[Oral anticoagulation. Quality control and standardization of the prothrombin time determination].
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Biomedical subjects
Publications and source records attributed to C Vorburger.
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1. In nineteen patients with normal or diseased kidneys, renal blood flow, transit times and vascular volume were determined by means of an indicator-dilution method. Two different indicators, plasma-bound Indocyanine Green (IG) and 99mTc-labelled erythrocytes, were used simultaneously. 2. Comparison of the results indicates that IG slightly overestimates renal blood flow, appearance time, mean transit time and vascular volume, as the erythrocyte/IG ratios averaged 0.972, 0.903, 0.93, and 0.921 respectively. Overestimation of the mean transit time was less apparent when it was prolonged. In patients with reduced renal function, the average blood flow values obtained with the two indicators were in good agreement. 3. It is unlikely that axial streaming of erythrocytes accounts for their shorter mean transit time, because the individual erythrocyte/IG mean transit time ratios were independent of the rate of blood flow and the peripheral packed cell volume. 4. Since the erythrocyte/IG mean transit time ratios correlated significantly with the erythrocyte/IG ratios for appearance time and renal blood flow, the common mechanism leading to a depression of all erythrocyte/IG ratios is presumably extravascular circulation and delayed recovery of a small fraction of IG.
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In patients with renal failure the administration of antiinfectious chemotherapeutic agents (antibiotics) raises two main problems. Antibiotics which are effective only by virtue of their high urinary concentration may lose their effect with reduced renal function (plasma creatinine above 1.5-1.7 mg%). This is true of nitrofurantoin, nalidixic acid, colistin and, to a lesser extent, sulfonamides. Decreased renal elimination of antibiotics may ultimately lead to accumulation and toxic side effects, and the dose of a given antibiotic should therefore be adapted to renal function. Simple dose-adaptation rules are proposed on the basis of plasma creatinine concentration as an index of renal function, a table listing the elimination constants of several antibiotics, and a nomogram which serves to determine graphically the appropriate global elimination constant for the individual patient and a given antibiotic.
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The mechanism responsible for the anuria in acute renal failure after shock is still controversial. Suppressed glomerular filtration and/or tubular back-diffusion of the filtrate are major possible causes. In the present investigation, seven patients with acute anuria, three of these seven again in the polyuric phase, six patients with moderate renal impairment, four patients with chronic renal failure, and eight subjects with normal renal function were studied by a multiple indicator-dilution method in which the total renal blood flow and renal distribution volumes of indocyanine green, [(51)Cr]EDTA, and (24)Na were determined. In normal subjects the average values for one kidney were 582 ml/min, 42 ml, 92 ml, and 139 ml, respectively. The measurements in the patients with moderate renal impairment were similar to those in the normal subjects, but were decreased in chronic renal failure. In acute anuria, the average values were 269 ml/min, 40 ml, 101 ml, and 114 ml and the kidney volume, estimated radiographically, was increased by 40%. When expressed as milliliters per milliliters kidney, the average distribution volume of (24)Na was decreased from 0.64 to 0.38. This decrease is consistent with the hypothesis that suppressed filtration is largely responsible for the anuria and that back-diffusion is, at most, a contributory factor. The apparent contradiction between the relatively well-preserved total blood flow and the suppressed filtration may be due to a combination of afferent vasoconstriction and efferent vasodilatation. This view is supported by the observation that low filtration fractions were found in clearance measurements performed during the polyuric phase.
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