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临床及实验性缺血性疼痛期间的血浆β-内啡肽

Plasma beta-endorphin during clinical and experimental ischaemic pain.

作者信息

Bach F W, Fahrenkrug J, Jensen K, Dahlstrøm G, Ekman R

机构信息

Department of Clinical Chemistry, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.

出版信息

Scand J Clin Lab Invest. 1987 Dec;47(8):751-8.

PMID:2963368
Abstract

An improved radio-immunoassay using an antiserum directed towards the N-terminal part of the endogenous opioid peptide beta-endorphin 1-31 (beta-EP) was validated and applied to a study of beta-EP in plasma during ischaemic pain. Experimental ischaemic pain induced in seven healthy volunteers by the submaximal effort tourniquet test did not change plasma beta-EP or adrenocorticotrophin. Plasma beta-EP was determined in 21 patients with acute myocardial infarction (AMI) and in seven patients with unstable angina pectoris. Plasma beta-EP was 4.9 fmol/ml with 95% confidence limits, 3.2-7.8 fmol/ml in AMI patients at admittance, and 2.9 (2.0-3.4) fmol/ml one week later in stable and pain-free condition (p less than 0.05). The level in 49 healthy persons was 2.8 (2.4-2.9) fmol/ml. Elevated beta-EP levels were found in five AMI patients with cardiogenic shock and in four AMI patients dying within 24 h after admittance compared to the rest of AMI patients (p less than 0.02). beta-EP was not elevated during unstable angina pectoris, although pain scores were similar to AMI. The AMI group revealed a significant, although weak, positive correlation between plasma beta-EP and pain score (Spearman r = 0.49, p less than 0.05), while there was no correlation during unstable angina pectoris. beta-EP was not correlated to the amount of morphine required within the 48 h after admittance of AMI patients. We conclude that the increase of beta-EP in plasma during AMI may be due to stressful factors other than ischaemic pain and that it is questionable whether beta-EP in plasma is related to antinociception.

摘要

一种改进的放射免疫分析方法得以验证,该方法使用针对内源性阿片肽β-内啡肽1 - 31(β-EP)N端部分的抗血清,并应用于缺血性疼痛期间血浆中β-EP的研究。通过次最大强度的止血带试验在7名健康志愿者中诱发的实验性缺血性疼痛,并未改变血浆β-EP或促肾上腺皮质激素水平。对21例急性心肌梗死(AMI)患者和7例不稳定型心绞痛患者的血浆β-EP进行了测定。AMI患者入院时血浆β-EP为4.9 fmol/ml,95%置信区间为3.2 - 7.8 fmol/ml,一周后在病情稳定且无痛状态下为2.9(2.0 - 3.4)fmol/ml(p < 0.05)。49名健康人的血浆β-EP水平为2.8(2.4 - 2.9)fmol/ml。与其余AMI患者相比,5例发生心源性休克的AMI患者及4例入院后24小时内死亡的AMI患者血浆β-EP水平升高(p < 0.02)。不稳定型心绞痛期间,尽管疼痛评分与AMI相似,但β-EP并未升高。AMI组血浆β-EP与疼痛评分之间存在显著但较弱的正相关(Spearman相关系数r = 0.49,p < 0.05),而不稳定型心绞痛期间则无相关性。β-EP与AMI患者入院后48小时内所需吗啡量无关。我们得出结论,AMI期间血浆β-EP升高可能是由于缺血性疼痛以外的应激因素所致,血浆β-EP是否与抗伤害感受相关尚存在疑问。

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