HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Norihiko Shiiya Keishu Yasuda Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wakamatsu, Y. Articles by Yasuda, K. Search for Related Content PubMed PubMed Citation Articles by Wakamatsu, Y. Articles by Yasuda, K. Related Collections Great vessels

J Thorac Cardiovasc Surg 2001;122:728-733
© 2001 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

The adenosine triphosphate–sensitive potassium channel opener nicorandil protects the ischemic rabbit spinal cord

From the Department of Cardiovascular Surgery^a and Department of Anatomy,^b Hokkaido University, Sapporo, Japan.

Received for publication Dec 1, 2000. Revisions requested Feb 16, 2001; revisions received Feb 28, 2001. Accepted for publication March 9, 2001. Address for reprints: Norihiko Shiiya, MD, Department of Cardiovascular Surgery, Hokkaido University Hospital, N14W5, kita-ku, Sapporo 060-8648, Japan (E-mail: shiyanor{at}med.hokudai.ac.jp).

Objective: We investigated the protective effects of an adenosine triphosphate–sensitive potassium channel opener nicorandil in the rabbit model of spinal cord ischemia.
Methods: Rabbits were randomized into 4 groups (each n = 6): the nicorandil group (100 µg/kg intravenous nicorandil 10 minutes before ischemia); the glibenclamide plus nicorandil group (3 mg/kg intravenous glibenclamide, an antagonist of adenosine triphosphate–sensitive potassium channels, 10 minutes before nicorandil administration); the vehicle group (vehicle alone); and the sham operation group (without spinal cord ischemia). Spinal cord ischemia was induced by balloon occlusion of the infrarenal abdominal aorta for 15 minutes at 39°C. Neurologic function was graded into Johnson&'s score at 8 hours, 1 day, and 2 days. Histopathologic examination was performed at 2 days, and the number of intact motor neuron cells was compared.
Results: Johnson scores of the glibenclamide plus nicorandil and vehicle groups were significantly lower than those of the sham operation and nicorandil groups at each time point, and no statistically significant difference was observed between the glibenclamide plus nicorandil and vehicle groups. Histopathologic examination revealed that motor neurons were almost normal in the nicorandil group, whereas about 55% of motor neurons were lost in the vehicle and glibenclamide plus nicorandil groups.
Conclusions: Nicorandil has a protective effect on the ischemic rabbit spinal cord, and the beneficial effect seems mediated through the activation of adenosine triphosphate–sensitive potassium channels.

This article has been cited by other articles:

				S. Wakasa, N. Shiiya, T. Tachibana, T. Ooka, and Y. Matsui A semiquantitative analysis of reactive astrogliosis demonstrates its correlation with the number of intact motor neurons after transient spinal cord ischemia J. Thorac. Cardiovasc. Surg., April 1, 2009; 137(4): 983 - 990. [Abstract] [Full Text] [PDF]

				T. Tachibana, N. Shiiya, T. Kunihara, Y. Wakamatsu, A. F. Kudo, T. Ooka, S. Watanabe, and K. Yasuda Immunophilin ligands FK506 and cyclosporine A improve neurologic and histopathologic outcome after transient spinal cord ischemia in rabbits J. Thorac. Cardiovasc. Surg., January 1, 2005; 129(1): 123 - 128. [Abstract] [Full Text] [PDF]