Effects of propylene glycol mannate sulfate on thrombosis in abdominal aorta in rabbits
Abstract
AIM: To study the effects of propylene glycol mannate sulfate (PGMS) on platelet adhesion, aggregation and thrombosis in abdominal aorta in rabbits.
METHODS: Platelet adhesion assay was performed with a platelet-adhesion-meter. The platelet concentration was determined with an electronic particle counter, and the total radio-activity was determined with Clinigamma-1272.
RESULTS: PGMS inhibited washed platelet aggregation induced by thrombin in vitro. The value of IC50 was 0.9 mg.L(-1). (95% confidence limit = 4.1-13.7 mg.L(-1). At 10, 30, and 60 min after i.v. PGMS 75 mg.kg(-1), the inhibition rates of platelet adhesion were 90.4%, 41.8%, and 26.3% and the inhibition rates of platelet aggregation induced by thrombin were 99%, 122%, and 110%, respectively. It did not exhibit any noticeable effect on platelet aggregation induced by ADP and collagen at this dosage. After 1.5 h of i.v. PGMS 75 mg.kg-1 and total autologous 111In-platelets 3.3 x 10(9) the radioactivity and dry weight of the injured and uninjured segments were determined. The PGMS group showed a significantly lower radioactivity (1.1 +/- 0.6 MBq), 111In-platelets (8.3 +/- s 3.3 x 10(8)) as well as the radioactivity deposited.g(-1) out of the total radioactivity infused % (0.24 +/- 0.21) compared with the control group (3.7 +/- 0.5 MBq, 24.6 +/- 3.5 x 10(8), and 0.86 +/- 0.25, respectively).
CONCLUSION: PGMS prevented the platelet adhesion and aggregation at the injured arterial wall.
Keywords:
METHODS: Platelet adhesion assay was performed with a platelet-adhesion-meter. The platelet concentration was determined with an electronic particle counter, and the total radio-activity was determined with Clinigamma-1272.
RESULTS: PGMS inhibited washed platelet aggregation induced by thrombin in vitro. The value of IC50 was 0.9 mg.L(-1). (95% confidence limit = 4.1-13.7 mg.L(-1). At 10, 30, and 60 min after i.v. PGMS 75 mg.kg(-1), the inhibition rates of platelet adhesion were 90.4%, 41.8%, and 26.3% and the inhibition rates of platelet aggregation induced by thrombin were 99%, 122%, and 110%, respectively. It did not exhibit any noticeable effect on platelet aggregation induced by ADP and collagen at this dosage. After 1.5 h of i.v. PGMS 75 mg.kg-1 and total autologous 111In-platelets 3.3 x 10(9) the radioactivity and dry weight of the injured and uninjured segments were determined. The PGMS group showed a significantly lower radioactivity (1.1 +/- 0.6 MBq), 111In-platelets (8.3 +/- s 3.3 x 10(8)) as well as the radioactivity deposited.g(-1) out of the total radioactivity infused % (0.24 +/- 0.21) compared with the control group (3.7 +/- 0.5 MBq, 24.6 +/- 3.5 x 10(8), and 0.86 +/- 0.25, respectively).
CONCLUSION: PGMS prevented the platelet adhesion and aggregation at the injured arterial wall.