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This study investigated the possible contribution of microvascular vasoconstriction to no-reflow following ischemia/reperfusion in a mouse skeletal muscle model. Using paired cremaster muscles, arterioles of diameter 10-100 microns were directly viewed and measured by the use of an in vivo videomicroscopy before and after a 6-hr period of complete ischemia at 27 degrees C. Following ischemia/reperfusion, feeder and arcading arterioles constricted significantly to 54.5 and 62% of pre-ischemic baseline diameters respectively (P < .05). While the calcium antagonist diltiazem and nitroprusside were both able to reverse arteriolar constriction, endothelium-dependent acetylcholine-induced dilatation was markedly impaired following reperfusion (P < 0.05). Superoxide dismutase did not attenuate the microvascular response, suggesting that the mechanism is likely to be at least partly free radical-independent.
M Pemberton, and
G L Anderson, and
J H Barker
September 1998,
Seminars in vascular surgery,
M Pemberton, and
G L Anderson, and
J H Barker
January 1989,
Microcirculation, endothelium, and lymphatics,
M Pemberton, and
G L Anderson, and
J H Barker
July 1997,
The American journal of physiology,
M Pemberton, and
G L Anderson, and
J H Barker
August 1997,
Journal of reconstructive microsurgery,
M Pemberton, and
G L Anderson, and
J H Barker
January 1994,
International journal of microcirculation, clinical and experimental,
M Pemberton, and
G L Anderson, and
J H Barker
December 1993,
International journal of microcirculation, clinical and experimental,
M Pemberton, and
G L Anderson, and
J H Barker
June 1990,
Journal of applied physiology (Bethesda, Md. : 1985),
M Pemberton, and
G L Anderson, and
J H Barker
September 1990,
The Journal of surgical research,
M Pemberton, and
G L Anderson, and
J H Barker
July 1991,
Annals of vascular surgery,
M Pemberton, and
G L Anderson, and
J H Barker
April 2005,
Plastic and reconstructive surgery,
