Production of endothelium-derived contracting factor is enhanced after coronary reperfusion. Ann Thorac Surg 1991 May;51(5):788-93
Date
05/01/1991Pubmed ID
1902653DOI
10.1016/0003-4975(91)90126-bScopus ID
2-s2.0-0026075421 (requires institutional sign-in at Scopus site) 47 CitationsAbstract
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.
Author List
Pearson PJ, Lin PJ, Schaff HVAuthor
Paul Joseph Pearson MD, PhD Chief, Professor in the Surgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBiological Factors
Carbon Dioxide
Coronary Vasospasm
Dinoprost
Dogs
Endothelins
Female
In Vitro Techniques
Male
Muscle Contraction
Muscle, Smooth, Vascular
Myocardial Reperfusion
Nitrogen
Oxygen
