Suppression and the sequential appearance of the galactose enzymes in a transferase amber mutant of E. coli.
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Biomedical subjects
Publications and source records attributed to G Michaelis.
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In 3 groups of 15 patients, respectively, we studied metabolic changes following tourniquet-release after operations of lower extremity. The influence of different anesthetic methods was evaluated by blood-gas-analyses up to 30 minutes after blood-circulation of the lower limb had been reinstalled. Our results demonstrate, that the patients under regional anesthesia with spontaneous respiration (group 1) could preserve their metabolic equilibrium with minor changes within the physiologic range. The intubated patients with controlled respiration (group 2) revealed a marked metabolic acidosis after tourniquet-release with insufficient respiratory compensation. Initial values were not reached within 30 minutes. The patients of group 3 (controlled respiration with a 25% increase of the normal minute volume for a period of 5 minutes after release of the tourniquet) had a less severe acidosis than those of group 2. The beneficial influence of spontaneous respiration in compensating metabolic acidosis--even in aged patients--following an ischemic tourniquet has been demonstrated by this investigation. Short-term hyperventilation seems to be the therapeutic tool in patients with controlled respiration to compensate for metabolic acidosis up to a certain extent.
An impairment of cortisol synthesis can be assumed for the new antimycotic fluconazole based on its chemical structure (triazole derivative) and mechanism of action (inhibition of ergosterol synthesis). In healthy volunteers, however, no influence on steroid hormone production could be found. The present study was undertaken to clarify whether this is also true for critically ill, long-term patients in an intensive care unit. The basal cortisol and adrenocorticotropic hormone (ACTH) levels were determined by means of radioimmunoassay in 11 patients being treated with antimycotics at fixed times. Antimycotic treatment was carried out using either fluconazole (n = 6) or a combination of amphotericin B and flucytosine (n = 5) for 14 days. Seven days after cessation of the treatment the above-mentioned hormones were again determined. Patients with the same baseline criteria who did not require antimycotic treatment (n = 8) served as controls. During the entire study period adequate cortisol synthesis was found after ACTH stimulation in all three patient groups. They all presented with relatively raised basal cortisol levels (range 16.4-31.0 micrograms dl-1) and an increase in ACTH-stimulated cortisol synthesis from 31% (group ampho B/flucytosine) to 78% (group fluconazole). The basal ACTH values were always within the normal range (9.2-16.4 pg ml-1). Neither the basal ACTH levels nor the basal cortisol levels as well as the cortisol levels determined after the ACTH test showed adrenocortical suppression in the patients of all three groups. Thus, according to the present results clinically relevant impairment of cortisol synthesis after treatment with fluconazole can be excluded.