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偏头痛发作时的间歇性内啡肽血症不足

Intermittent hypoendorphinaemia in migraine attack.

作者信息

Baldi E, Salmon S, Anselmi B, Spillantini M G, Cappelli G, Brocchi A, Sicuteri F

出版信息

Cephalalgia. 1982 Jun;2(2):77-81. doi: 10.1046/j.1468-2982.1982.0202077.x.

Abstract

Beta-endorphin (RIA method, previous chromatographic extraction) was evaluated in plasma of migraine sufferers in free periods and during attacks. Decreased levels of the endogenous opioid peptide were found in plasma sampled during the attacks but not in free periods. Even chronic headache sufferers exhibited significantly lowered levels of beta-endorphin, when compared with control subjects with a negative personal and family history of head pains. The mechanism of the hypoendorphinaemia is unknown: lowered levels of the neuropeptide, which controls nociception, vegetative functions and hedonia, could be important in a syndrome such as migraine, characterized by pain, dysautonomia and anhedonia. The impairment of monoaminergic synapses ("empty neuron" condition) constantly present in sufferers from serious headaches, could be due to the fact that opioid neuropeptides, because of a receptoral or metabolic impairment, poorly modulate the respective monoaminergic neurons, resulting in imbalance of synaptic neurotransmission.

摘要

采用放射免疫分析法(之前经过色谱提取)对偏头痛患者在缓解期和发作期的血浆中的β-内啡肽进行了评估。在发作期采集的血浆中发现内源性阿片肽水平降低,但在缓解期未发现这种情况。与无个人及家族头痛病史的对照受试者相比,即使是慢性头痛患者的β-内啡肽水平也显著降低。内啡肽血症水平降低的机制尚不清楚:这种控制伤害感受、自主功能和快感的神经肽水平降低,在偏头痛这样一种以疼痛、自主神经功能障碍和快感缺失为特征的综合征中可能具有重要意义。严重头痛患者中持续存在的单胺能突触损伤(“空神经元”状态),可能是由于阿片类神经肽因受体或代谢损伤,对各自的单胺能神经元调节不佳,导致突触神经传递失衡。

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