Suppr超能文献

弗朗茨·福尔哈德和西奥多·法尔:他们在肾脏疾病和高血压研究中的成就与争议

Franz Volhard and Theodor Fahr: achievements and controversies in their research in renal disease and hypertension.

作者信息

Heidland A, Gerabek W, Sebekova K

机构信息

Department of Internal Medicine, University of Wuerzburg, Germany.

出版信息

J Hum Hypertens. 2001 Jan;15(1):5-16. doi: 10.1038/sj.jhh.1001130.

Abstract

The clinician, Franz Volhard, and the pathologist, Theodor Fahr, worked closely together in Mannheim from 1909 until 1915 and introduced a novel classification of renal diseases. In the monograph entitled 'Die Bright'sche Nierenkrankheit, Klinik, Pathologie und Atlas' (1914) they differentiated between degenerative (nephroses), inflammatory (nephritides) and arteriosclerotic (scleroses) diseases. Nephrosclerosis was divided into the benign and malignant form, of which the latter stood the test of time as a new disease entity. Fahr further divided benign nephrosclerosis into the compensated and decompensated form--depending on the presence or absence of glomerular injury. In the pathogenesis of malignant nephrosclerosis, Volhard stressed the decisive role of severe blood pressure elevation, while Fahr postulated an inflammatory mechanism, a concept later confirmed by Adalbert Bohle for at least a minority of patients. A very far reaching concept of Franz Volhard was his idea that pale (renal) hypertension results from a pressor substance released from ischaemic kidney(s) contributing--via a vicious circle--to a further rise in blood pressure with subsequent renovascular injury and aggravation of hypertension. This hypothesis was supported in 1930 by initial experiments of his collaborator, Hartwich (demonstrating in dogs a mild rise in blood pressure after ligation of branches of the renal artery) and definitively proven by Goldblatt (1934) in dogs by induction of severe and persistent hypertension after clamping of both renal arteries. The consequent detection of the renin angiotensin system was the final confirmation of Volhard's postulated renal pressor substance. In the pathogenesis of red (essential) hypertension, Volhard stressed the role of hereditary factors, age, obesity and potentially of severe alcoholism. He emphasised a premature reduction of vascular distensibility (due to elastosis of the prearterioles), a high cardiac output as well as a dampening of baroceptor function. Additionally, Volhard made crucial advances in cardiology and pneumology. Journal of Human Hypertension (2001) 15, 5-16

摘要

临床医生弗朗茨·福尔哈德(Franz Volhard)和病理学家西奥多·法尔(Theodor Fahr)于1909年至1915年在曼海姆密切合作,引入了一种新的肾脏疾病分类方法。在1914年出版的名为《布赖特氏肾病:临床、病理及图谱》(Die Bright'sche Nierenkrankheit, Klinik, Pathologie und Atlas)的专著中,他们区分了退行性(肾病)、炎症性(肾炎)和动脉硬化性(硬化症)疾病。肾硬化被分为良性和恶性两种形式,其中后者作为一种新的疾病实体经受住了时间的考验。法尔进一步将良性肾硬化分为代偿性和失代偿性两种形式,这取决于肾小球损伤的有无。在恶性肾硬化的发病机制中,福尔哈德强调了严重血压升高的决定性作用,而法尔则假定存在一种炎症机制,这一概念后来至少在少数患者中被阿达尔贝特·博勒(Adalbert Bohle)证实。弗朗茨·福尔哈德一个极具深远意义的观点是,苍白(肾性)高血压是由缺血性肾脏释放的一种升压物质引起的,这种物质通过恶性循环导致血压进一步升高,随后引起肾血管损伤和高血压加重。1930年,他的合作者哈特里希(Hartwich)的初步实验支持了这一假设(在狗身上结扎肾动脉分支后血压出现轻度升高),1934年戈德布拉特(Goldblatt)通过钳夹狗的双侧肾动脉诱导出严重且持续的高血压,最终证实了这一假设。随后肾素 - 血管紧张素系统的发现最终证实了福尔哈德所假定的肾脏升压物质。在红色(原发性)高血压的发病机制中,福尔哈德强调了遗传因素、年龄、肥胖以及可能的严重酗酒的作用。他强调血管扩张性过早降低(由于小动脉前弹力组织变性)、高心输出量以及压力感受器功能减弱。此外,福尔哈德在心脏病学和肺病学方面也取得了关键进展。《人类高血压杂志》(2001年)15卷,5 - 16页

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验