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Oxidative modification of tropomyosin and myocardial dysfunction following coronary microembolization.

Abstract：

AIMS:We addressed a potential mechanism of myocardial dysfunction following coronary microembolization at the level of myofibrillar proteins. METHODS AND RESULTS:Anaesthetized pigs underwent intracoronary infusion of microspheres. After 6 h, the microembolized areas (MEA) had decreased systolic wall thickening to 38 +/- 7% of baseline and a 2.62 +/- 0.40-fold increase in the formation of disulphide cross-bridges (DCB) in tropomyosin relative to that in remote areas. The impairment in contractile function correlated inversely with DCB formation (r = -0.68; P = 0.015) and was associated with increased TNF-alpha content. DCB formation was reflected by increased tropomyosin immunoreactivity and abolished in vitro by dithiothreitol. Ascorbic acid prevented contractile dysfunction as well as increased DCB and TNF-alpha. In anaesthetized dogs, 8 h after intracoronary microspheres infusion, contractile function was reduced to 8+/-10% of baseline and DCB in MEA was 1.48+/-0.12 higher than that in remote areas. In conscious dogs, 6 days after intracoronary microspheres infusion, myocardial function had returned to baseline and DCB was no longer different between remote and MEA. Again contractile function correlated inversely with DCB formation (r = -0.83; P = 0.005). CONCLUSION:Myofibrillar protein oxidation may represent a mechanistic link between inflammation and contractile dysfunction following coronary microembolization.

journal_name

Eur Heart J

journal_title

European heart journal

authors

Canton M,Skyschally A,Menabò R,Boengler K,Gres P,Schulz R,Haude M,Erbel R,Di Lisa F,Heusch G

doi

10.1093/eurheartj/ehi751

subject

Has Abstract

pub_date

2006-04-01 00:00:00

pages

875-81

issue

7

eissn

0195-668X

issn

1522-9645

pii

ehi751

journal_volume

27

pub_type

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