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Title: Thromboxane A2 and prostacyclin do not modulate the systemic hemodynamic response to cold in humans
Authors: Gresele, P ×
Bounameaux, H
Arnout, Jozef
Perez-Requejo, J L
Deckmyn, Hans
Vermylen, Jozef #
Issue Date: Dec-1985
Series Title: The Journal of laboratory and clinical medicine vol:106 issue:5 pages:534-41
Abstract: The immersion of a limb in a mixture of water and ice induces in normal humans an initial vasoconstriction mediated mainly by catecholamine release. In some studies the cold pressor test was associated with an increase in vasoconstrictor thromboxane A2 and in vasodilating prostacyclin. Dazoxiben hydrochloride, a thromboxane synthase inhibitor, has been reported to suppress cold-induced vasoconstriction. We compared in a double-blind, crossover, placebo-controlled study the effects of indomethacin (a cyclooxygenase inhibitor), dazoxiben hydrochloride, and BM13.177 (a novel thromboxane receptor antagonist) on the changes in cutaneous vascular resistance and arterial blood pressure induced by cold in 12 healthy volunteers. Cold challenge produced an increase in blood pressure and an initial decrease in finger blood flow, reflecting an increase in cutaneous vascular resistance. Neither effective suppression of thromboxane A2 generation or of the effects of thromboxane A2 on platelets by the three active treatments nor increase in prostacyclin generation after ingestion of dazoxiben hydrochloride modified the hemodynamic response to cold. In conclusion, thromboxane A2 and prostacyclin do not play a significant role in the modulation of the systemic hemodynamic response to cold. In addition, thromboxane receptor antagonism in normal humans does not influence basal blood pressure.
ISSN: 0022-2143
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Molecular and Vascular Biology
Chemistry, Campus Kulak Kortrijk
Interdisciplinary Research Facility Life Sciences, Campus Kulak Kortrijk
Biomedical Sciences Group Management - miscellaneous
Faculty of Medicine - miscellaneous
× corresponding author
# (joint) last author

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