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短暂性心肌缺血刺激心房利钠因子释放。

Transient myocardial ischemia stimulates atrial natriuretic factor release.

作者信息

Malatino L S, Leonardi C, Stancanelli B, Polizzi G, Grassi R, Tamburino C, Tamburino G

机构信息

Istituto di Clinica Medica Luigi Condorelli, University of Catania, Italy.

出版信息

Am Heart J. 1992 Mar;123(3):693-8. doi: 10.1016/0002-8703(92)90508-s.

DOI:10.1016/0002-8703(92)90508-s
PMID:1531723
Abstract

Atrial natriuretic factor release during transient myocardial ischemia was investigated in 29 patients with coronary artery disease and symptoms of angina (Canadian Cardiovascular Association classes II-III). Eleven patients (group I) underwent single-vessel percutaneous transluminal coronary angioplasty. Repeat determinations of mean pulmonary artery wedge pressure and blood sampling from pulmonary artery for atrial natriuretic factor measurements were performed at baseline, and at 2, 5, and 15 minutes after percutaneous transluminal coronary angioplasty was begun. Baseline atrial natriuretic factor levels (34.6 +/- 4.5 pg/ml) rose to 56.3 +/- 7.3 pg/ml (p = 0.02) and decreased at 5 minutes (43.7 +/- 5.7 pg/ml, not significant) and 15 minutes (35.3 +/- 4.4 pg/ml, not significant). Changes in atrial natriuretic factor concentrations were significantly correlated with those in mean pulmonary artery wedge pressure (2 minutes: r = 0.69, p = 0.02; 5 minutes: r = 0.90, p less than 0.001). In group II (n = 10) the increase in atrial natriuretic factor after dye load occurred later (baseline: 25.8 +/- 2.1; 60 minutes: 40.6 +/- 2.6 pg/ml; p = 0.005) than that observed in group I after percutaneous transluminal coronary angioplasty. In group III, atrial natriuretic factor during angina rose as early (baseline 11.3 +/- 1.3; 5 minutes: 20 +/- 2.3 pg/ml; p = 0.006) as after percutaneous transluminal coronary angioplasty. Results indicate that transient myocardial ischemia stimulates atrial natriuretic factor release, probably through changes in cardiac function.

摘要

对29例患有冠状动脉疾病且有心绞痛症状(加拿大心血管协会II - III级)的患者,研究了短暂性心肌缺血期间心房利钠因子的释放情况。11例患者(第一组)接受了单支血管经皮腔内冠状动脉成形术。在基线时以及开始经皮腔内冠状动脉成形术后2、5和15分钟,重复测定平均肺动脉楔压,并从肺动脉采血以测量心房利钠因子。基线时心房利钠因子水平(34.6±4.5 pg/ml)升至56.3±7.3 pg/ml(p = 0.02),并在5分钟时下降(43.7±5.7 pg/ml,无显著差异),在15分钟时降至35.3±4.4 pg/ml(无显著差异)。心房利钠因子浓度的变化与平均肺动脉楔压的变化显著相关(2分钟:r = 0.69,p = 0.02;5分钟:r = 0.90,p<0.001)。在第二组(n = 10)中,染料负荷后心房利钠因子的升高出现得比第一组经皮腔内冠状动脉成形术后晚(基线:25.8±2.1;60分钟:40.6±2.6 pg/ml;p = 0.005)。在第三组中,心绞痛期间心房利钠因子升高的时间与经皮腔内冠状动脉成形术后一样早(基线11.3±1.3;5分钟:20±2.3 pg/ml;p = 0.006)。结果表明,短暂性心肌缺血可能通过心脏功能的改变刺激心房利钠因子的释放。

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Transient myocardial ischemia stimulates atrial natriuretic factor release.短暂性心肌缺血刺激心房利钠因子释放。
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