INCREASED PLASMA ENDOTHELIN-1 IN THE EARLY HOURS OF ACUTE MYOCARDIAL-INFARCTION

被引:285
作者
STEWART, DJ
KUBAC, G
COSTELLO, KB
CERNACEK, P
机构
[1] MCGILL UNIV,DEPT MED,DIV CARDIOL,MCGILL UNIT PREVENT CARDIOVASC DIS,MONTREAL H3A 2T5,QUEBEC,CANADA
[2] MCGILL UNIV,DEPT MED,DIV MED BIOCHEM,MONTREAL H3A 2T5,QUEBEC,CANADA
基金
英国医学研究理事会;
关键词
D O I
10.1016/S0735-1097(10)80214-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Endothelin is a novel endothelium-derived vasoactive peptide with potent vasoconstrictor action in the coronary bed; however, its possible contribution to myocardial ischemia and infarction is not known. Plasma endothelin-1 concentration was measured with use of a radioimmunoassay in serial venous samples from 22 patients over a 72 h period after acute myocardial infarction (14 patients with uncomplicated infarction [group I] and 8 patients with hemodynamic or ischemic sequelae [group II]). Twenty-two normal subjects and seven patients with stable angina served as the control subjects. Endothelin-1 levels in patients with stable coronary disease were not different from those of normal subjects (0.62 +/- 0.56 and 0.76 +/- 0.38 pg/ml, respectively). In group I, plasma levels of endothelin-1 rose sharply after myocardial infarction, reaching a peak of 4.95 +/- 0.78 pg/ml at 6 h after the onset of chest pain (p < 0.05 compared with values in control subjects) and returning rapidly toward the normal range by 24 h. Patients with complicated infarction (group II) demonstrated a similar rapid increase in plasma endothelin-1 to a peak value of 8.29 +/- 1.95 pg/ml; however, plasma endothelin-1 remained elevated in these patients, becoming significantly different from values in group I at 48 and 72 h. There was no correlation between peak increases in creatine kinase and peak endothelin-1 in either group, suggesting that the stimulus for elevation of endothelin-1 was not myocardial necrosis itself. Furthermore, left ventricular ejection fraction did not correlate with the increase in endothelin-1 in group I patients, whereas there was a significant inverse relation between ventricular function and plasma endothelin-1 in group II. Therefore, the rapid increase in plasma endothelin-1 associated with the onset of infarction suggests that this peptide may provide a marker of endothelial perturbation in the early phase of coronary ischemia or even contribute to alterations in myocardial perfusion. The sustained increase in plasma endothelin-1 in patients demonstrating complications of myocardial infarction might reflect continuing ischemia or marked depression in ventricular function in these patients.
引用
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页码:38 / 43
页数:6
相关论文
共 32 条
[1]  
ANGGARD E, 1989, J CARDIOVASC PHARM, V13, pS46
[2]   RELEASE OF ENDOTHELIN FROM THE PORCINE AORTA - INHIBITION BY ENDOTHELIUM-DERIVED NITRIC-OXIDE [J].
BOULANGER, C ;
LUSCHER, TF .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 85 (02) :587-590
[3]   IMMUNOREACTIVE ENDOTHELIN IN HUMAN-PLASMA - MARKED ELEVATIONS IN PATIENTS IN CARDIOGENIC-SHOCK [J].
CERNACEK, P ;
STEWART, DJ .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1989, 161 (02) :562-567
[4]   INFLUENCE OF ENDOTHELIN ON HUMAN CORONARY-ARTERIES AND LOCALIZATION OF ITS BINDING-SITES [J].
CHESTER, AH ;
DASHWOOD, MR ;
CLARKE, JG ;
LARKIN, SW ;
DAVIES, GJ ;
TADJKARIMI, S ;
MASERI, A ;
YACOUB, MH .
AMERICAN JOURNAL OF CARDIOLOGY, 1989, 63 (18) :1395-1398
[5]   EFFECTS OF ENDOTHELIN ON THE CORONARY VASCULAR BED IN OPEN-CHEST DOGS [J].
CLOZEL, JP ;
CLOZEL, M .
CIRCULATION RESEARCH, 1989, 65 (05) :1193-1200
[6]   ENDOTHELIN IS A POTENT CONSTRICTOR OF HUMAN VESSELS USED IN CORONARY REVASCULARIZATION SURGERY [J].
COSTELLO, KB ;
STEWART, DJ ;
BAFFOUR, R .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1990, 186 (2-3) :311-314
[7]  
DENUCCI G, 1988, P NATL ACAD SCI USA, V85, P9797
[8]   SECRETORY MECHANISM OF IMMUNOREACTIVE ENDOTHELIN IN CULTURED BOVINE ENDOTHELIAL-CELLS [J].
EMORI, T ;
HIRATA, Y ;
OHTA, K ;
SHICHIRI, M ;
MARUMO, F .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1989, 160 (01) :93-100
[9]   LETHAL ISCHEMIA DUE TO INTRACORONARY ENDOTHELIN IN PIGS [J].
EZRA, D ;
GOLDSTEIN, RE ;
CZAJA, JF ;
FEUERSTEIN, GZ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (01) :H339-H343