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Characterization of microvascular vasoconstriction following ischemia/reperfusion in skeletal muscle using videomicroscopy
Author(s) -
Pemberton Mark,
Anderson Gary L.,
Barker John H.
Publication year - 1996
Publication title -
microsurgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.031
H-Index - 63
eISSN - 1098-2752
pISSN - 0738-1085
DOI - 10.1002/(sici)1098-2752(1996)17:1<9::aid-micr2>3.0.co;2-k
Subject(s) - medicine , cremaster muscle , ischemia , vasoconstriction , constriction , vasodilation , microcirculation , skeletal muscle , diltiazem , cardiology , nitric oxide , sodium nitroprusside , anesthesia , arteriole , antagonist , calcium , receptor
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 μm 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°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). Super‐oxide dismutase did not attenuate the microvascular response, suggesting that the mechanism is likely to be at least partly free radical‐independent. © 1996 Wiley‐Liss, Inc.