Modulation of tendon healing by nitric oxide

G. A.C. Murrell; C. Szabo; J. A. Hannafin; D. Jang; M. M. Dolan; X. H. Deng; D. F. Murrell; R. F. Warren

doi:10.1007/s000110050027

Modulation of tendon healing by nitric oxide

G. A.C. Murrell, C. Szabo, J. A. Hannafin, D. Jang, M. M. Dolan, X. H. Deng, D. F. Murrell, R. F. Warren

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117 Scopus citations

Abstract

Nitric oxide (NO^.) is a small, diffusible free radical that is generated from L-arginine by a family of enzymes, collectively termed the nitric oxide synthases. We investigated the role of NO^. in tendon healing. NO^. synthase activity and immunoreactivity was absent in un-injured rat Achilles tendon. After surgical division there was a five-fold increase in NO^. synthase activity and immunoreactivity within the healing tendon at day 7, with a return to near baseline levels at day 14. Inhibition of NO^. synthase activity with oral administration of Nω-nitro-L-arginine methyl ester (L-NAME) resulted in a significant reduction in cross-sectional area (30% at day 7, p < 0.01, 50% at day 15, p < 0.001) and failure load (24% at day 7, p < 0.01) of the healing Achilles tendon constructs. Rats fed the same regimen of the enantiomer of L-NAME, (D-NAME) had normal tendon healing. These results indicate that nitric oxide synthase is induced during tendon healing and inhibition of nitric oxide synthase inhibits this tendon healing.

Original language	English (US)
Pages (from-to)	19-27
Number of pages	9
Journal	Inflammation Research
Volume	46
Issue number	1
DOIs	https://doi.org/10.1007/s000110050027
State	Published - 1997
Externally published	Yes

Keywords

Free radical
Nitric oxide
Nitric oxide synthase
Tendon healing
Wound healing

ASJC Scopus subject areas

Immunology
Pharmacology

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10.1007/s000110050027

Cite this

@article{07525f76f1fb4c119d5753feb1dea231,

title = "Modulation of tendon healing by nitric oxide",

abstract = "Nitric oxide (NO.) is a small, diffusible free radical that is generated from L-arginine by a family of enzymes, collectively termed the nitric oxide synthases. We investigated the role of NO. in tendon healing. NO. synthase activity and immunoreactivity was absent in un-injured rat Achilles tendon. After surgical division there was a five-fold increase in NO. synthase activity and immunoreactivity within the healing tendon at day 7, with a return to near baseline levels at day 14. Inhibition of NO. synthase activity with oral administration of Nω-nitro-L-arginine methyl ester (L-NAME) resulted in a significant reduction in cross-sectional area (30% at day 7, p < 0.01, 50% at day 15, p < 0.001) and failure load (24% at day 7, p < 0.01) of the healing Achilles tendon constructs. Rats fed the same regimen of the enantiomer of L-NAME, (D-NAME) had normal tendon healing. These results indicate that nitric oxide synthase is induced during tendon healing and inhibition of nitric oxide synthase inhibits this tendon healing.",

keywords = "Free radical, Nitric oxide, Nitric oxide synthase, Tendon healing, Wound healing",

author = "Murrell, {G. A.C.} and C. Szabo and Hannafin, {J. A.} and D. Jang and Dolan, {M. M.} and Deng, {X. H.} and Murrell, {D. F.} and Warren, {R. F.}",

note = "Funding Information: Acknowledgements. This work was supported by National Institutes of Health Grant AR42729 (G.A.C. Murrell) and by the Soft Tissue Research Fund. S. B. Doty contributed significantly to this work. We are also grateful to the Piedmont Foundation and the Orthopaedic Research and Education Foundation (OREF) for support for work which defined many of the techniques utilized in the project; to Eric Attia, Kitty Boch and Alexander Hu for technical assistance and to Cory Brayton and Carl Nathan for advice and constructive criticism. G.A.C. Murrell is supported by St. George Private Hospital/Health Care of Australia Pty Ltd.",

year = "1997",

doi = "10.1007/s000110050027",

language = "English (US)",

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journal = "Inflammation Research",

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T1 - Modulation of tendon healing by nitric oxide

AU - Murrell, G. A.C.

AU - Szabo, C.

AU - Hannafin, J. A.

AU - Jang, D.

AU - Dolan, M. M.

AU - Deng, X. H.

AU - Murrell, D. F.

AU - Warren, R. F.

N1 - Funding Information: Acknowledgements. This work was supported by National Institutes of Health Grant AR42729 (G.A.C. Murrell) and by the Soft Tissue Research Fund. S. B. Doty contributed significantly to this work. We are also grateful to the Piedmont Foundation and the Orthopaedic Research and Education Foundation (OREF) for support for work which defined many of the techniques utilized in the project; to Eric Attia, Kitty Boch and Alexander Hu for technical assistance and to Cory Brayton and Carl Nathan for advice and constructive criticism. G.A.C. Murrell is supported by St. George Private Hospital/Health Care of Australia Pty Ltd.

PY - 1997

Y1 - 1997

N2 - Nitric oxide (NO.) is a small, diffusible free radical that is generated from L-arginine by a family of enzymes, collectively termed the nitric oxide synthases. We investigated the role of NO. in tendon healing. NO. synthase activity and immunoreactivity was absent in un-injured rat Achilles tendon. After surgical division there was a five-fold increase in NO. synthase activity and immunoreactivity within the healing tendon at day 7, with a return to near baseline levels at day 14. Inhibition of NO. synthase activity with oral administration of Nω-nitro-L-arginine methyl ester (L-NAME) resulted in a significant reduction in cross-sectional area (30% at day 7, p < 0.01, 50% at day 15, p < 0.001) and failure load (24% at day 7, p < 0.01) of the healing Achilles tendon constructs. Rats fed the same regimen of the enantiomer of L-NAME, (D-NAME) had normal tendon healing. These results indicate that nitric oxide synthase is induced during tendon healing and inhibition of nitric oxide synthase inhibits this tendon healing.

AB - Nitric oxide (NO.) is a small, diffusible free radical that is generated from L-arginine by a family of enzymes, collectively termed the nitric oxide synthases. We investigated the role of NO. in tendon healing. NO. synthase activity and immunoreactivity was absent in un-injured rat Achilles tendon. After surgical division there was a five-fold increase in NO. synthase activity and immunoreactivity within the healing tendon at day 7, with a return to near baseline levels at day 14. Inhibition of NO. synthase activity with oral administration of Nω-nitro-L-arginine methyl ester (L-NAME) resulted in a significant reduction in cross-sectional area (30% at day 7, p < 0.01, 50% at day 15, p < 0.001) and failure load (24% at day 7, p < 0.01) of the healing Achilles tendon constructs. Rats fed the same regimen of the enantiomer of L-NAME, (D-NAME) had normal tendon healing. These results indicate that nitric oxide synthase is induced during tendon healing and inhibition of nitric oxide synthase inhibits this tendon healing.

KW - Free radical

KW - Nitric oxide

KW - Nitric oxide synthase

KW - Tendon healing

KW - Wound healing

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Modulation of tendon healing by nitric oxide

Abstract

Keywords

ASJC Scopus subject areas

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