Comparative pyridostigmine kinetics in plasma were measured in 10 healthy subjects given 4 mg iv and 60 mg oral pyridostigmine bromide. As determined from the AUC ratio, oral availability was 11.5% to 18.9% (means = 14.3%). Mean t 1/2 of the plasma level decline after oral dosing was 200 minutes, twice as long as the terminal elimination t1/2 after intravenous infusion (97 minutes). Thus absorption may proceed at a slower rate than elimination. Comparison of intraindividual data revealed strict dependence of the AUC on the infused dose (2, 4, and 8 mg) in one subject and variability in AUC up to a factor of two when two subjects took oral pyridostigmine three times. Patients with myasthenia who were receiving continuous therapy with oral pyridostigmine had AUC values per unit dose corresponding to those in healthy subjects. Storage stability of pyridostigmine in plasma required acidification of samples and storage at -75 degrees C. When native plasma was kept at -20 degrees C, there was appreciable loss of pyridostigmine within 1 to 2 months, the extent of which depended on the initial concentration.
During the first 48 h after 67% partial hepatectomy of female Wistar rats (160 g) the specific activities of the glucogenic fructose-bisphosphatase and of the glycolytic hexokinase, phosphofructokinase and pyruvate kinase in the kidney cortex remained essentially constant. The activity of the glucogenic glucose-6-phosphatase was increased slightly to 140% and that of phosphoe/?0/pyruvate carboxykinase to above 230% after 12 h. Since a metabolic acidosis and glucocorticoid hormones are the two well-known inducers of renal phosphoe;?o/pyruvate carboxykinase, the acid-base status and the corticosterone levels were determined after partial hepatectomy. The acid-base status remained unchanged. Corticosterone levels were enhanced after 12 h and 24 h to over 300%. Thus it appeared that the glucocorticoid hormone rather than a metabolic acidosis played a major role in the induction of renal phosphoe/70/pyruvate carboxykinase after partial hepatectomy. From these findings it is concluded that the considerable increase of the gluconeogenic capacity of the kidney is necessary in order to compensate the diminished capacity of the onethird liver remnant which, in spite of its own enhancement of gluconeogenic capacity, apparently cannot insure the glucose supply of the central nervous system and the erythrocytes in the postabsorptive phase.
Kompensatorische Steigerung der gluconeogenen Kapazität der Niere nach TeilhepatektomieZusammenfassung: Während der ersten 48 h nach 67% Teilhepatektomie weiblicher Wistar-Ratten (l 60 g) blieb in der Nierenrinde die spezifische Aktivität der glucogenen Fructose-bisphosphatase und der glycolytischen Hexokinase, 6-Phosphofructokinase and Pyruvat-Kinase praktisch konstant. Die Aktivität der glucogenen Glucose-6-phosphatase war leicht auf 140% und die der
In a 46-year-old female patient with malignant thymoma and concomitant myasthenia gravis relapse with gravitational metastases occurred 6 1/2 years after the first operation. Metastases could be removed surgically only partially and were subsequently irradiated with 50 Gy. After 3 1/2 years renewed metastatic growth occurred. Until then the concomitant myasthenia had been stable during treatment with pyridostigmine and azathioprin and intermittent prednisone; acetylcholine receptor antibody titres had remained largely stable. Combined cytostatic treatment with vincristine, cyclophosphamide, prednisone and doxorubicin or cisplatin led to regression of metastases during the observation period of 1 1/2 years and at the same time to stabilisation of the myasthenia. Acetylcholine receptor antibody titres decreased and this was roughly paralleled by clinical improvement. Whereas there is no obvious correlation of antibodies against acetylcholine-receptor protein and tendency of tumour growth there is good agreement with the course of the accompanying myasthenia.
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