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急性心肌梗死时血浆儿茶酚胺水平:β-肾上腺素能阻滞剂的影响及其与中心血流动力学的关系

Plasma catecholamine levels in acute myocardial infarction: influence of beta-adrenergic blockade and relation to central hemodynamics.

作者信息

Murray D P, Watson R D, Zezulka A V, Murray R G, Littler W A

机构信息

Department of Cardiovascular Medicine, University of Birmingham, East Birmingham Hospital, England.

出版信息

Am Heart J. 1988 Jan;115(1 Pt 1):38-44. doi: 10.1016/0002-8703(88)90515-7.

DOI:10.1016/0002-8703(88)90515-7
PMID:3336984
Abstract

In a prospective study, 20 patients with acute myocardial infarction were randomly assigned in a double-blind fashion to treatment with intravenous metoprolol followed by oral metoprolol or placebo. All patients underwent hemodynamic monitoring for 24 hours. Plasma adrenaline and noradrenalin levels were estimated at baseline (mean 6.0 +/- 0.9 hours from onset of symptoms) and at 1 and 24 hours after the start of therapy. Plasma adrenaline and noradrenalin levels were elevated in all but one patient, with a further increase at 1 hour after administration of metoprolol (p less than 0.05). At baseline pulmonary capillary wedge pressure was directly related to both plasma adrenaline (r = -0.44; p less than 0.05) and noradrenalin levels (r = -0.44; p less than 0.05). There was also an inverse relationship between stroke volume index and the plasma noradrenalin level (r = -0.44; p less than 0.05) but not the plasma adrenaline level. These relationships were lost after the baseline measurements. However, between baseline and 1 hour there was a close relationship between the change in systemic vascular resistance and the changes in both adrenaline (r = -0.48; p less than 0.05) and noradrenalin levels (r = -0.66; p less than 0.01). Thus, in the early stages of myocardial infarction high plasma catecholamine levels are associated with the hemodynamic markers of severe left ventricular damage. Beta-adrenergic blockade with metoprolol produced a further increase in catecholamine levels that was associated with an increase in systemic vascular resistance.

摘要

在一项前瞻性研究中,20例急性心肌梗死患者被随机双盲分配接受静脉注射美托洛尔随后口服美托洛尔或安慰剂治疗。所有患者均接受24小时血流动力学监测。在基线时(症状发作后平均6.0±0.9小时)以及治疗开始后1小时和24小时测定血浆肾上腺素和去甲肾上腺素水平。除1例患者外,所有患者的血浆肾上腺素和去甲肾上腺素水平均升高,在给予美托洛尔后1小时进一步升高(p<0.05)。基线时肺毛细血管楔压与血浆肾上腺素(r=-0.44;p<0.05)和去甲肾上腺素水平(r=-0.44;p<0.05)均直接相关。每搏量指数与血浆去甲肾上腺素水平之间也存在负相关(r=-0.44;p<0.05),但与血浆肾上腺素水平无关。这些关系在基线测量后消失。然而,在基线和1小时之间,全身血管阻力的变化与肾上腺素(r=-0.48;p<0.05)和去甲肾上腺素水平的变化(r=-0.66;p<0.01)均密切相关。因此,在心肌梗死的早期阶段,高血浆儿茶酚胺水平与严重左心室损害的血流动力学指标相关。美托洛尔的β肾上腺素能阻滞使儿茶酚胺水平进一步升高,这与全身血管阻力增加有关。

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