Timio M
Dipartimento di Medicina Interna, Nefrologia e Dialisi, Ospedale San Giovanni Battista, Foligno (PG), Italy.
G Ital Nefrol. 2003 Sep-Oct;20(5):512-5.
The existence of a clear relationship between renal ischemia and hypertension has been widely documented by Harry Goldblatt and his colleagues. In their original papers they showed that gross and persistent elevation of systolic blood pressure could be produced in dogs by clamping both renal artery, or one if the other kidney had been removed. If renal arteries constriction was not too severe, a stable hypertension unaccompanied by more than mild renal impairment was produced. Subsequently, Goldblatt showed that, with severe constriction, retinal changes, arteriolar impairment and left ventricular hypertension could occur. Goldblatt has remained steadily of the opinion that essential hypertension in man is similarly due to renal ischemia occasioned either by stenosis of a main artery, or by organic changes in the smaller renal arteries down to the size of the different glomerular arteries. At first sight, it might seem like a simple matter to correctly identify the chain of events that begins with renal artery constriction and ends with persistent hypertension. Observing that a link was missing in this chain of events, Goldblatt hypothesised that the link was a humoral mechanism. Tigersted and Bergman showed that renin was the missing link. Renal ischemia as cause of hypertension in dogs opened a new chapter in the connection between kidney circulation and blood pressure elevation. This quite unexpected connection is one of the most challenging issues today and clearly demonstrates that the development of Goldblatt's ideas on renal circulation is still important and has by no means ended. Goldblatt, in his epistemologic approach to hypertension scientific challenges, realised that ideas are the building blocks of science: not flights of fancy, not notions sculpted in snow, but enduring concepts. Goldblatt's lasting ideas are more than a function of time and place: they have inherent qualities that have survived up to the present day.
哈里·戈德布拉特及其同事已广泛证明肾缺血与高血压之间存在明确关联。在他们最初的论文中,他们表明通过钳夹双侧肾动脉,或者在切除另一侧肾脏的情况下钳夹一侧肾动脉,可使犬的收缩压显著且持续升高。如果肾动脉收缩不太严重,会产生稳定的高血压,且仅伴有轻度肾功能损害。随后,戈德布拉特表明,在严重收缩时,会出现视网膜变化、小动脉损害和左心室高血压。戈德布拉特一直坚定地认为,人类原发性高血压同样是由于主肾动脉狭窄或直至不同肾小球动脉大小的较小肾动脉发生器质性改变所导致的肾缺血引起的。乍一看,正确识别从肾动脉收缩开始并以持续性高血压结束的一系列事件似乎是一件简单的事情。戈德布拉特观察到这一系列事件中缺少一个环节,于是他推测这个环节是一种体液机制。蒂格斯泰德和伯格曼表明肾素就是这个缺失的环节。肾缺血作为犬高血压的病因,为肾循环与血压升高之间的联系开启了新的篇章。这种相当意外的联系是当今最具挑战性的问题之一,清楚地表明戈德布拉特关于肾循环的观点的发展仍然很重要,而且远未结束。戈德布拉特在其对高血压科学挑战的认识论方法中,意识到观念是科学的基石:不是幻想,不是雪雕般的概念,而是持久的概念。戈德布拉特的持久观念不仅仅是时间和地点的函数:它们具有一直存续至今的内在品质。