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Stroke, Vol 24, 1528-1533, Copyright © 1993 by American Heart Association

ARTICLES

Evidence from comparative investigations that impaired platelet activation is not specific for stroke-prone spontaneously hypertensive rats

A Klee, S Vater, GW Schmid-Schonbein and D Seiffge
Hoechst AG, Werk Kalle-Albert, Wiesbaden, Germany.

BACKGROUND AND PURPOSE: Platelet behavior of Sprague Dawley (SD), Wistar (WI), Wistar-Kyoto (WKY), spontaneously hypertensive (SHR), and stroke-prone spontaneously hypertensive rats (SHRSP) was studied in vivo to evaluate the importance of hypertension-related hemostatic disorders. METHODS: The study was based on the model of stimulus- induced pulmonary microembolization of labeled platelets. After injection of 51Cr-labeled homologous platelets into urethane- anesthetized rats, the organ distribution of the platelets was continuously monitored by gamma detectors. Count rates of two detectors- -one placed above the animals' thoraxes (C1), the other above their abdomens (C2)-and the ratio of C1:C2 were calculated. The following platelet activators were applied intravenously: adenosine diphosphate (ADP; 50 micrograms/kg), collagen (100 micrograms/kg), and thrombin (50 IU/kg). RESULTS: All three substances caused a reversible pulmonary accumulation of the labeled platelets and hence an increase in C1/C2 (delta C1/C2%). ADP induced a shift of 75% in SD, 52% in WI, 32% in WKY, 30% in SHR, and 31% in SHRSP. Thrombin-mediated shift was 79% in SD, 64% in WI, 58% in WKY, 48% in SHR, and 54% in SHRSP. Collagen induced a shift of 85% in SD, 96% in WI, 84% in WKY, 56% in SHR, and 62% in SHRSP. CONCLUSIONS: Because indistinguishable results were observed in both hypertensive strains, we conclude that impaired platelet aggregation is not specific for SHRSP. Hence, it may not primarily be responsible for the increased occurrence of stroke in these animals.