Constriction to hypoxia-reoxygenation in isolated mouse coronary
arteries: role of endothelium and superoxide.
Liu, Qiang.
Department of Medicine, The Johns Hopkins University School of
Medicine, Baltimore, Maryland 21224
APStracts 6:0277A, 1999.
The aim of the present study was to determine the role of endothelium
and superoxide in the responses of isolated mouse coronary arteries
to hypoxia and reoxygenation (H/R). Isolated mouse coronary artery
was cannulated, pressurized at 60 mmHg and constantly superfused with
recirculating Krebs-Ringer bicarbonate solution for continuous
measurement of internal diameter (ID) by video microscopy. Under a no
flow condition, hypoxia (0%O2, 30 min) caused vasoconstriction.
Reoxygenation caused a further vasoconstriction (ID = 111.4 ( 11.1 to
91 ( 16.5 (m) that was significantly reduced by removal of
endothelium (ID = 105.4 ( 27 to 109.9 ( 23.4 (m). Cu/Zn Superoxide
dismutase (SOD, 150 U/ml) did not alter the hypoxic vasoconstriction
but abolished the reoxygenation-caused endothelium-dependent
vasoconstriction. H/R markedly enhanced the generation of superoxide
that was significantly reduced by either removing the endothelium or
treated these endothelium intact vessels with SOD. These results
suggest that in isolated mouse coronary arteries, hypoxia caused
vasoconstriction that was independent of endothelium, whereas
reoxygenation caused vasoconstriction that was mediated by enhanced
generation of superoxide from endothelium.
Received 23 December 1998; accepted in final form 3 June 1999.
APS Manuscript Number A1175-8.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1999 The American Physiological Society.
Published in APStracts on 25 June 1999