Xanthine oxidase-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle

H. J. McCutchan, J. R. Schwappach, E. G. Enquist, D. L. Walden, L. S. Terada, O. K. Reiss, J. A. Leff, J. E. Repine

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

We hypothesized that xanthine oxidase (XO)-derived hydrogen peroxide (H2O2) contributes to ischemic skeletal muscle injury during reperfusion. We found that after ischemia (3 h) and then reperfusion (4 h) rat gastrocnemius muscles had decreased contractile function following direct stimulation. Three lines of investigation suggested that XO-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle. First, treatment with dimethylthiourea (DMTU), a highly permeant O2 metabolite scavenger, but not urea, just before reperfusion improved muscle function in legs subjected to ischemia and then reperfusion. Second, gastrocnemius muscles from rats fed tungsten or allopurinol had negligible XO activities and increased muscle function after ischemia and reperfusion. Third, as assessed by measurement of skeletal muscle catalase activity in the presence of aminotriazole, H2O2 was measured during reperfusion of ischemic muscles from untreated or urea-treated rats but not during reperfusion of muscles from rats treated with DMTU, tungsten, or allopurinol.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume258
Issue number5 27-5
StatePublished - 1990

Fingerprint

Xanthine Oxidase
Reperfusion Injury
Reperfusion
Skeletal Muscle
Muscles
Allopurinol
Tungsten
Ischemia
Urea
Amitrole
Catalase
Hydrogen Peroxide
Leg

Keywords

  • aminotriazole
  • Dimethylthiourea
  • oxygen radicals
  • vascular injury

ASJC Scopus subject areas

  • Physiology

Cite this

McCutchan, H. J., Schwappach, J. R., Enquist, E. G., Walden, D. L., Terada, L. S., Reiss, O. K., ... Repine, J. E. (1990). Xanthine oxidase-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle. American Journal of Physiology - Heart and Circulatory Physiology, 258(5 27-5).

Xanthine oxidase-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle. / McCutchan, H. J.; Schwappach, J. R.; Enquist, E. G.; Walden, D. L.; Terada, L. S.; Reiss, O. K.; Leff, J. A.; Repine, J. E.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 258, No. 5 27-5, 1990.

Research output: Contribution to journalArticle

McCutchan, HJ, Schwappach, JR, Enquist, EG, Walden, DL, Terada, LS, Reiss, OK, Leff, JA & Repine, JE 1990, 'Xanthine oxidase-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle', American Journal of Physiology - Heart and Circulatory Physiology, vol. 258, no. 5 27-5.
McCutchan, H. J. ; Schwappach, J. R. ; Enquist, E. G. ; Walden, D. L. ; Terada, L. S. ; Reiss, O. K. ; Leff, J. A. ; Repine, J. E. / Xanthine oxidase-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle. In: American Journal of Physiology - Heart and Circulatory Physiology. 1990 ; Vol. 258, No. 5 27-5.
@article{ceae53d226f6410d9801a8e0c1830a51,
title = "Xanthine oxidase-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle",
abstract = "We hypothesized that xanthine oxidase (XO)-derived hydrogen peroxide (H2O2) contributes to ischemic skeletal muscle injury during reperfusion. We found that after ischemia (3 h) and then reperfusion (4 h) rat gastrocnemius muscles had decreased contractile function following direct stimulation. Three lines of investigation suggested that XO-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle. First, treatment with dimethylthiourea (DMTU), a highly permeant O2 metabolite scavenger, but not urea, just before reperfusion improved muscle function in legs subjected to ischemia and then reperfusion. Second, gastrocnemius muscles from rats fed tungsten or allopurinol had negligible XO activities and increased muscle function after ischemia and reperfusion. Third, as assessed by measurement of skeletal muscle catalase activity in the presence of aminotriazole, H2O2 was measured during reperfusion of ischemic muscles from untreated or urea-treated rats but not during reperfusion of muscles from rats treated with DMTU, tungsten, or allopurinol.",
keywords = "aminotriazole, Dimethylthiourea, oxygen radicals, vascular injury",
author = "McCutchan, {H. J.} and Schwappach, {J. R.} and Enquist, {E. G.} and Walden, {D. L.} and Terada, {L. S.} and Reiss, {O. K.} and Leff, {J. A.} and Repine, {J. E.}",
year = "1990",
language = "English (US)",
volume = "258",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "5 27-5",

}

TY - JOUR

T1 - Xanthine oxidase-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle

AU - McCutchan, H. J.

AU - Schwappach, J. R.

AU - Enquist, E. G.

AU - Walden, D. L.

AU - Terada, L. S.

AU - Reiss, O. K.

AU - Leff, J. A.

AU - Repine, J. E.

PY - 1990

Y1 - 1990

N2 - We hypothesized that xanthine oxidase (XO)-derived hydrogen peroxide (H2O2) contributes to ischemic skeletal muscle injury during reperfusion. We found that after ischemia (3 h) and then reperfusion (4 h) rat gastrocnemius muscles had decreased contractile function following direct stimulation. Three lines of investigation suggested that XO-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle. First, treatment with dimethylthiourea (DMTU), a highly permeant O2 metabolite scavenger, but not urea, just before reperfusion improved muscle function in legs subjected to ischemia and then reperfusion. Second, gastrocnemius muscles from rats fed tungsten or allopurinol had negligible XO activities and increased muscle function after ischemia and reperfusion. Third, as assessed by measurement of skeletal muscle catalase activity in the presence of aminotriazole, H2O2 was measured during reperfusion of ischemic muscles from untreated or urea-treated rats but not during reperfusion of muscles from rats treated with DMTU, tungsten, or allopurinol.

AB - We hypothesized that xanthine oxidase (XO)-derived hydrogen peroxide (H2O2) contributes to ischemic skeletal muscle injury during reperfusion. We found that after ischemia (3 h) and then reperfusion (4 h) rat gastrocnemius muscles had decreased contractile function following direct stimulation. Three lines of investigation suggested that XO-derived H2O2 contributes to reperfusion injury of ischemic skeletal muscle. First, treatment with dimethylthiourea (DMTU), a highly permeant O2 metabolite scavenger, but not urea, just before reperfusion improved muscle function in legs subjected to ischemia and then reperfusion. Second, gastrocnemius muscles from rats fed tungsten or allopurinol had negligible XO activities and increased muscle function after ischemia and reperfusion. Third, as assessed by measurement of skeletal muscle catalase activity in the presence of aminotriazole, H2O2 was measured during reperfusion of ischemic muscles from untreated or urea-treated rats but not during reperfusion of muscles from rats treated with DMTU, tungsten, or allopurinol.

KW - aminotriazole

KW - Dimethylthiourea

KW - oxygen radicals

KW - vascular injury

UR - http://www.scopus.com/inward/record.url?scp=0025423889&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025423889&partnerID=8YFLogxK

M3 - Article

C2 - 2110780

AN - SCOPUS:0025423889

VL - 258

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 5 27-5

ER -