Secretion of prohormone of B-type natriuretic peptide, proBNP1-108, is increased in heart failure.
Secretion of prohormone of B-type natriuretic peptide, proBNP1-108, is increased in heart failure.
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DOI：
10.1016/j.jchf.2013.03.001
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发表时间：
2013-06
期刊：
影响因子：
--
通讯作者：
Burnett JC Jr
中科院分区：
文献类型：
--
作者：
Costello-Boerrigter LC;Lapp H;Boerrigter G;Lerman A;Bufe A;Macheret F;Heublein DM;Larue C;Burnett JC Jr
我们使用一种新的proBNP 1 -108特异性检测方法，检验了proBNP 1 -108由非衰竭和衰竭的人类心脏分泌以及proBNP 1 -108分泌在衰竭心脏中增加的假设。B型利钠肽的激素原（proBNP 1 -108）是一种108个氨基酸的肽，主要由心脏产生，并裂解成生物活性BNP 1 -32和生物无活性NT-proBNP 1 -76。尚不清楚心脏proBNP 1 -108分泌的增加与外周加工的减少相比在多大程度上导致心力衰竭（HF）患者中proBNP 1 -108水平与无HF的受试者相比升高。通过收集动脉血和冠状窦（CS）血液测定proBNP 1 -108的经心梯度。排除冠状动脉疾病后，在心导管插入术期间采集无明显心脏病受试者（n=9）的样本。在植入双心室起搏器期间采集HF患者（n=21）的样本。ProBNP 1 -108用新的测定法（BioRad）测量。数值为中位数（第25/75百分位数）。proBNP 1 -108跨非衰竭心脏的梯度为8（2/20）ng/L（主动脉：15（1/25）ng/dL，CS：24（8/41）ng/dL; p=0.018）。衰竭心脏中proBNP 1 -108的经心梯度为326（96/482）ng/dL（动脉：381（201/586）ng/dL，CS：709（408/1087）ng/dL; p<0.001）。衰竭心脏的跨心梯度大于非衰竭心脏（p=0.001）。ProBNP 1 -108由非衰竭和衰竭的人类心脏分泌，但在后者中更多。proBNP 1 -108的外周加工发生在何处以及如何受到疾病的影响仍有待确定。
Using a novel, specific assay for proBNP1–108 we tested the hypotheses that proBNP1–108 is secreted by both non-failing and failing human hearts and that proBNP1–108 secretion is increased in failing hearts. The prohormone of B-type natriuretic peptide (proBNP1–108) is a 108-amino acid peptide produced primarily by the heart and cleaved into biologically active BNP1–32 and the biologically inactive NT-proBNP1–76. It is unknown to what extent increased cardiac proBNP1–108 secretion as compared to reduced peripheral processing is responsible for elevated proBNP1–108 levels in patients with heart failure (HF) as compared to subjects without HF. The transcardiac gradient of proBNP1–108 was determined by collecting arterial blood and blood from the coronary sinus (CS). Samples from subjects without overt heart disease (n=9) were collected during cardiac catheterization after coronary artery disease had been excluded. Samples from HF patients (n=21) were collected during implantation of a biventricular pacemaker. ProBNP1–108 was measured with a new assay (BioRad). Values are median (25th/75th percentile). The gradient of proBNP1–108 across the non-failing hearts was 8 (2/20) ng/L (aorta: 15 (1/25) ng/dL, CS: 24 (8/41) ng/dL; p=0.018). The transcardiac gradient of proBNP1–108 in the failing hearts was 326 (96/482) ng/dL (arterial: 381 (201/586) ng/dL, CS: 709 (408/1087) ng/dL; p<0.001). The transcardiac gradient was greater in failing than non-failing hearts (p=0.001). ProBNP1–108 is secreted by non-failing and failing human hearts, but more so in the latter. It remains to be established where peripheral processing of proBNP1–108 occurs and how this is affected by disease.
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作者：
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影响因子：
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