Levosimendan displays anti-inflammatory effects and decreases MPO bioavailability in patients with severe heart failure

被引：20

作者：

Adam, Matti ^{[1
]}

Meyer, Sven ^{[2
,3
]}

Knors, Henning ^{[4
]}

Klinke, Anna ^{[5
,6
]}

Radunski, Ulf K. ^{[4
]}

Rudolph, Tanja K. ^{[5
,6
]}

Rudolph, Volker ^{[5
,6
]}

Spin, Joshua M. ^{[1
]}

Tsao, Philip S. ^{[1
]}

Costard-Jaeckle, Angelika ^{[4
]}

Baldus, Stephan ^{[5
,6
]}

机构：

[1] Stanford Univ, Div Cardiovasc Med, Stanford, CA 94305 USA

[2] Univ Groningen, Univ Med Ctr Groningen, Dept Cardiol, Groningen, Netherlands

[3] European Med Sch Oldenburg Groningen, Heart Ctr Oldenburg, Oldenburg, Germany

[4] Univ Hamburg, Ctr Heart, Dept Cardiovasc Med, Hamburg, Germany

[5] Univ Cologne, Dept Cardiol, D-50931 Cologne, Germany

[6] Cologne Cardiovasc Res Ctr, D-50931 Cologne, Germany

来源：

SCIENTIFIC REPORTS | 2015年 / 5卷

关键词：

ENDOTHELIAL DYSFUNCTION; NATRIURETIC-PEPTIDE; PULSE PRESSURE; MYELOPEROXIDASE; HYPERTENSION; DOBUTAMINE; MECHANISMS; NEUTROPHILS; ACTIVATION; STRESS;

D O I：

10.1038/srep09704

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Treatment of decompensated heart failure often includes administration of levosimendan. Myeloperoxidase (MPO) is released during polymorphonuclear neutrophil (PMN) degranulation, and mediates dysregulation of vascular tone in heart failure. We evaluated the effects of levosimendan-treatment on MPO in patients with acute decompensation of chronic heart failure over a one week course. Plasma MPO levels were significantly decreased after levosimendan treatment (from 252.1 +/- 31.1 pmol/l at baseline to 215.02 +/- 27.96 pmol/l at 6 h, p < 0.05). Ex vivo incubation of whole blood with levosimendan decreased MPO release after PMN-stimulation (8.2 +/- 1.4-fold increase at baseline vs. 6.0 +/- 1.1-fold increase with levosimendan). MPO levels also significantly correlated with diastolic blood pressure over the time course. In a multivariate linear model, the main contributor to systolic, diastolic and mean blood pressure was level of PMN elastase. MPO contributed only in heparin-treated patients, suggesting a more significant role for endothelial-bound MPO than for circulating MPO or elastase with respect to blood pressure regulation. We here provide the first evidence that levosimendan treatment inhibits MPO release by PMNs in decompensated heart failure patients. This mechanism may regulate endothelial function and vascular tone in heart failure patients.

引用

页码：1 / 9

页数：9

共 38 条

[1] Effects of Levosimendan versus Dobutamine on inflammatory and apoptotic pathways in acutely decompensated chronic heart failure [J].