Clinical experience and experimental studies have shown that hyperthermia can cause
cerebral ischaemia and brain damage. By in vitro experiments with heating, we previously
were able to induce carotid artery constriction. The objective of the present study
was to clarify the mechanism of this thermal response. Isometric tension was recorded
in rabbit carotid artery specimens using organ baths during stepwise temperature elevation.
The heating responses were investigated at basal tone, in precontracted vessels, after
blocking of adrenergic responses and administration of potassium (K)-channel activators
and inhibitors. Stepwise heating of carotid artery strips from 37°C to 47°C induced
reproducible graded contraction. The hyperthermic responses were not due to adrenergic
stimulation, which were reduced and resistant to neurogenic blockade by tetrodotoxin.
Heating-induced contractions were potentiated by the K-channel inhibitors tetraethylammonium,
BaCl2, charybdotoxin, and the Na+/K+ ATPase inhibitor ouabain. Levcromakalim (BRL), a K+-channel activator, reduced heating induced contractions. Heating of carotid artery
preparations induced reversible graded vasoconstriction proportional to temperature.
The heating-induced contractions were not mediated by an adrenergenic process, but
rather were due to inhibition of K+ channels, which increases Ca2+ entry. In vivo, this reaction may lead to a disturbance of autoregulation of cerebral
blood flow and ischemia with brain damage.
Key words
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Article info
Publication history
Accepted:
December 6,
2004
Received:
December 3,
2004
Identification
DOI: https://doi.org/10.1016/j.jstrokecerebrovasdis.2004.12.006
Copyright
© 2005 National Stroke Association. Published by Elsevier Inc. All rights reserved.
