Oxygen-dependent vasomotor responses are conducted upstream in the mouse cremaster microcirculation.
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.
Riemann
Mads
M
Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark. riemann @ dadlnet.dk
Rai
Amrit
A
Ngo
Anh Thuc
AT
Dziegiel
Morten Hanefeld
MH
Holstein-Rathlou
Niels-Henrik
NH
Torp-Pedersen
Christian
C
D000818:Animals; D001160:Arterioles / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008833:Microcirculation / Q000502:physiology*; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010100:Oxygen / Q000378:metabolism*; D014661:Vasoconstriction / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology*
D004791:Enzyme Inhibitors; D019001:Nitric Oxide Synthase; D010100:Oxygen; D019331:NG-Nitroarginine Methyl Ester