Premium
The Establishment of Acetic Acid‐Induced Cerebral Infarct Model, and Evaluation of Tissue Plasminogen Activator (t‐PA), Edaravone, Argatroban and Ticlopidine
Author(s) -
Shibata Keita,
Hashimoto Terumasa,
Nobe Koji,
Ohata Hisayuki,
Honda Kazuo
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.575.3
Subject(s) - edaravone , argatroban , medicine , tissue plasminogen activator , cerebral infarction , pharmacology , thrombolysis , anesthesia , ticlopidine , ischemia , cardiology , thrombin , aspirin , myocardial infarction , clopidogrel , platelet
The aim of the present study is to establish a novel embolic infarct model that was similar to human clinical condition and to evaluate the effects of some anti‐cerebral infarct agents were examined. Thrombotic occlusion was induced by local application of acetic acid to the right common carotid artery in the male Mongolian gerbil. Infarct area was assessed by the 2% TTC staining. Neurological scores were determined by a modified method described by Longa et al. The infarct area and the neurological scores increased in acetic acid concentration‐dependent manner (60, 80, 100%). Infarct area reached the maximum at 24 hr after ischemia and sustained until 5 days later. However, neurological scores decreased following the maximal response. Treatment with t‐PA reduced both values in a dose‐dependent manner (0.01, 0.1, 10 mg/kg). A free radical scavenger, edaravone (3 mg/kg), a thrombin inhibitor, argatroban (10 mg/kg), and an antiplatelet agent, ticlopidine (10 mg/kg) slightly affected. These results indicate that this model may be a useful for evaluating the cerebral infarct therapeutic drugs and provide the information about pathophysiological mechanisms of cerebral infarction.