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急性心肌梗死后的心房利钠肽、B型利钠肽及血清胶原蛋白标志物

Atrial natriuretic peptide, B-type natriuretic peptide, and serum collagen markers after acute myocardial infarction.

作者信息

Magga Jarkko, Puhakka Mikko, Hietakorpi Seppo, Punnonen Kari, Uusimaa Paavo, Risteli Juha, Vuolteenaho Olli, Ruskoaho Heikki, Peuhkurinen Keijo

机构信息

Department of Internal Medicine, Kuopio University Hospital, 70211 Kuopio, Finland.

出版信息

J Appl Physiol (1985). 2004 Apr;96(4):1306-11. doi: 10.1152/japplphysiol.00557.2003. Epub 2003 Nov 7.

Abstract

Experimental data suggest that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) act locally as antifibrotic factors in heart. We investigated the interrelationships of natriuretic peptides and collagen markers in 93 patients receiving thrombolytic treatment for their first acute myocardial infarction (AMI). Collagen formation following AMI, evaluated as serum levels of amino terminal propeptide of type III procollagen, correlated with NH(2)-terminal proANP (r = 0.45, P < 0.001), BNP (r = 0.55, P < 0.001) and NH(2)-terminal proBNP (r = 0.50, P < 0.01) on day 4 after thrombolysis. Levels of intact amino terminal propeptide of type I procollagen decreased by 34% (P < 0.001), and levels of carboxy terminal cross-linked telopeptide of type I collagen (ICTP) increased by 65% (P < 0.001). ICTP levels correlated with NH(2)-terminal proBNP (r = 0.25, P < 0.05) and BNP (r = 0.28, P < 0.05) on day 4. Our results suggest that ANP and BNP may act as regulators of collagen scar formation and left ventricular remodeling after AMI in humans. Furthermore, degradation of type I collagen is increased after AMI and may be regulated by BNP.

摘要

实验数据表明,心房利钠肽(ANP)和B型利钠肽(BNP)在心脏中作为局部抗纤维化因子发挥作用。我们调查了93例首次接受急性心肌梗死(AMI)溶栓治疗患者中利钠肽与胶原蛋白标志物之间的相互关系。AMI后的胶原蛋白形成,以血清III型前胶原氨基末端前肽水平评估,在溶栓后第4天与NH(2)-末端proANP(r = 0.45,P < 0.001)、BNP(r = 0.55,P < 0.001)和NH(2)-末端proBNP(r = 0.50,P < 0.01)相关。I型前胶原完整氨基末端前肽水平下降34%(P < 0.001),I型胶原羧基末端交联端肽(ICTP)水平升高65%(P < 0.001)。在第4天,ICTP水平与NH(2)-末端proBNP(r = 0.25,P < 0.05)和BNP(r = 0.28,P < 0.05)相关。我们的结果表明,ANP和BNP可能在人类AMI后作为胶原蛋白瘢痕形成和左心室重塑的调节因子。此外,AMI后I型胶原的降解增加,可能受BNP调节。

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