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Inhibitory effects of H2-receptor antagonists on platelet function in vitro

H Kariyazono

T Shinkawal

T Yamaguchi

T Yamashita

O Ayukawal

Department of Hospital Pharmacy, Faculty of Medicine, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima 890-8520, Japan

Y Moriyama

G Yotsumoto

H Toyohira

A Taira

Second Department of Surgery, Faculty of Medicine, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima 890-8520, Japan

K Yamada

Department of Hospital Pharmacy, Faculty of Medicine, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima 890-8520, Japan

1. 1 To evaluate in vitro inhibitory effects of four types of histamine H₂-receptor antagonist (H₂-receptor antagonists), famotidine, roxatidine, cimetidine and ranitidine, on platelet function, we examined aggregating potency and P-selectin levels with agonist-induced aggregation. Ranitidine and cimetidine inhibited, in concentration of 0.35 mM, the secondary aggregation induced by 5 pM adenosine diphosphate (ADP), the aggregation induced by 1,g/mL collagen and 3 gM arachidonic acid. All of H₂-receptor antagonists inhibited, in concentration of 1.4 mm, the aggregation induced by ADP, collagen and arachidonic acid. Ranitidine and cimetidine reduced markedly, in same concentration, P-selectin levels after induction of aggregation by 5 gm ADP, 1 ig/xmL collagen and 3 gM arachidonic acid. When classified by the strength of inhibitory action, ranitidine and cimetidine were strong, followed by famotidine and roxatidine.
   
2. 2 It is considered that inhibitory effects of H.-receptor antagonists on platelet function are weaker than those of acetylsalicylic acid (ASA), since ASA inhibited platelet aggregation in concentration of 100 MM.
   
3. 3 No relationship was observed between inhibitory effects of H₂-receptor antagonists on platelet aggregation induced by above agonists and the presence or absence of imidazole ring in the chemical structure.
   

Key Words: histamine H2-receptor antagonists • platelet aggregation • P-selectin • ADP • collagen • arachidonic acid

Human & Experimental Toxicology, Vol. 18, No. 8, 487-492 (1999)
DOI: 10.1191/096032799678847069


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