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.
