[Direct renal action of isoprenaline and propranolol].
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Biomedical subjects
Publications and source records attributed to D Durand.
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From the kinetic study of the effects of one single growth hormone (GH) injection on the phosphate metabolism, it appears that the influence of GH on the serum phosphate level is biphasic: a decrease is followed by an increase. Conversely GH leads to an early decrease of the urinary phosphate excretion.
The object of the present work was to determine the part played by thyroxine (T4) in chronic effects of GH on phosphocalcium metabolism. Therefore, we used hypophysectomized-thyroparathyroidectomized female rats. The results were that: 1. Repeated daily administration of GH to female rats which had been operated on was not followed by the hyperphosphatemia classically observed in normal animals. GH always decreased urinary calcium and phosphorus excretion, indicating a direct renal effect of this hormone, irrespective of blood variations in the ions. 2. Chronic administration of infra-physiological doses of L-thyroxine (0.25 mug/100 g per day) enabled one again to obtain in operated rats the increase of phosphatemia specifically due to GH. 3. With the doses of GH and thyroxine used in these experiments, the blood calcium level of rats which have been operated on decreased. In conclusion, GH intervenes directly in phosphocalcium metabolism and it helps maintain a high phosphatemia. Thyroxine permits this last mentioned effect.
14 cases of idiopathic rapidly progressive glomerulonephritis (I. R. P. G. N.) treated by heparin between 1968 and 1974 were collected by the authors. Extra-capillary crescents (E. C. C.) occurred in 75 to 100% of glomeruli in ten patients and in 50 to 75% in four. Gross proteinuria, hematuria and renal failure were always present. 9 patients were admitted with primary oligo-anuric renal failure. 11 patients were treated by repeated hemodialysis before and during anticoagulant treatment. Heparin was given by intra-venous injection every 3 hours for one to two months with Howell times range from 150 to 200% of control. Heparin was the only treatment in 6 cases, and was given with dipyridamole in 4, with prednisone in 3 and with azathioprine in one case. 5 severe or fatal hemorragic complications were observed. The clinical course was usually unfavorable with 5 early deaths, 3 provisional steady-states with 2 late deaths. Six patients were treated by periodic hemodialysis. Repeat kidney biopsies were obtained in 8 patients. The findings suggest that heparin affects mainly the E. C. C. and fibrinoid deposits but not glomerular sclerosis. The inefficiency of all current treatments of primary oligo-anuric IRPGN is stressed. In patients with better initial renal function choice between anticoagulant and/or immuno-depressive drugs must be scrutinized in individual cases bearing in mind potential iatrogenic complications. In equivocal cases, patients should be referred to the chronic hemodialysis and/or transplantation program.
Superimposition of an adrenal scan on a renal scan revealed a kidney defect not appreciated on the renal scan alone. The defect proved to be ischemia of the upper pole of the kidney. Resection of the lesion alleviated the patient's hypertension.
Vibrio cholerae neuraminidase treatment increases the cell sensitivity to complement and antibodies cytotoxic action. This property can be applied to the microlymphocytotoxicity technic for antibodies study in dialysed and kidney transplanted patients and for pretransplantation cross-matches. The enzymatic treatment usually employed needs a great deal of lymphocytes submitted in a second step to antibodies cytotoxic action. But this method appeared difficult to be routinely applied. We developed a simpler method consisting in treating only the lymphocytes needed to perform the test, on the reaction plate itself. This method gives the same results as the classical enzymatic treatment: the intensity of the weakly positive reaction is strongly increased, after pretreatment of cells; in certain cases, it allows one to detect cytotoxic antibodies not revealed without neuraminidase. These antibodies can be related (or not) to HLA system but practically the more important fact is the ability of this method to reveal an eventual incompatibility.
Masive intestinal necrosis due to any cause is associated with a chemical complex that may be helpful in the early diagnosis of these conditions. This consists of elevated serum phosphate level, metabolic acidosis with significant base deficit, elevated white blood count, and elevated hemoglobin and hematocrit values. This chemical complex associated with clinical signs and symptoms, may indicate the need for laparotomy. In this way, the time period between vascular occlusion and operation could be shortened and possible lead to more gratifying results than the present day extremely high morbidity and mortality rates which are associated with massive intestinal necrosis.
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