Thromb Haemost 1993; 70(05): 826-833
DOI: 10.1055/s-0038-1649678
Platelets
Schattauer GmbH Stuttgart

Different Roles of Prostaglandins in Thromboembolic Processes in Arterioles and Venules In Vivo

Mirjam G A oude Egbrink
The Departments of Physiology and Biophysics, Cardiovascular Research Institute Maastricht, University of Limburg, Maastricht, The Netherlands
,
Geert-Jan Tangelder
The Departments of Physiology and Biophysics, Cardiovascular Research Institute Maastricht, University of Limburg, Maastricht, The Netherlands
,
Dick W Slaaf
The Departments of Physiology and Biophysics, Cardiovascular Research Institute Maastricht, University of Limburg, Maastricht, The Netherlands
,
Robert S Reneman
The Departments of Physiology and Biophysics, Cardiovascular Research Institute Maastricht, University of Limburg, Maastricht, The Netherlands
› Author Affiliations
Further Information

Publication History

Received 08 January 1993

Accepted after revision 21 June 1993

Publication Date:
05 July 2018 (online)

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Summary

The involvement of prostaglandins in thromboembolic processes, as induced by wall puncture, was studied in rabbit mesenteric arterioles and venules using intravital videomicroscopy. Inhibition of prostaglandin formation with aspirin (100 mg/kg, i. v.) significantly increased in arterioles duration of embolization (from 91 to 200 s) and number of emboli produced (from 4 to 8.5 per vessel), while rate of embolus production was not influenced. In venules, aspirin only influenced embolization rate (a significant decrease from one embolus/14 s to one/23 s). Specific blockade of TXA2-receptors by sulotroban (30 mg/kg, i. v) only influenced the arteriolar reaction: it significantly decreased embolization duration (from 560 to 218 s) and number of emboli produced (from 23 to 10 emboli per vessel), without affecting embolization rate. These findings indicate that both platelet activating and inhibiting prostaglandins play a more important role in thromboembolism in arterioles than in venules; this suggests a difference in prostaglandin synthetic capacity between arteriolar and venular endothelium.