Production of endothelium-derived contracting factor is enhanced after coronary reperfusion

Paul J. Pearson, Pyng J. Lin, Hartzell V Schaff

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

To determine whether coronary reperfusion enhances the production of endothelium-derived contracting factor, we investigated dogs subjected to global cardiac ischemia (45 minutes) followed by reperfusion (60 minutes). Segments of reperfused and control coronary arteries were suspended in organ chambers to measure isometric force. Perfusate hypoxia caused endothelium-dependent contraction in the control and reperfused arteries. However, reperfused arteries exhibited hypoxic contraction that was significantly greater than control segments. The hypoxic contractions in both the control and reperfused arteries could be inhibited by NG-monomethyl-l-arginine (L-NMMA), the blocker of endothelial cell synthesis of nitric oxide from l-arginine. The action of L-NMMA could be reversed by l-arginine but not d-arginine. Thus, after reperfusion, augmented production of endothelium-derived contracting factor occurs by an l-arginine-dependent pathway. We hypothesize that nitric oxide produced by l-arginine metabolism combines with superoxide anion to produce the peroxynitrite anion (ONOO-), which is metabolized to endothelium-derived contracting factor or induces its synthesis. Augmented production of endothelium-derived contracting factor would favor vasospasm after reperfusion.

Original languageEnglish (US)
Pages (from-to)788-793
Number of pages6
JournalThe Annals of Thoracic Surgery
Volume51
Issue number5
DOIs
StatePublished - 1991

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Myocardial Reperfusion
Endothelium
Arginine
Reperfusion
omega-N-Methylarginine
Arteries
Nitric Oxide
Peroxynitrous Acid
Superoxides
Anions
Coronary Vessels
Ischemia
Endothelial Cells
Dogs

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Production of endothelium-derived contracting factor is enhanced after coronary reperfusion. / Pearson, Paul J.; Lin, Pyng J.; Schaff, Hartzell V.

In: The Annals of Thoracic Surgery, Vol. 51, No. 5, 1991, p. 788-793.

Research output: Contribution to journalArticle

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AB - To determine whether coronary reperfusion enhances the production of endothelium-derived contracting factor, we investigated dogs subjected to global cardiac ischemia (45 minutes) followed by reperfusion (60 minutes). Segments of reperfused and control coronary arteries were suspended in organ chambers to measure isometric force. Perfusate hypoxia caused endothelium-dependent contraction in the control and reperfused arteries. However, reperfused arteries exhibited hypoxic contraction that was significantly greater than control segments. The hypoxic contractions in both the control and reperfused arteries could be inhibited by NG-monomethyl-l-arginine (L-NMMA), the blocker of endothelial cell synthesis of nitric oxide from l-arginine. The action of L-NMMA could be reversed by l-arginine but not d-arginine. Thus, after reperfusion, augmented production of endothelium-derived contracting factor occurs by an l-arginine-dependent pathway. We hypothesize that nitric oxide produced by l-arginine metabolism combines with superoxide anion to produce the peroxynitrite anion (ONOO-), which is metabolized to endothelium-derived contracting factor or induces its synthesis. Augmented production of endothelium-derived contracting factor would favor vasospasm after reperfusion.

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