TY - JOUR
T1 - Oxygen-dependent vasomotor responses are conducted upstream in the mouse cremaster microcirculation
AU - Riemann, Mads
AU - Rai, Amrit
AU - Ngo, Anh Thuc
AU - Dziegiel, Morten Hanefeld
AU - Holstein-Rathlou, Niels-Henrik
AU - Torp-Pedersen, Christian
AU - Riemann, Mads Achen
AU - Rai, Amrit
AU - Ngo, Anh Thuc
AU - Dziegiel, Morten Hanefeld
AU - Holstein-Rathlou, Niels-Henrik
AU - Torp-Pedersen, Christian
N1 - Copyright © 2010 S. Karger AG, Basel.
PY - 2010/12
Y1 - 2010/12
N2 - 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.
AB - 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.
U2 - 10.1159/000318777
DO - 10.1159/000318777
M3 - Journal article
C2 - 20639650
SN - 1018-1172
VL - 48
SP - 79
EP - 89
JO - Journal of Vascular Research
JF - Journal of Vascular Research
IS - 1
ER -