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Arterial baroreflex control during mild-to-moderate nitrous oxide narcosis.
KTH, School of Technology and Health (STH), Environmental Physiology (Closed 20130701).ORCID iD: 0000-0001-6361-8965
1999 (English)In: Undersea & Hyperbaric Medicine, ISSN 1066-2936, Vol. 26, no 1, 15-20 p.Article in journal (Refereed) Published
Abstract [en]

We hypothesized that light-to-moderate inert gas narcosis might play a role in bradycardia in divers by altering sensitivity or response dynamics of arterial baroreflexes. Carotid-cardiac and carotid-mean arterial pressure (MAP) baroreflex response curves were generated by applying multiple levels of neck pressure and suction. Seven healthy volunteers were studied during air breathing (control) and during inhalation of 39% nitrous oxide (N2O). Baseline (pre-stimulus) heart rate (HR) and MAP were not altered by N2O. Range, threshold level, saturation level, and delay of responses did not differ between conditions. For hypertensive stimuli, sensitivity of responses did not differ between air control and N2O inhalation, but for hypotensive stimuli, maximal response gain for HR tended to be reduced with N2O inhalation (P = 0.054). Our results speak against inert gas narcosis as a primary mechanism for hyperbaric bradycardia, but it remains possible that an attenuation of tachycardic responses to hypotensive stimuli plays a role.

Place, publisher, year, edition, pages
1999. Vol. 26, no 1, 15-20 p.
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URN: urn:nbn:se:kth:diva-123250OAI: diva2:625575
NR 20140805Available from: 2013-06-05 Created: 2013-06-05 Last updated: 2014-01-20Bibliographically approved

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Sundblad, Patrik
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