RESUMO
As is known, hypoxia leads to an increase in microcirculatory blood flow of the skin in healthy volunteers. In this pilot study, we investigated microcirculatory blood flow and reactive hyperemia of the skin in healthy subjects in normobaric hypoxia. Furthermore, we examined differences in microcirculation between hypoxic subjects with and without short-term acclimatization, whether or not skin microvasculature can acclimatize. Fourty-six healthy persons were randomly allocated to either short-term acclimatization using intermittent hypoxia for 1 h over 7 days at an FiO2 0.126 (treatment, n = 23) or sham short-term acclimatization for 1 h over 7 days at an FiO2 0.209 (control, n = 23). Measurements were taken in normoxia and at 360 and 720 min during hypoxia (FiO2 0.126). Microcirculatory cutaneous blood flow was assessed with a laser Doppler flowmeter on the forearm. Reactive hyperemia was induced by an ischemic stimulus. Measurements included furthermore hemodynamics, blood gas analyses and blood lactate. Microcirculatory blood flow increased progressively during hypoxia (12.3 ± 7.1-19.0 ± 8.1 perfusion units; p = 0.0002) in all subjects. The magnitude of the reactive hyperemia was diminished during hypoxia (58.2 ± 14.5-40.3 ± 27.4 perfusion units; p = 0.0003). Short-term acclimatization had no effect on microcirculatory blood flow. When testing for a hyperemic response of the skin's microcirculation we found a diminished signal in hypoxia, indicative for a compromised auto-regulative circulatory capacity. Furthermore, hypoxic short-term acclimatization did not affect cutaneous microcirculatory blood flow. Seemingly, circulation of the skin was unable to acclimatize using a week-long short-term acclimatization protocol. A potential limitation of our study may be the 7 days between acclimatization and the experimental test run. However, there is evidence that the hypoxic ventilatory response, an indicator of acclimatization, is increased for 1 week after short-term acclimatization. Then again, 1 week is what one needs to get from home to a location at significant altitude.
RESUMO
Repression of enzymes contributing to degradation of aromatic compounds via the beta-ketoadipate pathway in the presence of additional carbon sources (carbon catabolite repression) in the bacterium Acinetobacter sp. strain ADP1 is described. The phenomenon was investigated on the level of specific activity of protocatechuate 3,4-dioxygenase and p-hydroxybenzoate hydroxylase participating in catabolism of protocatechuate and p-hydroxybenzoate. Strong repression (90%) was found in cells grown on succinate and acetate in addition to the aromatic carbon source; partial derepression occurred towards the end of the logarithmic growth phase. Glucose, pyruvate, or lactate as secondary carbon sources had no repressing effect. The consumption of the aromatic substrate from the medium was delayed in the presence of acetate and succinate. The differences in specific enzyme activities were reflected at the transcript level for three operons connected to catabolism of aromatic compounds (pob, pca, van) as shown by Northern blot hybridization. Transcriptional fusions between the promoters of the pob and the pca operon identified the transcriptional level as the regulatory one. A mechanism of global regulation is postulated, which enables the organism to consume the offered carbon sources hierarchically in the most efficient manner.
