In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 288, No. 2 ( 2005-02), p. H525-H531
Abstract:
The role of nitric oxide (NO) and reactive oxygen species (ROS) in regulating capillary perfusion was studied in the hamster cheek pouch model during normoxia and after 20 min of exposure to 10% O 2 -90% N 2 . We measured Po 2 by using phosphorescence quenching microscopy and ROS production in systemic blood. Identical experiments were performed after treatment with the NO synthase inhibitor N G -monomethyl-l-arginine (l-NMMA) and after the reinfusion of the NO donor 2,2′-(hydroxynitrosohydrazono)bis-etanamine (DETA/NO) after treatment with l-NMMA. Hypoxia caused a significant decrease in the systemic Po 2 . During normoxia, arteriolar intravascular Po 2 decreased progressively from 47.0 ± 3.5 mmHg in the larger arterioles to 28.0 ± 2.5 mmHg in the terminal arterioles; conversely, intravascular Po 2 was 7–14 mmHg and approximately uniform in all arterioles. Tissue Po 2 was 85% of baseline. Hypoxia significantly dilated arterioles, reduced blood flow, and increased capillary perfusion (15%) and ROS (72%) relative to baseline. Administration of l-NMMA during hypoxia further reduced capillary perfusion to 47% of baseline and increased ROS to 34% of baseline, both changes being significant. Tissue Po 2 was reduced by 33% versus the hypoxic group. Administration of DETA/NO after l-NMMA caused vasodilation, normalized ROS, and increased capillary perfusion and tissue Po 2 . These results indicate that during normoxia, oxygen is supplied to the tissue mostly by the arterioles, whereas in hypoxia, oxygen is supplied to tissue by capillaries by a NO concentration-dependent mechanism that controls capillary perfusion and tissue Po 2 , involving capillary endothelial cell responses to the decrease in lipid peroxide formation controlled by NO availability during low Po 2 conditions.
Type of Medium:
Online Resource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.00426.2004
Language:
English
Publisher:
American Physiological Society
Publication Date:
2005
detail.hit.zdb_id:
1477308-9
SSG:
12
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