TY - JOUR
T1 - Intracoronary endothelin-1 increases coronary retrograde pressure by constricting arterioles
AU - Fukuda, Keiichi
AU - Hori, Shingo
AU - Kusuhara, Masatoshi
AU - Satoh, Toru
AU - Kyotani, Shingo
AU - Inoue, Soushin
AU - Ohno, Hideto
AU - Yamaguchi, Ken
AU - Handa, Shunnosuke
AU - Nakamura, Yoshiro
N1 - Funding Information:
We thank Dr Muneyuki Horikawa for valuable discussions and Ms Mary Sibuya for assistance in preparation of the manuscript. This work was supported by grants-in-aid (1989) for scientific research from the Ministry of Education, Science and Culture, Japan, and a grant from the Keio Medical Society (1989).
PY - 1990/12
Y1 - 1990/12
N2 - Study objective - The aim was to determine the site of coronary vasoconstriction induced by endothelin, by investigating the response in terms of retrograde pressure and reactive hyperaemia.Experimental material - Twelve anaesthetised mongrel dogs, 12-14 kg, were used for the studies.Design - The left anterior descending coronary artery was cannulated and perfused with blood through an extracorporeal bypass. The effects of intracoronary endothelin-l (1-500 pmol) on coronary blood flow, coronary flow reserve (the peak reactive flow and the repayment after 15 s coronary occlusion), and retrograde coronary pressure during coronary occlusion were studied (n=7). The retrograde coronary flow was collected from the bypass at each dose (n=5).Measurements and main results - At doses of greater than 20 pmol the coronary flow decreased dose dependently and reached almost zero flow at 500 pmol. The coronary flow reserve also decreased; however, the retrograde pressure was raised dose dependently at doses of greater than 10 pmol. At a dose of 500 pmol, the retrograde pressure was increased to 61 mm Hg [82(SEM 12)% of the coronary perfusion pressure]. Retrograde flow remained unchanged throughout the experiment.Conclusions - The endothelin-1 induced rise in retrograde pressure is in accordance with a dose dependent reduction in coronary flow reserve, and collateral flow was not augmented by endothelin. It is concluded that the effect of endothelin-1 on coronary circulation in situ was mainly due to the constriction of small resistant vessels.
AB - Study objective - The aim was to determine the site of coronary vasoconstriction induced by endothelin, by investigating the response in terms of retrograde pressure and reactive hyperaemia.Experimental material - Twelve anaesthetised mongrel dogs, 12-14 kg, were used for the studies.Design - The left anterior descending coronary artery was cannulated and perfused with blood through an extracorporeal bypass. The effects of intracoronary endothelin-l (1-500 pmol) on coronary blood flow, coronary flow reserve (the peak reactive flow and the repayment after 15 s coronary occlusion), and retrograde coronary pressure during coronary occlusion were studied (n=7). The retrograde coronary flow was collected from the bypass at each dose (n=5).Measurements and main results - At doses of greater than 20 pmol the coronary flow decreased dose dependently and reached almost zero flow at 500 pmol. The coronary flow reserve also decreased; however, the retrograde pressure was raised dose dependently at doses of greater than 10 pmol. At a dose of 500 pmol, the retrograde pressure was increased to 61 mm Hg [82(SEM 12)% of the coronary perfusion pressure]. Retrograde flow remained unchanged throughout the experiment.Conclusions - The endothelin-1 induced rise in retrograde pressure is in accordance with a dose dependent reduction in coronary flow reserve, and collateral flow was not augmented by endothelin. It is concluded that the effect of endothelin-1 on coronary circulation in situ was mainly due to the constriction of small resistant vessels.
KW - Collateral circulation
KW - Coronary circulation
KW - Coronary retrograde flow
KW - Coronary retrograde pressure
KW - Coronary spasm
KW - Endothelin-1
KW - Resistance vessel
KW - Vasoconstriction
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U2 - 10.1093/cvr/24.12.987
DO - 10.1093/cvr/24.12.987
M3 - Review article
C2 - 2097065
AN - SCOPUS:85047678842
VL - 24
SP - 987
EP - 992
JO - Cardiovascular Research
JF - Cardiovascular Research
SN - 0008-6363
IS - 12
ER -