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Flow-induced arterial enlargement is inhibited by suppression of nitric oxide synthase activity in vivo.

Authors :
Guzman RJ
Abe K
Zarins CK
Source :
Surgery [Surgery] 1997 Aug; Vol. 122 (2), pp. 273-9; discussion 279-80.
Publication Year :
1997

Abstract

Background: Acute flow-induced arterial dilation is mediated by nitric oxide (NO). The role of NO in chronic flow-induced adaptive enlargement is unknown. We assessed the role of NO in arterial adaptation to increased blood flow (BF).<br />Methods: Iliac artery BF was increased in adult male rats by creating a left femoral arteriovenous fistula. Left iliac BF and diameter were measured, and wall shear stress was calculated. The effect of the NO synthase inhibitor N omega-nitro-L-arginine-methyl ester (L-NAME) was studied in arteriovenous fistula rats divided into three groups (group 1, vehicle, group 2, 0.5 mg/ml; group 3, 2 mg/ml) in drinking water. Arterial diameter, blood pressure, and medial cell density were assessed after 21 days. Left iliac cyclic guanosine monophosphate content was measured in an additional group of animals.<br />Results: BF and wall shear stress in the left iliac artery increased fourfold immediately after arteriovenous fistula. Arterial enlargement was evident after 7 days, and wall shear stress normalized after 42 days. Flow-induced arterial enlargement was inhibited by both low- and high-dose L-NAME compared with control (analysis of variance p < 0.05). Blood pressure was elevated only in animals treated with high-dose L-NAME. Left iliac cyclic guanosine monophosphate content was lower in rats treated with L-NAME than in the control group (p < 0.05).<br />Conclusions: NO suppression by L-NAME inhibits flow-induced iliac artery enlargement in rats. This finding suggests that NO plays a role in flow-induced arterial remodeling.

Details

Language :
English
ISSN :
0039-6060
Volume :
122
Issue :
2
Database :
MEDLINE
Journal :
Surgery
Publication Type :
Academic Journal
Accession number :
9288132
Full Text :
https://doi.org/10.1016/s0039-6060(97)90018-0