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Reperfusion injury in skeletal muscle is reduced in inducible nitric oxide synthase knockout mice.

Publication ,  Journal Article
Qi, W-N; Chen, L-E; Zhang, L; Eu, JP; Seaber, AV; Urbaniak, JR
Published in: J Appl Physiol (1985)
October 2004

Inducible nitric oxide synthase (iNOS) participates in many pathological events, and selective inhibition of iNOS has been shown to reduce ischemia-reperfusion (I/R) injury in different tissues. To further confirm its role in this injury process, I/R injury was observed in denervated cremaster muscles of iNOS-deficient (iNOS-/-) and wild-type mice. After 3-h ischemia and 90-min reperfusion, blood flow in reperfused muscle was 80 +/- 8.5% (mean +/- SE) of baseline at 10-min reperfusion and completely returned to the preischemia baseline after 20 min in iNOS-/- mice. In contrast, blood flow was 32 +/- 7.4% at 10 min and increased to 60 +/- 20% of the baseline level at 90 min in wild-type mice (P < 0.001 vs. iNOS-/- mice at all time points). The increased muscle blood flow in iNOS-/- mice was associated with significantly less vasospasm in all three sizes of arterial vessel size categories. The weight ratio to the contralateral muscle not subjected to I/R was greater in wild-type mice (173 +/- 11%) than in iNOS-/- mice (117 +/- 3%; P < 0.01). Inflammation and neutrophil extravasation were also more severe in wild-type mice. Western blot analysis demonstrated an absence of iNOS protein band in iNOS-/- mice and upregulation of iNOS protein expression in wild-type mice. Our results confirm the importance of iNOS in I/R injury. Upregulated iNOS exacerbates I/R injury and appears to be a therapeutic target in protection of tissues against this type of injury.

Duke Scholars

Published In

J Appl Physiol (1985)

DOI

ISSN

8750-7587

Publication Date

October 2004

Volume

97

Issue

4

Start / End Page

1323 / 1328

Location

United States

Related Subject Headings

  • Severity of Illness Index
  • Reperfusion Injury
  • Recovery of Function
  • Physiology
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase
  • Muscle, Skeletal
  • Mice, Knockout
  • Mice
  • Male
 

Citation

APA
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ICMJE
MLA
NLM
Qi, W.-N., Chen, L.-E., Zhang, L., Eu, J. P., Seaber, A. V., & Urbaniak, J. R. (2004). Reperfusion injury in skeletal muscle is reduced in inducible nitric oxide synthase knockout mice. J Appl Physiol (1985), 97(4), 1323–1328. https://doi.org/10.1152/japplphysiol.00380.2004
Qi, Wen-Ning, Long-En Chen, Li Zhang, Jerry P. Eu, Anthony V. Seaber, and James R. Urbaniak. “Reperfusion injury in skeletal muscle is reduced in inducible nitric oxide synthase knockout mice.J Appl Physiol (1985) 97, no. 4 (October 2004): 1323–28. https://doi.org/10.1152/japplphysiol.00380.2004.
Qi W-N, Chen L-E, Zhang L, Eu JP, Seaber AV, Urbaniak JR. Reperfusion injury in skeletal muscle is reduced in inducible nitric oxide synthase knockout mice. J Appl Physiol (1985). 2004 Oct;97(4):1323–8.
Qi, Wen-Ning, et al. “Reperfusion injury in skeletal muscle is reduced in inducible nitric oxide synthase knockout mice.J Appl Physiol (1985), vol. 97, no. 4, Oct. 2004, pp. 1323–28. Pubmed, doi:10.1152/japplphysiol.00380.2004.
Qi W-N, Chen L-E, Zhang L, Eu JP, Seaber AV, Urbaniak JR. Reperfusion injury in skeletal muscle is reduced in inducible nitric oxide synthase knockout mice. J Appl Physiol (1985). 2004 Oct;97(4):1323–1328.

Published In

J Appl Physiol (1985)

DOI

ISSN

8750-7587

Publication Date

October 2004

Volume

97

Issue

4

Start / End Page

1323 / 1328

Location

United States

Related Subject Headings

  • Severity of Illness Index
  • Reperfusion Injury
  • Recovery of Function
  • Physiology
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase
  • Muscle, Skeletal
  • Mice, Knockout
  • Mice
  • Male