Elevation of serum endothelins and cardiotoxicity induced by particulate matter (PM2.5) in rats with acute myocardial infarction

被引：37

作者：

Kang Y.J. ^{[1
,3
,4
,5
]}

Li Y. ^{[1
]}

Zhou Z. ^{[1
]}

Roberts A.M. ^{[2
]}

Cai L. ^{[1
]}

Myers S.R. ^{[3
]}

Wang L. ^{[1
]}

Schuschke D.A. ^{[2
]}

机构：

[1] Department of Medicine, Univ. of Louisville Sch. of Medicine, Louisville

[2] Department of Physiology, Univ. of Louisville Sch. of Medicine, Louisville

[3] Dept. of Pharmacology/Toxicology, Univ. of Louisville Sch. of Medicine, Louisville

[4] Jewish Hosp. Heart/Lung Institute, Louisville

[5] Department of Medicine, Univ. of Louisville Sch. of Medicine, Louisville, KY 40202

来源：

Cardiovascular Toxicology | 2002年 / 2卷 / 4期

基金：

美国国家卫生研究院;

关键词：

Cardiac arrhythmia; Electrocardiogram; Endothelin receptor; Myocardial infarction; Particulate matter;

D O I：

10.1385/CT:2:4:253

中图分类号：

学科分类号：

摘要：

Epidemiological studies have defined a significant positive association of acute exposure to ambient concentrations of particulate matter (PM) with increased daily mortality and hospital admission for cardiovascular diseases. Experimental studies have shown that animals with pre-existing cardiovascular diseases are more susceptible to the cardiac effect of PM exposure. The present study was undertaken to investigate possible involvement of upregulation of the endothelin system in PM exposure-induced cardiotoxicity in rats with acute myocardial infarction (MI). Adult male Sprague-Dawley rats were subjected to occlusion of the left coronary artery and displayed myocardial infarction 12 h after the surgery. The heart rate significantly decreased and premature ventricular complexes of the electrocardiogram occurred in the myocardial infarct animals. Exposure to PM2.5 via intratracheal instillation with 2.0 mg in 0.3 mL normal saline significantly worsened the ventricular arrhythmia along with a further decrease in heart rate. The same PM exposure only caused slight cardiac changes in the sham-operated animals. Serum total endothelin concentrations were significantly elevated in both myocardial infarct rats and sham-operated controls in response to PM exposure. However, increased numbers of the endothelin receptor type A on the cardiomyocytes were observed only in the infarct myocardium. This study thus suggests that upregulation of the endothelin system in rats with MI is likely involved in the PM exposure-induced cardiotoxicity.

引用

页码：253 / 261

页数：8

共 36 条

[1]

Dockery D.W., Epidemiologic evidence of cardiovascular effects of particulate air pollution, Environ. Health Perspect., 109, pp. 483-486, (2001)

[2]

Gordon T., Reibman J., Cardiovascular toxicity of inhaled ambient particulate matter, Toxicol. Sci., 56, pp. 2-4, (2000)

[3]

Peters A., Liu E., Verrier R.L., Et al., Air pollution and incidence of cardiac arrhythmia, Epidemiology, 11, pp. 11-17, (2000)

[4]

Wellenius G.A., Saldiva P.H.N., Batalha J.R.F., Et al., Electrocardiographic changes during exposure to residual oil fly ash (ROFA) particles in a rat model of myocardial infarction, Toxicol. Sci., 66, pp. 327-335, (2002)

[5]

Bouthillier L., Vincent R., Goegan P., Et al., Acute effects of inhaled urban particles and ozone: Lung morphology, macrophage activity, and plasma endothelin-1, Am. J. Pathol., 153, pp. 1873-1884, (1998)

[6]

Inoue A., Yanagisawa M., Kimura S., Et al., The human endothelin family: Three structurally and pharmacologically distinct isopeptides predicted by three separate genes, Proc. Natl. Acad. Sci. USA, 86, pp. 2863-2867, (1989)

[7]

Xu D., Emoto N., Giaid A., Et al., ECE-1: A membrane bound metalloprotease that catalyses the proteolytic activation of big endothelin-1, Cell, 78, pp. 473-485, (1994)

[8]

Harai H., Hori S., Aramori I., Ohkuba H., Nakanishi S., Cloning and expression of a cDNA encoding an endothelin receptor, Nature, 348, pp. 732-735, (1990)

[9]

Molenaar P., O'Reilly G., Sharkey A., Et al., Characterization and localization in the human atrioventricular conducting system and myocardium, Circ. Res., 72, pp. 526-538, (1993)

[10]

Davenport A.P., Maguire J.J., Is endothelin-induced vasoconstriction mediated only by ET-A receptors in humans?, Trends Pharmacol. Sci., 15, pp. 9-11, (1994)

← 1 2 3 4 →