JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
		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 Services Email this article to a colleague Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Umehara, S. Articles by Nishikawa, T. Search for Related Content PubMed PubMed Citation Articles by Umehara, S. Articles by Nishikawa, T.

---

CARDIOVASCULAR ANESTHESIA

Effects of Sevoflurane Anesthesia on Carotid-Cardiac Baroreflex Responses in Humans

Department of Anesthesia, Akita University School of Medicine, Akita-city, Japan

Address correspondence and reprint requests to Makoto Tanaka, MD, Department of Anesthesia, Akita University School of Medicine, Hondo 1-1-1, Akita-city 010-8543, Japan. Address e-mail to mtanaka{at}med.akita-u.ac.jp.

Sevoflurane depresses cardio-vagal baroreflex gain (ability of vagally mediated R-R interval response to arterial blood pressure change). We examined the effects of sevoflurane anesthesia on maximum buffering capacity of vagally mediated hemodynamic control (baroreflex range) by examining the entire stimulus-response baroreflex relation. Electrocardiogram and invasive arterial blood pressure were monitored in 11 healthy volunteers. Carotid-cardiac baroreflex responses were elicited by increasing neck chamber pressure (external pressure applied over the bilateral carotid sinuses) to 40 mm Hg for 5 heartbeats followed by decreasing chamber pressure by successive 15-mm Hg R-wave triggered decrements to –65 mm Hg during held expiration. R-R intervals were plotted as functions of preceding carotid distending pressure. Range, maximum gain, and operational point (relative position of the resting set point within the entire baroreflex response curve) were determined at conscious baseline, during 2% (end-tidal) sevoflurane anesthesia, without and with phenylephrine infusion to maintain conscious arterial blood pressure, and at 30, 60, 120, and 180 min after emergence from anesthesia. Sevoflurane anesthesia significantly depressed maximum gain (from 3.84 ± 0.99 to 1.04 ± 0.40 ms/mm Hg [mean ± sd]; P < 0.001) and range (from 207 ± 43 to 52 ± 19 ms; P < 0.001) of the reflex relation, both of which recovered at 120 and 180 min after emergence. Phenylephrine infusion only partially restored these variables. The operational point was unchanged throughout the study. Our results indicate that maximum cardio-vagal compensatory response to buffer hemodynamic perturbation is depressed during sevoflurane anesthesia. Sevoflurane-induced hypotension, which produced vagal withdrawal, did not play an important role in depressing cardio-vagal reflex function.

This article has been cited by other articles:

				A. Silvani, D. Grimaldi, S. Vandi, G. Barletta, R. Vetrugno, F. Provini, G. Pierangeli, C. Berteotti, P. Montagna, G. Zoccoli, et al. Sleep-dependent changes in the coupling between heart period and blood pressure in human subjects Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2008; 294(5): R1686 - R1692. [Abstract] [Full Text] [PDF]

				C. J. Barrett and C. P. Bolter The influence of heart rate on baroreceptor fibre activity in the carotid sinus and aortic depressor nerves of the rabbit Exp Physiol, September 1, 2006; 91(5): 845 - 852. [Abstract] [Full Text] [PDF]

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999