Summary. Serial measurements of intrarenal distribution of blood flow have been recorded in anesthetized dogs with the 133xenon "washout" technique. The results showed that normal kidneys redistributed their blood flow after laparotomy and mobilization of the kidney. This alteration consisted of a diminution in percentage of total renal blood flow supplied to the fastest flowing component, and a diminution of renal mass supplied by that component. This effect lasted for as long as 7 days. Thereafter, the blood flow distribution remained stable.Autotransplanted kidneys had a stable distribution of blood flow between 0 and 77 days after operation, the values being identical with the stable normal kidney. Homotransplanted kidneys had the same intrarenal distribution of blood flow after operation as the autotransplanted kidneys. Whereas the intrarenal distribution of blood flow of the autotransplanted kidneys remained stable, a redistribution occurred in the homotransplanted kidneys as rejection progressed.. This phenomenon occurred before marked elevation of blood urea nitrogen.The redistribution was due to a decrease in percentage of blood flow supplied to the fastest flowing component, and a relative reduction of tissue mass perfused by this component.Radioautography of the kidneys before rejection demonstrated that the cortex was homogeneously perfused by the fastest flowing component of blood flow. As rejection progressed, a reduced area of cortex was perfused by this component. Terminally, the fastest flowing component was located in the outer medulla.It is suggested that the reduction in cortical blood flow produced by immunological mechanisms may play a prominent role in the ensuing renal failure. IntroductionAnatomical changes in the intrarenal vasculature are a prominent feature in the homotransplated *

Haemorrhagic hypotension (HH) causes a redistribution of intrarenal blood flow characterized by a patchy cortical hypoperfusion. Previous studies indicated that the sYmpathoadrenergic system is mainly responsible for these redistribution processes. The relative role of renal nerves and of circulating catecholamines was studied in the present experiments. Intrarenal haemodynamics were analysed by means of the Xenon washout technique and Krypton autoradiographics. 8 autotransplanted (and, therefore, chronically denervated) kidneys showed the same typical response to severe and prolonged HH as 11 normal control organs. In 2 additional dogs, the intrarenal distribution of blood flow (IDBF) and local blood flow rates (F ) of an acutely denervated kidney before and during HH did not show any differences as compared with the contralateral control organ. It is concluded that the patchy cortical hypoperfusion observed in the dog during severe haemorrhagic hypotension does not depend on an intact innervation of the kidney, but that it is mainly mediated by circulating catecholamines.

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Untersuchungen der intrarenalen Hämodynamik an normalen (nicht-transplantierten), autotransplantierten und homotransplantierten Hundenieren zeigten folgende Resultate: 1. Transplantation per se führt trotz der eingreifenden Veränderungen der Innervation, des Lymphabflusses und der Blutversorgung der Niere nicht zu einer Veränderung der intrarenalen Blutverteilung, noch der lokalen Durchfluβraten. 2. Ausgelöst durch die auf der genetischen Verschiedenheit von Spender und Empfänger beruhenden immunpathologischen Prozesse entwickeln sich als früheste Zeichen der Abstoβung fleckige, subcapsuläre, langsam sich ausbreitende Ischämiezonen, die schlieβlich zu einem völligen hämodynamischen Ausfall der Nierenrinde und damit zum Funktionsverlust des Transplantates führen. Die Abstoβung des Nierenhomotransplantates kann damit als fortschreitende Infarzierung vor allem der Nierenrinde charakterisiert werden. Die Beziehungen dieser Beobachtungen zu den immunologischen Grundprozessen werden diskutiert.