Abstract:
BACKGROUND:A new method was evaluated where local changes in oxygen tension were induced in a tissue while being studied under a microscope in vivo. We tested whether hypoxic vasodilation and hyperoxic vasoconstriction in arterioles in striated muscle are being propagated upstream, and whether the endothelium and smooth muscle cell layers are necessary components in the signaling pathway. METHODS:The study was performed in mouse cremaster muscle superfused with Krebs buffer. A section of the capillary bed was then superfused with human red blood cell suspension equilibrated with either 95% nitrogen or 95% oxygen, and 5% carbon dioxide. RESULTS:The superfusions caused a 12.9 ± 2.4% (p < 0.01) dilation and a 12.3 ± 2.7% (p < 0.01) constriction of the supplying non-exposed arteriole. Vasomotor responses could be detected 1 mm upstream of the stimulation site. The responses to hypoxia and hyperoxia were not affected by inhibition of nitric oxide (NO) synthases by L-NAME. Damage to the wall of an intervening segment of the arteriole abolished upstream changes. CONCLUSIONS:The method is capable of changing the oxygen tension locally in a membranous tissue and elicits NO-independent local and upstream vasomotor responses. Upstream responses were transmitted by a conducted vascular response.
journal_name
J Vasc Resjournal_title
Journal of vascular researchauthors
Riemann M,Rai A,Ngo AT,Dziegiel MH,Holstein-Rathlou NH,Torp-Pedersen Cdoi
10.1159/000318777subject
Has Abstractpub_date
2011-01-01 00:00:00pages
79-89issue
1eissn
1018-1172issn
1423-0135pii
000318777journal_volume
48pub_type
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journal_title:Journal of vascular research
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