Inhibition of NO Synthase Prevents Acute Collateral Artery Dilation in the Rat Hindlimb

The role of endothelium-derived nitric oxide (EDNO) in the initial opening and sustained dilation of collateral vessels in the peripheral circulation was investigated. Abrupt arterial occlusion was produced by clamping the rat superficial femoral artery (SFA). Arterial pressures were measured proxim...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of surgical research 1996-03, Vol.61 (2), p.463-468
Main Authors: Unthank, Joseph L., Nixon, J.Craig, Dalsing, Michael C.
Format: Article
Language:English
Subjects:
Animals
Arginine - analogs & derivatives
Arginine - pharmacology
Biological and medical sciences
Blood Pressure - drug effects
Collateral Circulation
Hindlimb - blood supply
Male
Medical sciences
NG-Nitroarginine Methyl Ester
Nitric Oxide - physiology
Nitric Oxide Synthase - antagonists & inhibitors
Rats
Rats, Sprague-Dawley
Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases
Vascular surgery: aorta, extremities, vena cava. Surgery of the lymphatic vessels
Vasodilation - drug effects
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The role of endothelium-derived nitric oxide (EDNO) in the initial opening and sustained dilation of collateral vessels in the peripheral circulation was investigated. Abrupt arterial occlusion was produced by clamping the rat superficial femoral artery (SFA). Arterial pressures were measured proximal (MAP) and distal (PD) to the occlusion site. In one group (INITIAL DILATION), the clamp was removed after PDreached a plateau, and then the nitric oxide synthase inhibitor,Nω-nitro-L-arginine methyl ester (L-NAME), was administered and the occlusion repeated in the same limb to evaluate the role of nitric oxide in the initial opening of collateral vessels. In another group (SUSTAINED DILATION), L-NAME was administered after acute compensation to SFA occlusion had occurred to determine if inhibition of nitric oxide synthase would reverse any acute compensation. Collateral dilation was evaluated by recovery in PDrelative to MAP (PD-%MAP) and by the percent of total resistance in the collateral-dependent circuit due primarily to collaterals (%RC). The acute compensation indicated by an increase in PD-%MAP (14 ± 1.9% to 27 ± 2.6%) and decrease in %RC(86 ± 1.9 to 73 ± 2.6%) in the INITIAL DILATION group was prevented by L-NAME (P< 0.0005). L-NAME also reversed the compensation in the SUSTAINED DILATION group; PD-%MAP decreased from 28 ± 2.3% to 11 ± 1.9% and %RCincreased from 72 ± 2.3% to 93 ± 1.1% after administration of L-NAME. Although collateral flow was not measured, the results are consistent with the hypothesis that acute collateral dilation is mediated by increases in flow or shear stress which stimulate the release of EDNO.
ISSN:0022-4804
1095-8673
DOI:10.1006/jsre.1996.0147