TY - JOUR
T1 - Flow-independent myocardial ischemia induced by endothelin-1
T2 - An NADH fluorescence analysis
AU - Inoue, Soushin
AU - Hori, Shingo
AU - Adachi, Takeshi
AU - Miyazaki, Koji
AU - Kyotani, Shingo
AU - Fukuda, Keiichi
AU - Mori, Hidezo
AU - Nakazawa, Hiroe
AU - Aikawa, Naoki
AU - Ogawa, Satoshi
PY - 2005/12/1
Y1 - 2005/12/1
N2 - The endothelin-1 (ET-1) is known to cause myocardial ischemia; however, whether this effect is entirely dependent on vasoconstriction is uncertain. The aim of this study was to characterize the myocardial ischemia after the intracoronary administration of endothelin-1, and compare it with that induced by coronary stenosis.In the left anterior descending coronary artery of 15 dogs, a mild inflow reduction (30%) was produced for 10 minutes using intracoronary endothelin-1 (46 ± 33 pmol/min) or coronary stenosis. The hearts were rapidly cross-sectioned at short axial plane and freeze-clamped within 120 milliseconds using a specially developed device to visualize and quantify the area of ischemia (%IA) with NADH fluorescence photography. The %IA was larger in the endothelin-1 group than in the stenosis group (66 ± 23 versus 18 ± 18, P = 0.0005); furthermore, the ischemia was transmural in the ET-1 group, but limited to subendocardium in the stenosis group. ET-1 increased the coronary arterial resistance especially in subepicardial region and produced smaller ischemic foci in microcirculation. The mechanism of larger ischemia produced by ET-1 might depend on pro-ischemic effects on myocytes and vasoconstriction of the coronary microcirculation, predominantly in the subepicardium in vivo.
AB - The endothelin-1 (ET-1) is known to cause myocardial ischemia; however, whether this effect is entirely dependent on vasoconstriction is uncertain. The aim of this study was to characterize the myocardial ischemia after the intracoronary administration of endothelin-1, and compare it with that induced by coronary stenosis.In the left anterior descending coronary artery of 15 dogs, a mild inflow reduction (30%) was produced for 10 minutes using intracoronary endothelin-1 (46 ± 33 pmol/min) or coronary stenosis. The hearts were rapidly cross-sectioned at short axial plane and freeze-clamped within 120 milliseconds using a specially developed device to visualize and quantify the area of ischemia (%IA) with NADH fluorescence photography. The %IA was larger in the endothelin-1 group than in the stenosis group (66 ± 23 versus 18 ± 18, P = 0.0005); furthermore, the ischemia was transmural in the ET-1 group, but limited to subendocardium in the stenosis group. ET-1 increased the coronary arterial resistance especially in subepicardial region and produced smaller ischemic foci in microcirculation. The mechanism of larger ischemia produced by ET-1 might depend on pro-ischemic effects on myocytes and vasoconstriction of the coronary microcirculation, predominantly in the subepicardium in vivo.
KW - Coronary circulation
KW - Endothelin-1
KW - Microcirculation
KW - Myocardial ischemia
KW - NADH fluorescence
KW - Pro-ischemia
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U2 - 10.1097/01.fjc.0000188280.03123.60
DO - 10.1097/01.fjc.0000188280.03123.60
M3 - Article
C2 - 16306806
AN - SCOPUS:33644672454
SN - 0160-2446
VL - 46
SP - 810
EP - 816
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
IS - 6
ER -