Thromb Haemost 1991; 65(05): 588-595
DOI: 10.1055/s-0038-1648195
Original Article
Schattauer GmbH Stuttgart

Evaluation of Pulmonary Accumulation of 51Chromium-Labelled Rat Platelets following Intravenous Application of ADP and Collagen

Andreas Klee
*   The University of Würzburg, Dept, of Experimental Surgery, Würzburg, FRG
,
Dirk Seiffge
**   The Dept. of Pharmacology, Hoechst AG, Werk Kalle-Albert, Wiesbaden, FRG
› Author Affiliations
Further Information

Publication History

Received 28 July 1990

Accepted after revision 15 January 1991

Publication Date:
24 July 2018 (online)

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Summary

We examined the effects of ADP- and collagen-induced pulmonary platelet embolism in the rat. Homologous 51Chromium-labelled platelets were used to monitor extracorporally the distribution of platelets in the circulation. For that purpose, collimated iodide scintillation detectors were placed above thorax (C1) and abdomen (C2). A dose-dependent increase in thoracic radioactivity, paralleled by a decrease in the abdomen, was observed after intravenous injection of ADP and collagen. This resulted in a shift of C1/C2, so that the effect of collagen was more pronounced (maximal increase of C1/C2 = 134%) than ADP (maximal increase of C1/C2 = 79%). The increase in thoracic radioactivity was caused by the uptake of platelets in the lung as was shown after administration of collagen (6-fold enrichment of labelled platelets). Lung platelet sequestration resulted in a dose-dependent thrombocytopenia. The ADP-and collagen-induced pulmonary platelet embolism reversibly provoked cardiovascular symptoms of shock: hypotension and bradycardia. Impaired gas exchange during platelet accumulation manifested itself in a reversible arterial hypoxaemia and hyper-capnia, followed by a weak acidosis. We were able to inhibit ADP-dependent thoracic platelet accumulation by ticlopidine in a dose-related manner as well as collagen-induced thoracic platelet accumulation by acetylsalicylic acid. The results indicate that behaviour of homologous labelled rat platelets in vivo can easily be monitored, thus offering the opportunity to investigate the effects of antiaggregatory drugs on platelets in their natural environment.