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Regional Hypoxia In Ischemic Cremaster Muscle Microcirculation
Author(s) -
Duggan William,
Ashby Marc,
Hui Pan,
Damaser Margot S.,
Siemionow Maria
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.730.35
Subject(s) - cremaster muscle , microcirculation , hypoxia (environmental) , ischemia , medicine , immunohistochemistry , in vivo , anesthesia , anatomy , chemistry , oxygen , biology , microbiology and biotechnology , organic chemistry
Purpose: The purpose of our study was to test the hypothesis that ischemia of the cremaster muscle induces extensive hypoxia and significantly reduces blood flow of the microcirculation. Methods: 12 Lewis rats (75–100g) divided into 4 experimental groups underwent cremaster muscle preparations for in vivo microcirculatory recordings. Group 1 acted as the control group, whilst groups 2, 3 and 4 underwent 2, 4 and 6 hours of ischemia respectively by clamping the cremaster pedicle. After ischemia hypoxyprobe‐1 (pimonidazole hydrochloride, which demonstrates hypoxia by adducting with proteins in cells having oxygen concentrations <14 ìM) was applied topically to the isolated cremaster muscle. In the control group the hypoxyprobe‐1 was applied after 6 hours without any ischemia. Hydroxyprobe‐1 was localized by primary mouse monoclonal antibody. Results: All cremaster muscles within the ischemic groups demonstrated hypoxia as indicted by the immunohistochemistry for hypoxyprobe‐1. No tissue hypoxia was seen in the control group. Conclusions: We have proved our hypothesis that 2,4 and 6 hours of induced ischemia within the cremaster muscle results in local hypoxia which increases with increased ischemic time