[Refractory diseases. 1. Primary care in refractory diseases].
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Biomedical subjects
Publications and source records attributed to T Murase.
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A sensitive and specific radioimmunoassay for arginine vasopressin (AVP) was developed utilizing the antisera against lysine vasopressin (LVP) in combination with a labeled AVP. The assay employs an acetone extraction procedure and detects as little as 0.8 pg. per milliliter of AVP in human plasma. In normal subjects the mean (+/- S.D.) plasma concentration of AVP was 4.9 +/- 1.2 pg. per mililiter after fluid deprivation and 1.2 +/- 0.4 pg. per milliliter after water loading. Plasma AVP levels correlated significantly with plasma osmolalities. In four patients with diabetes insipidus, plasma AVP concentrations ranged from less than 0.8 to 1.2 pg. per milliliter, whereas six patients with the syndrome of inappropriate ADH secretion showed plasma levels of AVP which correspond to those of the dehydrated state in normal subjects or greater, although plasma osmolalities were low in all cases. It was concluded that the present radioimmunoassay method for AVP provides a useful way of assessing neurohypophyseal function in man.
In an attempt to define pathogenesis of the previously described impaired triglyceride (TG) removal in uremia, the effects of the addition of normal and uremic plasma on the activity of lipoprotein lipase (LPL) from rat epididymal adipose tissue were examined. Six uremic patients on chronic dialysis and 13 normals were studied. Adding increments of normal and uremic plasma increased the LPL activity to maximal levels when 0.1 ml of plasma was added. Larger aliquots of uremic plasma produced marked inhibition of LPL activity. This inhibition was not observed with the normal plasma. When increasing amounts of uremic plasma were added to an incubation mixture already maximally activated by 0.1 ml of normal plasma, inhibition of LPL was again observed. This inhibition was still present in uremic plasma which had been dialysed against cold saline. The inhibitor was in the lipoprotein-free (d greater than 1.225) fraction of the plasma. The results indicate that uremic plasma has an LPL inhibitor which is probably a protein and may play a role in the pathogenesis of uremic hypertriglyceridemia.
Two different methods of examining triglyceride turnover are described. One measures the clearance of endogenously labeled triglyceride glycerol, the radioglyceride method. The other assesses the hydrolysis of endogenous very low density lipoproteins after a primed infusion of maximal doses of heparin, the lipolytic rate. Both depend on widely different assumptions. A comparison of data obtained by both methods at the same time in single individuals with widely differing triglyceride concentrations revealed them to agree quite closely. This correspondence indirectly suggests the validity of the procedures. The procedures have been applied to show that fat-free high-carbohydrate diets accelerate triglyceride production in some humans.
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