Xanthine oxidase mediates myocardial injury after hepatoenteric ischemia-reperfusion

Vance G. Nielsen, Sidhartha Tan, Manuel S. Baird, Paul N. Samuelson, Andrew T. McCammon, Dale A. Parks

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

Objectives: To determine if myocardial injury results from hepatoenteric ischemia-reperfusion. We also proposed to determine if this remote heart injury is mediated by a xanthine oxidase-dependent mechanism. Design: Randomized, controlled animal study. Setting: University-based animal research facility. Subjects: Thirty-six New Zealand white male rabbits, weighing 1.8 to 3 kg. Interventions: Anesthetized rabbits were randomly assigned to one of four groups (n = 9 per group): a) a sham-operated group; b) a sham-operated group pretreated with sodium tungstate (xanthine oxidase inactivator); c) an sorts occlusion group; and d) an aorta occlusion group pretreated with sodium tungstate. Descending thoracic aorta occlusion was maintained for 40 mins with a 4-Fr Fogarty embolectomy catheter, followed by 2 hrs of reperfusion. Measurements and Main Results: Myocardial injury, manifested by increased circulating creatine kinase-MB fraction activity, was significantly associated with aortic occlusion and reperfusion (p < .05). Sodium tungstate pretreatment significantly (p < .05) reduced circulating and myocardial xanthine oxidase activity. Xanthine oxidase inactivation by sodium tungstate significantly decreased circulating creatine kinase-MB fraction activity after hepatoenteric ischemia-reperfusion (p < .05). Finally, circulating creatine kinase-MB fraction activity was significantly associated with circulating xanthine oxidase activity (r2 = .85; p < .001). Conclusions: We conclude that remote myocardial injury is caused by hepatoenteric ischemia-reperfusion. The pathoetiology of this myocardial injury involves s xanthine oxidase-dependent mechanism.

Original languageEnglish (US)
Pages (from-to)1044-1050
Number of pages7
JournalCritical Care Medicine
Volume25
Issue number6
DOIs
StatePublished - Jun 1997
Externally publishedYes

Fingerprint

Xanthine Oxidase
Reperfusion
Ischemia
MB Form Creatine Kinase
Wounds and Injuries
Thoracic Aorta
Heart Injuries
Rabbits
Embolectomy
Aorta
Catheters
sodium tungstate(VI)

Keywords

  • Critical care
  • Free radicals
  • Heart
  • Ischemia
  • Liver
  • Oxidants
  • Reperfusion
  • Shock
  • Sodium tungstate
  • Xanthine oxidoreductase

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Nielsen, V. G., Tan, S., Baird, M. S., Samuelson, P. N., McCammon, A. T., & Parks, D. A. (1997). Xanthine oxidase mediates myocardial injury after hepatoenteric ischemia-reperfusion. Critical Care Medicine, 25(6), 1044-1050. https://doi.org/10.1097/00003246-199706000-00023

Xanthine oxidase mediates myocardial injury after hepatoenteric ischemia-reperfusion. / Nielsen, Vance G.; Tan, Sidhartha; Baird, Manuel S.; Samuelson, Paul N.; McCammon, Andrew T.; Parks, Dale A.

In: Critical Care Medicine, Vol. 25, No. 6, 06.1997, p. 1044-1050.

Research output: Contribution to journalArticle

Nielsen, VG, Tan, S, Baird, MS, Samuelson, PN, McCammon, AT & Parks, DA 1997, 'Xanthine oxidase mediates myocardial injury after hepatoenteric ischemia-reperfusion', Critical Care Medicine, vol. 25, no. 6, pp. 1044-1050. https://doi.org/10.1097/00003246-199706000-00023
Nielsen, Vance G. ; Tan, Sidhartha ; Baird, Manuel S. ; Samuelson, Paul N. ; McCammon, Andrew T. ; Parks, Dale A. / Xanthine oxidase mediates myocardial injury after hepatoenteric ischemia-reperfusion. In: Critical Care Medicine. 1997 ; Vol. 25, No. 6. pp. 1044-1050.
@article{7e6bc517bba544e69ef9bfe2bcacb0e7,
title = "Xanthine oxidase mediates myocardial injury after hepatoenteric ischemia-reperfusion",
abstract = "Objectives: To determine if myocardial injury results from hepatoenteric ischemia-reperfusion. We also proposed to determine if this remote heart injury is mediated by a xanthine oxidase-dependent mechanism. Design: Randomized, controlled animal study. Setting: University-based animal research facility. Subjects: Thirty-six New Zealand white male rabbits, weighing 1.8 to 3 kg. Interventions: Anesthetized rabbits were randomly assigned to one of four groups (n = 9 per group): a) a sham-operated group; b) a sham-operated group pretreated with sodium tungstate (xanthine oxidase inactivator); c) an sorts occlusion group; and d) an aorta occlusion group pretreated with sodium tungstate. Descending thoracic aorta occlusion was maintained for 40 mins with a 4-Fr Fogarty embolectomy catheter, followed by 2 hrs of reperfusion. Measurements and Main Results: Myocardial injury, manifested by increased circulating creatine kinase-MB fraction activity, was significantly associated with aortic occlusion and reperfusion (p < .05). Sodium tungstate pretreatment significantly (p < .05) reduced circulating and myocardial xanthine oxidase activity. Xanthine oxidase inactivation by sodium tungstate significantly decreased circulating creatine kinase-MB fraction activity after hepatoenteric ischemia-reperfusion (p < .05). Finally, circulating creatine kinase-MB fraction activity was significantly associated with circulating xanthine oxidase activity (r2 = .85; p < .001). Conclusions: We conclude that remote myocardial injury is caused by hepatoenteric ischemia-reperfusion. The pathoetiology of this myocardial injury involves s xanthine oxidase-dependent mechanism.",
keywords = "Critical care, Free radicals, Heart, Ischemia, Liver, Oxidants, Reperfusion, Shock, Sodium tungstate, Xanthine oxidoreductase",
author = "Nielsen, {Vance G.} and Sidhartha Tan and Baird, {Manuel S.} and Samuelson, {Paul N.} and McCammon, {Andrew T.} and Parks, {Dale A.}",
year = "1997",
month = "6",
doi = "10.1097/00003246-199706000-00023",
language = "English (US)",
volume = "25",
pages = "1044--1050",
journal = "Critical Care Medicine",
issn = "0090-3493",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Xanthine oxidase mediates myocardial injury after hepatoenteric ischemia-reperfusion

