TY - JOUR
T1 - Production of endothelium-derived contracting factor is enhanced after coronary reperfusion
AU - Pearson, Paul J.
AU - Lin, Pyng J.
AU - Schaff, Hartzell V.
PY - 1991/5
Y1 - 1991/5
N2 - 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.
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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U2 - 10.1016/0003-4975(91)90126-B
DO - 10.1016/0003-4975(91)90126-B
M3 - Article
C2 - 1902653
AN - SCOPUS:0026075421
SN - 0003-4975
VL - 51
SP - 788
EP - 793
JO - The Annals of thoracic surgery
JF - The Annals of thoracic surgery
IS - 5
ER -