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Reperfusion injury is reduced in skeletal muscle by inhibition of inducible nitric oxide synthase.

Publication ,  Journal Article
Zhang, L; Looney, CG; Qi, W-N; Chen, L-E; Seaber, AV; Stamler, JS; Urbaniak, JR
Published in: J Appl Physiol (1985)
April 2003

This study evaluated the effects of the selective inducible nitric oxide synthase (iNOS) inhibitor N-[3-(aminomethyl)benzyl]acetamidine (1400W) on the microcirculation in reperfused skeletal muscle. The cremaster muscles from 32 rats underwent 5 h of ischemia followed by 90 min of reperfusion. Rats received either 3 mg/kg 1400W or PBS subcutaneously before reperfusion. We found that blood flow in reperfused muscles was <45% of baseline in controls but sharply recovered to near baseline levels in 1400W-treated animals. There was a significant (P < 0.01 to P < 0.001) difference between the two groups at each time point throughout the 90 min of reperfusion. Vessel diameters remained <80% of baseline in controls during reperfusion, but recovered to the baseline level in the 1400W group by 20 min, and reached a maximum of 121 +/- 14% (mean +/- SD) of baseline in 10- to 20-micro m arterioles, 121 +/- 6% in 21- to 40-micro m arterioles, and 115 +/- 8% in 41- to 70-micro m arteries (P < 0.01 to P < 0.001). The muscle weight ratio between ischemia-reperfused (left) and non-ischemia-reperfused (right) cremaster muscles was 193 +/- 42% of normal in controls and 124 +/- 12% in the 1400W group (P < 0.001). Histology showed that neutrophil extravasation and edema were markedly reduced in 1400W-treated muscles compared with controls. We conclude that ischemia-reperfusion leads to increased generation of NO from iNOS in skeletal muscle and that the selective iNOS inhibitor 1400W reduces the negative effects of ischemia-reperfusion on vessel diameter and muscle blood flow. Thus 1400W may have therapeutic potential in treatment of ischemia-reperfusion injury.

Duke Scholars

Published In

J Appl Physiol (1985)

DOI

ISSN

8750-7587

Publication Date

April 2003

Volume

94

Issue

4

Start / End Page

1473 / 1478

Location

United States

Related Subject Headings

  • Vasodilation
  • Respiratory Mechanics
  • Reperfusion Injury
  • Rats, Sprague-Dawley
  • Rats
  • Physiology
  • Organ Size
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase
  • Muscle, Skeletal
 

Citation

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Zhang, L., Looney, C. G., Qi, W.-N., Chen, L.-E., Seaber, A. V., Stamler, J. S., & Urbaniak, J. R. (2003). Reperfusion injury is reduced in skeletal muscle by inhibition of inducible nitric oxide synthase. J Appl Physiol (1985), 94(4), 1473–1478. https://doi.org/10.1152/japplphysiol.00789.2002
Zhang, Li, Colin G. Looney, Wen-Ning Qi, Long-En Chen, Anthony V. Seaber, Jonathan S. Stamler, and James R. Urbaniak. “Reperfusion injury is reduced in skeletal muscle by inhibition of inducible nitric oxide synthase.J Appl Physiol (1985) 94, no. 4 (April 2003): 1473–78. https://doi.org/10.1152/japplphysiol.00789.2002.
Zhang L, Looney CG, Qi W-N, Chen L-E, Seaber AV, Stamler JS, et al. Reperfusion injury is reduced in skeletal muscle by inhibition of inducible nitric oxide synthase. J Appl Physiol (1985). 2003 Apr;94(4):1473–8.
Zhang, Li, et al. “Reperfusion injury is reduced in skeletal muscle by inhibition of inducible nitric oxide synthase.J Appl Physiol (1985), vol. 94, no. 4, Apr. 2003, pp. 1473–78. Pubmed, doi:10.1152/japplphysiol.00789.2002.
Zhang L, Looney CG, Qi W-N, Chen L-E, Seaber AV, Stamler JS, Urbaniak JR. Reperfusion injury is reduced in skeletal muscle by inhibition of inducible nitric oxide synthase. J Appl Physiol (1985). 2003 Apr;94(4):1473–1478.

Published In

J Appl Physiol (1985)

DOI

ISSN

8750-7587

Publication Date

April 2003

Volume

94

Issue

4

Start / End Page

1473 / 1478

Location

United States

Related Subject Headings

  • Vasodilation
  • Respiratory Mechanics
  • Reperfusion Injury
  • Rats, Sprague-Dawley
  • Rats
  • Physiology
  • Organ Size
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase
  • Muscle, Skeletal