AU - Nielsen, Vance G.

AU - Tan, Sidhartha

AU - Baird, Manuel S.

AU - Samuelson, Paul N.

AU - McCammon, Andrew T.

AU - Parks, Dale A.

PY - 1997/6

Y1 - 1997/6

N2 - Objectives: To determine if myocardial injury results from hepatoenteric ischemia-reperfusion. We also proposed to determine if this remote heart injury is mediated by a xanthine oxidase-dependent mechanism. Design: Randomized, controlled animal study. Setting: University-based animal research facility. Subjects: Thirty-six New Zealand white male rabbits, weighing 1.8 to 3 kg. Interventions: Anesthetized rabbits were randomly assigned to one of four groups (n = 9 per group): a) a sham-operated group; b) a sham-operated group pretreated with sodium tungstate (xanthine oxidase inactivator); c) an sorts occlusion group; and d) an aorta occlusion group pretreated with sodium tungstate. Descending thoracic aorta occlusion was maintained for 40 mins with a 4-Fr Fogarty embolectomy catheter, followed by 2 hrs of reperfusion. Measurements and Main Results: Myocardial injury, manifested by increased circulating creatine kinase-MB fraction activity, was significantly associated with aortic occlusion and reperfusion (p < .05). Sodium tungstate pretreatment significantly (p < .05) reduced circulating and myocardial xanthine oxidase activity. Xanthine oxidase inactivation by sodium tungstate significantly decreased circulating creatine kinase-MB fraction activity after hepatoenteric ischemia-reperfusion (p < .05). Finally, circulating creatine kinase-MB fraction activity was significantly associated with circulating xanthine oxidase activity (r2 = .85; p < .001). Conclusions: We conclude that remote myocardial injury is caused by hepatoenteric ischemia-reperfusion. The pathoetiology of this myocardial injury involves s xanthine oxidase-dependent mechanism.

AB - Objectives: To determine if myocardial injury results from hepatoenteric ischemia-reperfusion. We also proposed to determine if this remote heart injury is mediated by a xanthine oxidase-dependent mechanism. Design: Randomized, controlled animal study. Setting: University-based animal research facility. Subjects: Thirty-six New Zealand white male rabbits, weighing 1.8 to 3 kg. Interventions: Anesthetized rabbits were randomly assigned to one of four groups (n = 9 per group): a) a sham-operated group; b) a sham-operated group pretreated with sodium tungstate (xanthine oxidase inactivator); c) an sorts occlusion group; and d) an aorta occlusion group pretreated with sodium tungstate. Descending thoracic aorta occlusion was maintained for 40 mins with a 4-Fr Fogarty embolectomy catheter, followed by 2 hrs of reperfusion. Measurements and Main Results: Myocardial injury, manifested by increased circulating creatine kinase-MB fraction activity, was significantly associated with aortic occlusion and reperfusion (p < .05). Sodium tungstate pretreatment significantly (p < .05) reduced circulating and myocardial xanthine oxidase activity. Xanthine oxidase inactivation by sodium tungstate significantly decreased circulating creatine kinase-MB fraction activity after hepatoenteric ischemia-reperfusion (p < .05). Finally, circulating creatine kinase-MB fraction activity was significantly associated with circulating xanthine oxidase activity (r2 = .85; p < .001). Conclusions: We conclude that remote myocardial injury is caused by hepatoenteric ischemia-reperfusion. The pathoetiology of this myocardial injury involves s xanthine oxidase-dependent mechanism.

KW - Critical care

KW - Free radicals

KW - Heart

KW - Ischemia

KW - Liver

KW - Oxidants

KW - Reperfusion

KW - Shock

KW - Sodium tungstate

KW - Xanthine oxidoreductase

UR - http://www.scopus.com/inward/record.url?scp=0030961760&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030961760&partnerID=8YFLogxK

U2 - 10.1097/00003246-199706000-00023

DO - 10.1097/00003246-199706000-00023

M3 - Article

C2 - 9201059

AN - SCOPUS:0030961760

VL - 25

SP - 1044

EP - 1050

JO - Critical Care Medicine

JF - Critical Care Medicine

SN - 0090-3493

IS - 6

ER -