Effects of the antiplatelet agent TA-993 and its metabolite MB3 on the hemorheological properties of rat and human erythrocytes.

Abstract

In the present study, we investigated the effects of the antiplatelet agent TA-993 and its metabolite MB3 on the hemorheological properties of rat and human erythrocytes in comparison with ticlopidine and aspirin. TA-993 and MB3 concentration-dependently lowered the viscosity of rat erythrocyte suspensions. TA-993 and MB3 inhibited both the hypotonic hemolysis of human erythrocytes and the mechanical hemolysis of rat erythrocytes induced by turbulent flow. Treatment of rats with TA-993 (10 mg/kg/day po) for 10 days significantly increased blood filterability, but ticlopidine and aspirin did not show this effect. TA-993 and MB3 enhanced the interaction of 1-anilino-8-naphthalene sulfonate (ANS), a hydrophobic probe, with human erythrocyte ghosts and reduced the fluorescence polarization in 1,6-diphenyl 1,3,5-hexatriene (DPH, a fluidity probe)-labeled human erythrocyte ghosts. TA-993 and MB3 induced aggregation of liposome suspensions prepared from acidic phospholipids. These findings suggest that TA-993 and MB3 may affect the erythrocyte membrane by interacting with acidic phospholipids and thus improve the hemorheological properties.

• Authors: M Katoh, T Karasawa, H Doi, A Odawara
• Journal: Thrombosis research (Thromb Res) Vol. 104 Issue 2 Pg. 105-12 (Oct 15 2001) ISSN: 0049-3848 [Print] United States
• PMID: 11672754 (Publication Type: Comparative Study, Journal Article)

Chemical References

• Phospholipids
• Platelet Aggregation Inhibitors
• metabolite MB3
• TA 993
• Diltiazem
• Ticlopidine
• Aspirin

Topics

• Animals
• Aspirin (pharmacology)
• Blood Viscosity (drug effects)
• Diltiazem (analogs & derivatives, metabolism, pharmacology)
• Dose-Response Relationship, Drug
• Erythrocytes (drug effects)
• Hemolysis (drug effects)
• Hemorheology (drug effects)
• Humans
• Phospholipids (metabolism)
• Platelet Aggregation Inhibitors (metabolism, pharmacology)
• Rats
• Ticlopidine (pharmacology)