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 Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lei, B. Articles by Koehler, R. C. Search for Related Content PubMed PubMed Citation Articles by Lei, B. Articles by Koehler, R. C. Related Collections Animal models of human disease Transient Ischemic Attacks Endothelium/vascular type/nitric oxide

(Stroke. 1999;30:669-677.)
© 1999 American Heart Association, Inc.

Original Contributions

Nitric Oxide Production in the CA1 Field of the Gerbil Hippocampus After Transient Forebrain Ischemia

Effects of 7-Nitroindazole and N^G-Nitro-L-Arginine Methyl Ester

Baiping Lei, MD; Naoto Adachi, MD, PhD; Takumi Nagaro, MD Tatsuru Arai, MD

From the Department of Anesthesiology and Resuscitology, Ehime University School of Medicine, Ehime, Japan.

Correspondence to Naoto Adachi, MD, PhD, Department of Anesthesiology and Resuscitology, Ehime University School of Medicine, Shitsukawa, Shigenobu-cho, Onsen-gun, Ehime 791-0295, Japan.

Background and Purpose—The present study was designed to examine the time course of nitric oxide (NO) production and the source of NO in the CA1 field of the gerbil hippocampus after transient forebrain ischemia.

Methods—The production of NO in the CA1 field of the hippocampus after transient ischemia was monitored consecutively by measuring total NO metabolites (NO_x^-, NO₂^- plus NO₃^-) with the use of brain microdialysis. 7-Nitroindazole (7-NI) and N^G-nitro-L-arginine methyl ester were used to dissect the relative contributions of neuronal NO synthase and endothelial NO synthase to the NO production. The histological outcomes of 7-NI in 5- and 10-minute global ischemia were also evaluated.

Results—The production of NO in the CA1 field of the hippocampus after ischemia was dependent on the severity of ischemia. Ischemia for 2 or 5 minutes did not induce a significant increase in NO_x^- levels in the CA1 field of the hippocampus after reperfusion, whereas the 10- and 15-minute ischemias produced significant and persistent increases in NO_x^- levels. 7-NI did not inhibit the basal NO_x^- levels and showed no effects on NO_x^- levels after 5 minutes of ischemia. However, it completely inhibited the increased NO_x^- levels after 10 or 15 minutes of ischemia. 7-NI provided minor neuroprotection in 5 minutes but not in 10 minutes of global ischemia.

Conclusions—The increased NO level in the CA1 field of the hippocampus after ischemia is produced mostly by neuronal NO synthase, whereas the basal NO level mainly originates from endothelial NO synthase. The observed neuroprotective effect of 7-NI in 5-minute global ischemia in gerbils may not be due to neuronal NO synthase inhibition by this drug.

Editorial Comment

Effects of 7-Nitroindazole and N^G-Nitro-L-Arginine Methyl Ester

Raymond C. Koehler, PhD, Guest Editor

Department of Anesthesiology/Critical Care Medicine, The Johns Hopkins University, Baltimore, Maryland

This article has been cited by other articles:

				K. Fassbender, M. Fatar, A. Ragoschke, M. Picard, T. Bertsch, S. Kuehl, and M. Hennerici Subacute But Not Acute Generation of Nitric Oxide in Focal Cerebral Ischemia Stroke, September 1, 2000; 31(9): 2208 - 2211. [Abstract] [Full Text] [PDF]