Institute for Surgical Research, Ludwig-Maximilians-University, Munich, Germany
,
Józefa Węsierska-Gądek
3   Institute for Cancer Research, University of Vienna, Vienna, Austria
,
Alwin E. Goetz
1   Department of Anesthesiology, Ludwig-Maximilians-University, Munich, Germany
› Author Affiliations
Further Information

Publication History

Received 11 November 2003

Accepted after revision 21 January 2004

Publication Date:
06 December 2017 (online)

Summary

Accumulation of platelets might contribute to acute lung injury during systemic inflammation. The aim of the study was to elucidate the role of the poly (ADP-ribose) synthetase, a nucleotide-polymerizising enzyme, in mediation of platelet-endothelial cell interaction through regulation of adhesion molecules within the pulmonary microcirculation during endotoxemia. We used in vivo fluorescence microscopy to quantify kinetics of fluorescently labeled erythrocytes and platelets in rabbit pulmonary arterioles and venules. Six hours after onset of endotoxin infusion we observed a massive interaction of platelets with the microvascular endothelial cells, whereas under control conditions, no platelet sequestration was measured. An up-regulation of P- and E-selectin was detected in lung tissue following endotoxin infusion by immunohistochemistry and Western blot analysis. Blockade of endothelial P-selectin with fucoidin resulted in a reduction of the endotoxin-induced platelet-endothelial cell interaction. Inhibition of poly (ADP-ribose) synthetase by 3-aminobenzamide inhibited the endotoxin-induced expression of endothelial P- and E-selectin and the subsequent recruitment of platelets. In summary, we provide first in vivo evidence that platelets accumulate in pulmonary microcirculation following endotoxemia. Poly (ADP-ribose) synthetase seems to mediate this platelet-endothelial cell interaction via P- and E-selectin expressed on the surface of microvascular endothelium.

 
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