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Histaminergic and cholinergic neuron systems in the impairment of human thermoregulation during motion sickness
KTH, School of Technology and Health (STH), Environmental Physiology.
KTH, School of Technology and Health (STH), Environmental Physiology.
KTH, School of Technology and Health (STH), Environmental Physiology.
2010 (English)In: Brain Research Bulletin, ISSN 0361-9230, E-ISSN 1873-2747, Vol. 82, no 3-4, 193-200 p.Article in journal (Refereed) Published
Abstract [en]

Motion sickness (MS) exaggerates body cooling during cold-water immersion. The aim of the present study was to investigate whether such MS-induced predisposition to hypothermia is influenced by two anti-MS drugs: the histamine-receptor blocker dimenhydrinate (DMH) and the muscarine-receptor blocker scopolamine (Scop). Nine healthy male subjects were immersed in 15 degrees C water for a maximum of 90 min in five conditions: (1) control (CN): no medication, no MS provocation; (2) MS-control (MS-CN): no medication, MS provocation; (3) MS-placebo (MS-P): placebo DMH and placebo Scop, MS provocation; (4) MS-DMH: DMH and placebo Scop, MS provocation; (5) MS-Scop: Scop and placebo DMH, MS provocation. MS was induced by use of a rotating chair. Throughout the experiments rectal temperature (T-re), the difference in temperature between the non-immersed right forearm and third finger (T-ff) as an index of peripheral vasoconstriction, and oxygen uptake (VO2) as a measure of shivering thermogenesis, were recorded. DMH and Scop were similarly efficacious in ameliorating nausea. The fall in T-re was greater in the MS-CN and MS-P conditions than in the CN condition. DMH, but not Scop, prevented the MS-induced increase in body-core cooling. MS attenuated the cold-induced vasoconstriction, an effect which was fully prevented by DMH but only partially by Scop. MS provocation did not affect VO2 in any condition. The results suggest that the MS-induced predisposition to hypothermia is predominantly mediated by histaminergic mechanisms and that DMH might be useful in conjunction with maritime accidents or other scenarios where exposure to cold and MS are imminent features.

Place, publisher, year, edition, pages
2010. Vol. 82, no 3-4, 193-200 p.
Keyword [en]
Hypothermia, Histamine, Acetylcholine, Temperature regulation, Motion illness
URN: urn:nbn:se:kth:diva-26360DOI: 10.1016/j.brainresbull.2010.04.004ISI: 000279972700007ScopusID: 2-s2.0-77953542507OAI: diva2:371999
QC 20101123Available from: 2010-11-23 Created: 2010-11-23 Last updated: 2010-11-23Bibliographically approved
In thesis
1. Effects of Motion Sickness on Human Thermoregulatory Mechanisms
Open this publication in new window or tab >>Effects of Motion Sickness on Human Thermoregulatory Mechanisms
2010 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The presented studies were performed to investigate the effects of motion sickness (MS) on human autonomic and behavioural thermoregulatory mechanisms during cold stress and in a thermoneutral environment. The roles of histaminergic and cholinergic neuron systems in autonomic thermoregulation and MS-dependent dysfunction of autonomic thermoregulation were studied using a histamine-receptor blocker, dimenhydrinate (DMH), and a muscarine-receptor blocker, scopolamine (Scop). In addition, the effects of these substances on MS-induced nausea and perceptual thermoregulatory responses were studied. MS was found to lower core temperature, during cold stress by attenuation of cold-induced vasoconstriction and decreased shivering thermogenesis, and in a thermoneutral environment by inducing sweating and vasodilatation. The increased core cooling during cold stress was counteracted by DMH but not by Scop. In a thermoneutral environment, the temperature was perceived as uncomfortably warm during and after the MS provocation despite decreases in both core and skin temperature. No such effect was seen during cold-water immersion. Both pharmacologic substances had per se different effects on autonomic thermoregulatory responses during cold stress. Scop decreased heat preservation, but did not affect core cooling, while DMH reduced the rate of core cooling through increased shivering thermogenesis. Both DMH and Scop per se decreased thermal discomfort during cold-water immersion.Findings support the notion of modulating roles of histamine (H) and acetylcholine (Ach) in autonomic thermoregulation and during MS. MS activates cholinergic and histaminergic pathways, thereby increasing the levels of H and Ach in several neuro-anatomical structures. As a secondary effect, MS also elevates blood levels of several neuropeptides, which in turn would influence central and/or peripheral thermoregulatory responses.In conclusion, MS may predispose to hypothermia, by impairment of autonomic thermoregulation in both cold and thermoneutral environments and by modulation of behavioural thermoregulatory input signals. This might have significant implications for survival in maritime accidents.

Place, publisher, year, edition, pages
Stockholm: KTH, 2010. v, 41 p.
Trita-STH : report, ISSN 1653-3836 ; 2010:6
Motion Sickness, autonomic thermoregulation, behavioural thermoregulation, hypothermia, acetylcholine, histamine
National Category
urn:nbn:se:kth:diva-26058 (URN)978-91-7415-795-6 (ISBN)
Public defence
2010-12-10, sal 3:221, Alfred Nobels alle 10, Huddinge, 13:30 (English)

Medicine doktorsexamen

Available from: 2010-11-23 Created: 2010-11-11 Last updated: 2013-06-05Bibliographically approved

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