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Background: As it remains unclear whether hypoxia of cardiomyocytes could trigger the release of brain natriuretic peptide (BNP) in humans, we investigated whether breathing normobaric hypoxic gas mixture increases the circulating NT-proBNP in healthy male subjects.Methods: Ten healthy young men (age 29 ± 5 yrs, BMI 24.7 ± 2.8 kg/m2) breathed normobaric hypoxic gas mixture (11% O2/89% N2) for one hour. Venous blood samples were obtained immediately before, during, and 2 and 24 hours after hypoxic exposure. Cardiac function and flow velocity profile in the middle left anterior descending coronary artery (LAD) were measured by Doppler echocardiography.Results: Arterial oxygen saturation decreased steadily from baseline value of 99 ± 1% after the initiation hypoxia challenge and reached steady-state level of 73 ± 6% within 20-30 minutes. Cardiac output increased from 6.0 ± 1.2 to 8.1 ± 1.6 L/min and ejection fraction from 67 ± 4% to 75 ± 6% (both p < 0.001). Peak diastolic flow velocity in the LAD increased from 0.16 ± 0.04 to 0.28 ± 0.07 m/s, while its diameter remained unchanged. In the whole study group, NT-proBNP was similar to baseline (60 ± 32 pmol/ml) at all time points. However, at 24 h, concentration of NT-proBNP was higher (34 ± 18%) in five subjects and lower (17 ± 17%), p = 0.002 between the groups) in fi

The present contribution reviews current knowledge of apparently oxygen-dependent ion transport in erythrocytes and presents modern hypotheses on their regulatory mechanisms and physiological roles. In addition to molecular oxygen as such, reactive oxygen species, nitric oxide, carbon monoxide, regional variations of cellular ATP and hydrogen sulphide may play a role in the regulation of transport, provided that they are affected by oxygen tension. It appears that the transporter molecules themselves do not have direct oxygen sensors. Thus, the oxygen level must be sensed elsewhere, and the effect transduced to the transporter. The possible pathways involved in the regulation of transport, including haemoglobin as a sensor, and phosphorylation/dephosphorylation reactions both in the transporter and its upstream effectors, are discussed.

Effects of acute cold exposure (at 1°C and 5°C) on tissue redox state and oxidative stress parameters, as well as the onset of hypoxic signaling were investigated in the North Sea eelpout, Zoarces viviparus. Activation of the transcription factor HIF-1 (hypoxia inducible factor) was detected in liver samples after acute cold exposure. At this temperature the cellular redox milieu was significantly reduced (below -270 mV) as compared to controls (-250 to -267 mV). Increased levels of oxidative stress parameters (TBARS and protein carbonyls) were observed mainly during recovery at control temperature (12°C). This increase in oxidative stress parameters, in spite of maintained antioxidant capacity, indicates that acute cold stress and recovery mimic ischemia/reperfusion events as found in mammals. Notably the non-enzymatic antioxidant defense (e.g. glutathione) may play an important role for eelpout ROS scavenging capacity under cold stress.

The interplay between antioxidants, heat shock proteins and hypoxic signaling is supposed to be important for passive survival of critical temperature stress, e.g. during unfavorable conditions in hot summers. We investigated the effect of mild (18°C), critical (22°C) and severe (26°C) experimental heat stress, assumed to induce different degrees of functional hypoxia, as well as the effect of recovery following heat stress on these parameters in liver samples of the common eelpout Zoarces viviparus.Upon heat exposure to critical and higher temperatures we found an increase in oxidative damage markers such as TBARS (thiobarbituric reactive substances) and a more oxidized cellular redox potential, combined with reduced activities of the antioxidant enzyme SOD at 26°C. Together, this points to higher oxidative stress levels during stressful hyperthermia. In a recovery-time series, heat induced hypoxia and subsequent reoxygenation upon return of the fishes to 12°C led to increased protein oxidation and chemiluminescence rates within the first 12 hours upon recovery, therein resembling ischemia/reperfusion injury in mammals.HSP70 levels were found only slightly elevated after recovery from sub-lethal heat stress, indicating minor importance of the heat shock response in this species. The DNA binding activity of the hypoxia inducible transcription factor (HIF-1) was elevated only during mild heat exposure (18°C), but appeared impaired at more severe heat stress. We suppose that the more oxidized redox state during extreme heat may interfere with the hypoxic signaling response.

We investigated whether exposure to heavy metal pollution affected the immune function of individuals in a free living population of a small insectivorous passerine bird, the pied flycatcher Ficedula hypoleuca. We measured humoral immune responses in two study areas: a polluted area in the vicinity of a copper smelter and a control area far from the smelter. Plasma corticosterone level and blood heterophil/lymphocyte ratio (H/L) were used as more general physiological measures of stress. The immune response of F hypoleuca was not suppressed by pollution stress. In contrast, we found that F hypoleuca males showed stronger Immoral immune responses to a novel antigen (tetanus toxoid) in the polluted environment than in the unpolluted one. After the immunization of males, numbers of lymphocytes rose significantly more in the polluted area, leading to a smaller H/L ratio than in males from the control area. Females showed no pollution related effects on their immune responses. Corticosterone levels of males and nestlings were not related to pollution levels. Nestlings showed somewhat higher H/L ratios and lower fledging success in the polluted area, both factors indicating increased stress levels in a polluted area. Our results suggest that Immoral immune response of male F hypoleuca may be enhanced under moderate levels of heavy metal Pollution. Enhanced immune function may, however, also be costly for birds and the higher humoral immune responses in polluted areas may thus have negative effects on the birds' breeding performance and survival.