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Irreversible shock of rats after acute renal vein thrombosis
Authors:Michael Steinhausen  Frederick D. Dallenbach  Rudolf Jäckh  Niranjan Parekh  Bernd Zimmerhackl  Rainer Zimmermann
Affiliation:(1) I. Physiologisches Institut der Universität Heidelberg, Im Neuenheimer Feld 326, D-6900 Heidelberg, Federal Republic of Germany;(2) Institut f. Experimentelle Pathologie, DKFZ, Heidelberg;(3) Medizinische Universitätsklinik, Heidelberg
Abstract:
Summary After occlusion of the renal veins rats die quickly in progressive shock (within 4.5 h), but after ligating the renal hilum of both Kidneys they survive 27 h. To learn why renal vein occlusion is so rapidly lethal, and what substances are given off and by what method from the hemorrhagically infarcted kidneys, we studied eight groups of rats, each containing at least seven animals. The groups differed in the combination of hilar structures (renal veins, ureters, lymphatics) ligated. We compared: survival times, changes in blood pressure, blood volume, levels of plasma kinins, adenosine, and lactate, changes of blood pH, responses to Indomethacin, Trasylol®, and plasma expanders, tubular and capillary flow rates, histopathological changes in organs and cerebral blood flow and changes in the blood coagulation system. Our results suggest that the venous stasis, anoxia, and hemorrhagic necrosis caused by bilateral venous occlusion release into renal lymphatics toxic substances which reach the systemic circulation and induce irreversible shock. We have excluded prostaglandins and adenosine as the toxic substances inducing shock but could not rule out an action of the kallikrein-kinin-system. We postulate that the striking degenerative changes occurring in the arterioles of the brain after bilateral venous occlusion may mean these vessels are especially susceptible to high levels of lactic acid and that this may explain why these animals die so quickly. Our conclusions should help not only in understanding why high levels of lactate in shock portend a poor prognosis but also help in formulating appropriate therapy for circulatory failure of renal origin and for protracted hypotension after extensive tissue injury.The studies were supported by the German Research Foundation within the SFB 90 lsquoCardiovasculäres SystemrsquoPresented in part: Jäckh and Steinhausen, 1976; Dallenbach et al., 1978; Zimmerhackl et al., 1979We dedicate this paper to Wilhelm Doerr, Dr. med., Professor of Pathology, University of Heidelberg on the occasion of his 65th birthday (August 25th, 1979)
Keywords:Rat kidney  Renal vein occlusion  Prostaglandins  Kallikreins  Renal microcirculation  Renal lymphflow  Lactate acidosis
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