节段性动脉中膜溶解:单用去甲肾上腺素和高密度肾上腺素或与其他压力药物串扰引起的伴侧系膜细胞增生和心脏毒性的多形性血管痉挛动脉病变。

IF 2.5 Q2 PERIPHERAL VASCULAR DISEASE
International Journal of Vascular Medicine Pub Date : 2021-11-23 eCollection Date: 2021-01-01 DOI:10.1155/2021/2046566
Richard E Slavin
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引用次数: 3

摘要

节段性动脉介质溶解(SAM)是一种罕见的血管痉挛性动脉病,发生在由外周交感神经系统支配的肌肉动脉中,通常表现为老年患者腹部和腹膜后出血。SAM是由去甲肾上腺素与动脉肌膜上α -1肾上腺素能受体的塑性衍生的高密度灶偶联引起的。这种配体是由医源性拟交感神经激动剂、某些β -2激动剂或肾上腺儿茶酚胺过度释放的刺激信号产生的。这种配体与细胞质异三聚体Gq蛋白的偶联过度地发出了一系列生化事件的信号,产生了两种主要的损伤期sam损伤——外膜剪切和细胞质钙离子过载,对线粒体有毒,导致介质溶解和/或凋亡。大出血是由内侧肌肉的损失造成的间隙动脉瘤破裂引起的。去甲肾上腺素导向的修复反应迅速发展,要么解决血管造影损伤病变,要么产生血管疾病,这是具有缺血性临床特征的SAM的新形式。常见于心外膜动脉、椎动脉、肠动脉和腹膜后动脉,常见于年轻女性,表现为纤维肌肉发育不良、解剖性血肿和持续性动脉瘤。去甲肾上腺素可与其他降压药物相互作用产生SAM损伤——5 -羟色胺与特发性肺动脉高压和新生儿持续性肺动脉高压有关,组胺与自发性冠状动脉夹层伴嗜酸性粒细胞增多有关,内皮素-1与SAM产生的场效应有关,可造成静脉纤维肌肉发育不良。在心率明显升高的受试者中,去甲肾上腺素也参与系膜增生伴局灶节段性肾小球硬化、心肌介质溶解和细胞凋亡的侧枝发展。结论。去甲肾上腺素与可塑性升高的α -1肾上腺素受体或其他加压剂偶联产生SAM,这是一种组织学上可识别的血管痉挛性动脉疾病,随着修复,SAM转变为几种不同的标准化动脉疾病,将SAM的临床特征从出血性疾病转变为缺血性疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Segmental Arterial Mediolysis: A Multiguised Vasospastic Arteriopathy with Collateral Mesangial Cell Hyperplasia and Cardiac Toxicity Generated by Norepinephrine and Hyperdense Adrenoceptors Alone or by Crosstalk with Other Pressor Agents.

Segmental Arterial Mediolysis: A Multiguised Vasospastic Arteriopathy with Collateral Mesangial Cell Hyperplasia and Cardiac Toxicity Generated by Norepinephrine and Hyperdense Adrenoceptors Alone or by Crosstalk with Other Pressor Agents.

Segmental Arterial Mediolysis: A Multiguised Vasospastic Arteriopathy with Collateral Mesangial Cell Hyperplasia and Cardiac Toxicity Generated by Norepinephrine and Hyperdense Adrenoceptors Alone or by Crosstalk with Other Pressor Agents.

Segmental Arterial Mediolysis: A Multiguised Vasospastic Arteriopathy with Collateral Mesangial Cell Hyperplasia and Cardiac Toxicity Generated by Norepinephrine and Hyperdense Adrenoceptors Alone or by Crosstalk with Other Pressor Agents.

Segmental arterial mediolysis (SAM), an uncommon vasospastic arteriopathy occurring in the muscular arteries innervated by the peripheral sympathetic nervous system, usually presents with catastrophic abdominal and retroperitoneal hemorrhages in elderly patients. SAM is initiated by the coupling of norepinephrine to plastically derived hyperdense foci of alpha-1 adrenergic receptors on the sarcolemma of arterial muscle. This ligand is created by stimuli signaled by iatrogenic sympathomimetic agonists, some beta-2 agonists, or an excessive release of adrenal catecholamines. Coupling of this ligand with cytoplasmic heterotrimeric Gq protein excessively signals a cascade of biochemical events generating two principal lesions of injurious-phase SAM-the shearing of the outer media from the adventitia and an overload of cytoplasmic calcium ions toxic to mitochondria causing mediolysis and/or apoptosis. The massive hemorrhages are caused by ruptured gap aneurysms created by the transmedial loss of the medial muscle. A norepinephrine-directed reparative response rapidly develops either resolving angiographic injurious lesions or creating a body of vascular disorders, the new guises of SAM with ischemic clinical profiles. These present in the epicardial, vertebral, intestinal, and retroperitoneal arteries, often in younger females as fibromuscular dysplasia, dissecting hematomas, and persistent aneurysms. Norepinephrine can crosstalk with other pressor agents to create SAM lesions-serotonin with idiopathic pulmonary hypertension and persistent pulmonary hypertension in the newborn, histamine in spontaneous coronary artery dissections with eosinophilia, and endothelin-1 in a field effect generated by SAM that creates venous fibromuscular dysplasia. Norepinephrine also participates in the collateral development of mesangial hyperplasia with focal segmental glomerulosclerosis and myocardial mediolysis and apoptosis in subjects with markedly elevated heart rates. Conclusion. Norepinephrine coupling with plastically elevated alpha-1 adrenoceptor or other pressor agents generates SAM, a histologically recognizable vasospastic arteriopathy, that with repair is transformed into several different standardized arterial diseases that alter SAM's clinical profile from a hemorrhagic to an ischemic disorder.

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来源期刊
International Journal of Vascular Medicine
International Journal of Vascular Medicine PERIPHERAL VASCULAR DISEASE-
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