Inhibition of NO synthase prevents acute collateral artery dilation in the rat hindlimb

Joseph L. Unthank, J. Craig Nixon, Michael Dalsing

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Abstract

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 (P(D)) to the occlusion site. In one group (INITIAL DILATION), the clamp was removed after P(D) reached a plateau, and then the nitric oxide synthase inhibitor, N(ω)-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 P(D) relative to MAP (P(D)-%MAP) and by the percent of total resistance in the collateral-dependent circuit due primarily to collaterals (%R(C)). The acute compensation indicated by an increase in P(D)-%MAP (14 ± 1.9% to 27 ± 2.6%) and decrease in %Re (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; P(D)-%MAP decreased from 28 ± 2.3% to 11 ± 1.9% and %R(C) increased 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.

Original languageEnglish
Pages (from-to)463-468
Number of pages6
JournalJournal of Surgical Research
Volume61
Issue number2
DOIs
StatePublished - Mar 1996

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NG-Nitroarginine Methyl Ester
Hindlimb
Nitric Oxide Synthase
Dilatation
Arteries
Nitric Oxide
Femoral Artery
Constriction
Arterial Pressure
Extremities

ASJC Scopus subject areas

  • Surgery

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Inhibition of NO synthase prevents acute collateral artery dilation in the rat hindlimb. / Unthank, Joseph L.; Nixon, J. Craig; Dalsing, Michael.

In: Journal of Surgical Research, Vol. 61, No. 2, 03.1996, p. 463-468.

Research output: Contribution to journalArticle

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abstract = "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 (P(D)) to the occlusion site. In one group (INITIAL DILATION), the clamp was removed after P(D) reached a plateau, and then the nitric oxide synthase inhibitor, N(ω)-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 P(D) relative to MAP (P(D)-{\%}MAP) and by the percent of total resistance in the collateral-dependent circuit due primarily to collaterals ({\%}R(C)). The acute compensation indicated by an increase in P(D)-{\%}MAP (14 ± 1.9{\%} to 27 ± 2.6{\%}) and decrease in {\%}Re (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; P(D)-{\%}MAP decreased from 28 ± 2.3{\%} to 11 ± 1.9{\%} and {\%}R(C) increased 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.",
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