腎虚血, 腎鬱血, アノキシアにおける腎循環と代謝, 特に蛋白尿に関する実験的研究
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To clarify the effects of acute renal ischemia, congestion and anoxic anoxia on renel hemodynamics and metabolism, renal catheterization was carried out in 32 dogs, composed of 12 cases of ischemia, 14 cases of congestion and 6 cases of anoxic anoxia. Renal ischemia was produced by clamping of A. renalis, renal congestion by clamping of V. re-nalis and anoixia by inhalation of N2 gas. Under these conditions, renal oxygen and glucose consumption Na and K excretion, renal PAH extraction (EPAH), RBF, GFR, FF and urine volume were determined, and further the relation between occurence of proteinuria and changes of renal hemodynamics was investigated. The results obtained were as follows.The decrease of RBF caused increase of renal arterio-venous O2 difference (ΔO2) and fall of tubular reabsorption rate of Na (RNa), and when RBF decreased unde 30% of control value, EPAH showed to fall and FF to rise. Severe decrease of GFR caused oliguria. Following progressive elevation of renal venous pressure (RVP), RBF showed to decrease, FF to rise, ΔO2 to increase and RNa to fall.RBF, GFR, urine volume and CNa showed no change or slight increase in mild anoxic anoxia, they decreased, however, in severe anoxia.Renal O2 consnmption was observed to be maintained normal unless RBF decreased under 30% of control value or below, because renal ΔO2 rised compensationally as renal O2 supply decreased.No relation was found between renal glucose supply and consumption, and no difinite changes were observed in renal glucose metabolism by ischemia, congestion or anoxia.Proteinuria was found to occur, both when renal O2 supply decreased under 30% of control value by decrease of RBF or by fall of renal arterial O2 content, and when RVP rised over about 250mm H2O.It was suggested that decrease of renal O2 surpply and elevation of RVP might be both causative factors of proteinuria independent with each other.Minimum glomerular protein content (Min. G. prot.) was observed to rise before proteinuria became manifest, and it was presumed that proteinuria in these cases was caused by way of elevation of glomerular permeability to protein.In these experimental proteinuria A/G ratio of urinary protein and CA1/CG1 showed rema kable rise as compared to normal control values.It was further noted in discussion that some clinical findings could be explained by these experimental results.
- 社団法人 日本内科学会の論文