Possible role of thrombolytics in reocclusion after MI PHARMACOLOGY Reocc1usion occurs in some patients during thrombolytic therapy for the treatment of acute myocardial infarction (MI), and thrombolytic agents may in fact be involved in the reocclusion phenomenon after thrombolysis has been achieved, say researchers from Japan. They obtained platelet-rich plasma from venous blood samples of 12 healthy volunteers; the platelet count of the plasma samples was adjusted to lOx 10 4 /1l1. 90111 aliquots of the plasma samples were combined with IOllg of either urokinase or alteplase (tPA), each at 3 different concentrations, or saline (control samples); the samples were then incubated and the platelets fixed with paraformaldehyde. The volunteers then received aspirin 160 or 660 mg/day for 7 days. Platelet-rich plasma samples were then prepared again as described above. The researchers measured platelet surface P-selectin expression as a marker of platelet activity and demonstrated that platelets were activated by urokinase and alteplase in a concentration-dependent manner. In addition, the study data indicate that administration of aspirin at a certain dose level may be useful for the prevention of reocclusion after thrombolytic therapy. P-selectin expression was suppressed with administration of aspirin 660 mg/day, but no significant effect was observed with aspirin 160 mg/day. Kawano K, Aoki I, Aoki N, Homori M, Maki A. et aI. Human platelet activation by thrombolytic agents: effects of tissue-type plasminogen activator and urokinase on platelet surface P-selectin expression. American Heart Journal 135: 268-271. Part 1. Feb 1998 100647214 1173-832419811131-000191$01.00° Adlslntern8tIONlI LlmIlecl1898. All rights I'8MmId 19 Inpharma- 4 Apr 1898 No. 1131

Possible role of thrombolytics in reocclusion after MI

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Possible role of thrombolytics in reocclusion after MI

PHARMACOLOGY

Reocc1usion occurs in some patients during thrombolytic therapy for the treatment of acute myocardial infarction (MI), and thrombolytic agents may in fact be involved in the reocclusion phenomenon after thrombolysis has been achieved, say researchers from Japan.

They obtained platelet-rich plasma from venous blood samples of 12 healthy volunteers; the platelet count of the plasma samples was adjusted to lOx 104/1l1. 90111 aliquots of the plasma samples were combined with IOllg of either urokinase or alteplase (tPA), each at 3 different concentrations, or saline (control samples); the samples were then incubated and the platelets fixed with paraformaldehyde. The volunteers then received aspirin 160 or 660 mg/day for 7 days. Platelet-rich plasma samples were then prepared again as described above.

The researchers measured platelet surface P-selectin expression as a marker of platelet activity and demonstrated that platelets were activated by urokinase and alteplase in a concentration-dependent manner.

In addition, the study data indicate that administration of aspirin at a certain dose level may be useful for the prevention of reocclusion after thrombolytic therapy. P-selectin expression was suppressed with administration of aspirin 660 mg/day, but no significant effect was observed with aspirin 160 mg/day. Kawano K, Aoki I, Aoki N, Homori M, Maki A. et aI. Human platelet activation

by thrombolytic agents: effects of tissue-type plasminogen activator and urokinase on platelet surface P-selectin expression. American Heart Journal 135:

268-271. Part 1. Feb 1998 100647214

1173-832419811131-000191$01.00° Adlslntern8tIONlI LlmIlecl1898. All rights I'8MmId

Inpharma- 4 Apr 1898 No. 1131