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急性乙醇摄入后的心肌脂肪酸代谢

Myocardial fatty acid metabolism after acute ethanol consumption.

作者信息

Höck A, Notohamiprodjo G, Spohr G, Kaiser K P, Freundlieb C, Vyska K, Shreeve W W, Schweitzer H, Feinendegen L E

出版信息

Nucl Med Commun. 1986 Sep;7(9):671-82.

PMID:3774262
Abstract

This study was undertaken to assess the effect of ethanol ingestion on myocardial fatty acid metabolism in man. Nine individuals with informed consent and with a habitual ethanol consumption of approximately 40 g per day, but without any clinical signs of heart and metabolic disease, were examined after i.v. injection of omega-123I-heptadecanoic acid (IHA). Eight days later, these individuals were similarly examined after 2 h of continuous ingestion of a body weight dependent amount of ethanol, which was calculated to produce a blood level of 100 mg per 100 ml (1%). Then the subjects had been asked to reduce their ethanol consumption rigorously for 15 months. Subsequently after 2 weeks of abstinence a follow-up investigation without ethanol loading was carried out. The investigations were performed with an Anger scintillation camera in LAO-45 degrees projection. The measurement period was 40 min. Tracer accumulation and regional elimination half-times of IHA were analysed. In all patients, acute ethanol loading produced significant changes in pattern of accumulation and/or regional elimination half-times. Ethanol-induced alterations in segmental accumulation did not appear to be predictably correlated with changes in segmental elimination half-times. After rigorous reduction of ethanol consumption followed by 2 weeks of abstinence a normalization of the tracer uptake was observed; the distribution pattern was almost homogeneous. Also the regional elimination half-times became normal. The data demonstrate the significant effects of both chronic ethanol consumption and particularly acute ethanol loading on myocardial fatty acid metabolism and the reversibility of the effects.

摘要

本研究旨在评估摄入乙醇对人体心肌脂肪酸代谢的影响。九名个体在签署知情同意书后参与了研究,他们有每日摄入约40克乙醇的习惯,但无任何心脏和代谢疾病的临床症状。在静脉注射ω-123I-十七烷酸(IHA)后对他们进行了检查。八天后,在这些个体连续2小时摄入依体重而定的乙醇量(经计算可使血液浓度达到每100毫升100毫克(1%))后,同样对其进行了检查。然后要求受试者严格减少乙醇摄入量,持续15个月。随后,在戒酒2周后进行了一次无乙醇负荷的随访调查。使用安格闪烁相机在左前斜45度投影下进行检查。测量期为40分钟。分析了IHA的示踪剂蓄积和区域消除半衰期。在所有患者中,急性乙醇负荷导致蓄积模式和/或区域消除半衰期出现显著变化。乙醇引起的节段性蓄积改变似乎与节段性消除半衰期的变化没有可预测的相关性。在严格减少乙醇摄入量并戒酒2周后,观察到示踪剂摄取恢复正常;分布模式几乎均匀。区域消除半衰期也恢复正常。数据表明,长期摄入乙醇,尤其是急性乙醇负荷,对心肌脂肪酸代谢有显著影响,且这些影响具有可逆性。

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