This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science 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 Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Goyagi, T. Articles by Masaki, Y. Search for Related Content PubMed PubMed Citation Articles by Goyagi, T. Articles by Masaki, Y. Related Collections Resuscitation Neuroanesthesia

---

NEUROSURGICAL ANESTHESIA

ß-Adrenoreceptor Antagonists Attenuate Brain Injury After Transient Focal Ischemia in Rats

From the Department of Anesthesia and Intensive Care Medicine, Akita University School of Medicine, Akita, Japan.

Address correspondence and reprint requests to Toru Goyagi, MD, Akita University School of Medicine, 1-1-1 Hondo, Akita-city, Akita, 010-8543, Japan. Address e-mail to tgoyagi{at}doc.med.akita-u.ac.jp.

ß-adrenoreceptor antagonists experimentally reduce cardiac and renal injury after ischemia and are also clinically useful for myocardial infarction and severe burns. In addition, ß-adrenoreceptor antagonists provide neuroprotective effects after focal cerebral ischemia in experimental settings. We conducted the present study to compare the neuroprotective effects of several ß-adrenoreceptor antagonists in rat transient focal cerebral ischemia. Halothane-anesthetized normothermic adult male Sprague-Dawley rats were subjected to 2 h of middle cerebral artery occlusion using the intraluminal suture technique confirmed by laser Doppler flowmetry. Rats received an IV infusion of saline 0.5 mL/h, propranolol 100 µg · kg^–1 · min^–1, carvedilol 4 µg · kg^–1 · min^–1, esmolol 200 µg · kg^–1 · min^–1, or landiolol 50 µg · kg^–1 · min^–1 (n = 6 in each group). Infusion was initiated 30 min before middle cerebral artery occlusion and continued for 24 h. Additional rats received esmolol 50 µg · kg^–1 · min^–1 or landiolol 10 µg · kg^–1 · min^–1 intrathecally (IT) via the cisterna magna (n = 5 in each group), according to the same experimental protocol. The neurological deficit score was evaluated at 22 h after reperfusion, and the brains were removed and stained with triphenyltetrazolium chloride for evaluation of infarct volume. Additional rats that received saline, esmolol, and landiolol IV (n = 6 in each group) were allowed to survive for 7 days followed by measurement of infarct size. Neurological deficit scores were smaller in rats treated with propranolol-IV, carvedilol-IV, esmolol-IV, landiolol-IV, esmolol-IT, and landiolol-IT compared with saline-treated rats (P < 0.05). Cortical and striatum infarct volumes were less in the rats receiving ß-adrenoreceptor antagonists via either IV or IT than in saline-treated rats (P < 0.05). We conclude that ß-adrenoreceptor antagonists improve neurological and histological outcomes after transient focal cerebral ischemia in rats independent of administration route.

This article has been cited by other articles:

				R.-Q. Han, Y.-B. Ouyang, L. Xu, R. Agrawal, A. J. Patterson, and R. G. Giffard Postischemic Brain Injury Is Attenuated in Mice Lacking the {beta}2-Adrenergic Receptor Anesth. Analg., January 1, 2009; 108(1): 280 - 287. [Abstract] [Full Text] [PDF]