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嗜铬细胞瘤作为外周交感神经兴奋的临床模型:新老发现。

Pheochromocytoma as a Clinical Model of Peripheral Sympathetic Overdrive: Old and New Findings.

机构信息

Clinica Medica, Department of Medicine and Surgery, University of Milano-Bicocca, Via Pergolesi 33, 20052, Monza (Milan), Italy.

University of Milano-Bicocca, Milan, Italy.

出版信息

Curr Hypertens Rep. 2019 Oct 10;21(11):90. doi: 10.1007/s11906-019-0989-9.

Abstract

PURPOSE OF REVIEW

The present paper will review the results of experimental and clinical studies aimed at defining the functional behavior of the central and peripheral nervous system in adrenal pheochromocytoma.

RECENT FINDINGS

The contribution of sympathetic neural influences to the development of high blood pressure values in pheochromocytoma is complex. Studies performed in experimental animal models have shown that hypertension and the concomitant high circulating levels of catecholamines can lead to inhibition of central sympathetic neural outflow by reflex mechanisms and direct stimulation of central adrenergic receptors, respectively. However, these studies have also shown that high circulating levels of catecholamines favor a downregulation of alpha- and beta-adrenergic receptors, lessening their response to endogenous and exogenous adrenergic stimulation. The present paper reviews results of human studies performed by our group and others on the behavior of the central and peripheral nervous system in human pheochromocytoma. We discuss data collected in patients with different levels of peripheral sympathetic drive, i.e., before and after surgical removal of the adrenal pheochromocytoma. In the presence of elevated plasma catecholamine level, such as that characterizing adrenal pheochromocytoma, microneurography shows that central sympathetic neural activity is normal or even inhibited. At the peripheral vascular level, pheochromocytoma is characterized by a reduced vascular reactivity to exogenous sympathetic stimulation but a normal response by the vessels to endogenous adrenergic stimulation.

摘要

目的综述

本文将回顾旨在确定肾上腺嗜铬细胞瘤中枢和周围神经系统功能行为的实验和临床研究结果。

最新发现

交感神经影响对嗜铬细胞瘤中高血压值的发展的贡献是复杂的。在实验动物模型中进行的研究表明,高血压和随之而来的高循环儿茶酚胺水平可分别通过反射机制抑制中枢交感神经传出,并直接刺激中枢肾上腺素能受体,导致高血压。然而,这些研究还表明,高循环儿茶酚胺水平有利于 α 和 β 肾上腺素能受体的下调,从而降低其对内源性和外源性肾上腺素刺激的反应。本文回顾了我们小组和其他小组在人类嗜铬细胞瘤中中枢和周围神经系统行为方面进行的人类研究结果。我们讨论了在不同水平的外周交感神经驱动下收集的数据,即在肾上腺嗜铬细胞瘤切除前后。在血浆儿茶酚胺水平升高的情况下,如嗜铬细胞瘤的特征,微神经记录显示中枢交感神经活动正常甚至受到抑制。在外周血管水平,嗜铬细胞瘤的特征是对外源交感刺激的血管反应性降低,但对内源性肾上腺素刺激的血管反应正常。

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