Thromb Haemost 1988; 60(02): 319-323
DOI: 10.1055/s-0038-1647053
Original Article
Schattauer GmbH Stuttgart

Autoradiographic Observation of Platelets in Cerebrovascular Injuries Induced by Arachidonic Acid and its Prevention by Ticlopidine

Tsukasa Fujimoto
The Department of Neurosurgery, Showa University Fujigaoka Hospital, Yokohama, Kanagawa, and Department of Cardiovascular Research, The Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
,
Hidenori Suzuki
The Department of Neurosurgery, Showa University Fujigaoka Hospital, Yokohama, Kanagawa, and Department of Cardiovascular Research, The Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
,
Kenjiro Tanoue
The Department of Neurosurgery, Showa University Fujigaoka Hospital, Yokohama, Kanagawa, and Department of Cardiovascular Research, The Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
,
Yoshiharu Fukushima
The Department of Neurosurgery, Showa University Fujigaoka Hospital, Yokohama, Kanagawa, and Department of Cardiovascular Research, The Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
,
Hiroh Yamazaki
The Department of Neurosurgery, Showa University Fujigaoka Hospital, Yokohama, Kanagawa, and Department of Cardiovascular Research, The Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
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Publikationsverlauf

Received 22. Oktober 1986

Accepted after revision 01. Juli 1988

Publikationsdatum:
28. Juni 2018 (online)

Summary

The behavior of circulating 111In-labeled platelets in cerebrovascular injuries induced by arachidonic acid injection was studied. Fourteen rabbits were pretreated with the antiplatelet agent ticlopidine, and 10 rabbits were used for controls. Arachidonic acid (AA, 0.7 mg/kg) was injected into the internal carotid artery. Prior to the injection, platelets labeled with 111In- oxine were injected for autoradiography of the brain. Evans blue was injected as an indicator of blood-brain barrier disturbance. Nine control animals showed marked blue staining, and one showed slight blue staining. Seven out of the 14 pretreated animals showed slight or no staining, while 7 showed intensive staining. The distributions of the blue staining and the radioactivity showed high correlation. In the rabbits whose platelet aggrega- bility was depressed by ticlopidine, lower blue staining as well as lower radioactivity was observed. Our findings suggest that activated platelets have an important role in the genesis of cerebrovascular injuries.

 
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