Role of Endothelium -Derived Relaxing Factor in the Pathogenesis of Coronary Artery Spasm and Its Relationship with Ethanol.
10.4070/kcj.1992.22.5.768
- Author:
Jung Don SEO
;
Jae Kwan SONG
;
Cheol Ho KIM
;
Dae Won SOHN
;
Byung Hee OH
;
Myoung Mook LEE
;
Young Bae PARK
;
Yun Shick CHOI
;
Young Woo LEE
- Publication Type:Original Article
- Keywords:
EDRF(endothelium-derived relaxing factor);
Coronary vasospasm;
Ethyl alcohol
- MeSH:
Aorta;
Arginine;
Coronary Vasospasm;
Coronary Vessels*;
Endothelium*;
Endothelium, Vascular;
Ethanol*;
Humans;
Myocardial Ischemia;
Spasm*;
Vasodilation
- From:Korean Circulation Journal
1992;22(5):768-783
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Isometric tension recording was performed in the transverse strips of porcine coronary arteries and rabbit aorta to observe the effects of the endothelium and endothelium-derived relaxing factor(EDRF) on vasomotor tone and to test the hypothesis that alcohol may have the deleterious effect on endothelium-dependent vasorelaxation. Tension-development by vasoconstrictor was markedly attenuated in the endothelium-intact strips compared to the endothelium denuded strips. Administration of hemoglobin(10-5M) to inhibit the action of EDRF increased tension selectively in the endothelium-infarct strips, which is suggestive of basal EDRF secretion. Nitro L-arginine(10-5M). an analogue of L-arginine(10-4M) partially reversed the inhibitory effect of nitro L-arginine. Ethyl alchol inhibited bradykinin-induced endothelium-dependent vasorelaxation of porcine coronary artery in dose dependent manner. These data suggest that the protective effect of vascular endothelium to the action of vasoconstirctor can be explained by exercise of basal EDRF release and damaged endothelium would be a great risk of induction of vasospasm. Also we believe that there is a relationship of competive inhibition between L-arginine. a precursor of EDRF, and its analogues on the action of EDRF and alcohol intake would be hazardous to the patients with coronary artey disease because its inhibitory action on endothelium-dependent vasorelaxation may evoke myocardial ischemia.
