Influence of hyperoxia on diastolic myocardial and arterial endothelial function.

OBJECTIVE: Hyperoxia is known to influence cardiovascular and endothelial function, but it is unknown if there are differences between younger and older persons. The aim of this study was to monitor changes in myocardial diastolic function and flow-mediated dilatation (FMD) in younger and elderly volunteers, before and after exposure to relevant hyperbaric hyperoxia. METHODS: 51 male patients were separated into two groups for this study. Volunteers in Group 1 (n=28, mean age 26 ±6, "juniors") and Group 2 (n=23, mean age 53 ±9, "seniors") received standard HBO2 protocol (240kPa oxygen). Directly before and after hyperoxic exposure in a hyperbaric chamber we took blood samples (BNP, hs-troponin-t), assessed the FMD and echocardiographic parameters with focus on diastolic function. RESULTS: After hyperoxia we observed a high significant decrease in heart rate and systolic/diastolic FMD. Diastolic function varied in both groups: E/A ratio showed a statistically significant increase in Group 1 and remained unchanged in Group 2. E/e' ratio showed a slight but significant increase in Group 1, whereas e'/a' ratio increased in both groups. Deceleration time increased significantly in all volunteers. Isovolumetric relaxation time remained unchanged and ejection fraction showed a decrease only in Group 2. There were no changes in levels of BNP and hs-troponin-t in either group. CONCLUSION: Hyperoxia seems to influence endothelial function differently in juniors and seniors: FMD decreases more in seniors, possibly attributable to pre-existing reduced vascular compliance. Hyperoxia-induced bradycardia induced a more pronounced improvement in diastolic function in juniors. The ability of Group 1 to cope with hyperoxia-induced effects did not work in the same manner as with Group 2.

Influence of hyperoxia and physical exercise on *OH-radical stress in humans as measured by dihydroxylated benzoates (DHB) in urine.

BACKGROUND: Hyperoxia and physical exercise are known to produce reactive oxygen species (ROS), and the *OH radical is the most aggressive among them. However, knowledge is limited about *OH stress during physical work under hyperoxic conditions. METHODS: This study monitored *OH stress in human volunteers before and after a total of 135 exposures to ambient air (control), different levels of hyperoxia at rest and challenging open-water closed-circuit dives by measurement of dihydroxylated benzoates (DHB) with HPLC by electrochemical detection in urine. RESULTS: Changes in DHB in urine after control were only 3.43 +/- 4.8% (n = 9). After exposures to 100 kPa oxygen (O2) for 110 minutes DHB revealed increases in urine of 23.14 +/- 5.12% (n = 9); exposures to 240 kPa O2 for 90 minutes increases of 22.38 +/- 8.91% (n = 8); and 280 kPa 02 for 30 minutes of 21.92 +/- 10.76% (n = 17). Closed-circuit dives in open water (45-54 minutes of 125-160 kPa O2) revealed DHB increases of 66.34 +/- 25.73% (n = 92). All results differed significantly from control (p < 0.001). The closed-circuit dives also differed significantly from all exposures to hyperoxia without exercise (p < 0.001). Standardization of "oxygen burden" during each exposure (pO2 x exposure time x VO2) allowed for comparison of different exposures vs. DHB changes and revealed goodness of linear fit of r2 = 0.432 (p < 0.0001). CONCLUSIONS: Increases in urine DHB after exposures to different levels of hyperoxia at rest and during exercise are consistent with *OH stress that is greater during exercise than at rest, although other interpretations are possible. Standardization of the individual "oxygen burden" for a given exposure may become useful in future for the estimation of *OH stress.

Physical exercise might influence the risk of oxygen-induced acute neurotoxicity.

OBJECTIVE: Hyperoxia can induce acute neurotoxicity with generalized seizures. Hyperoxia-induced reduction in cerebral blood flow velocity (CBFV) might be protective. It is unclear whether dynamic exercise during hyperoxia can overcome CBFV-reduction and thus possibly increase the risk of neurotoxicity. METHODS: We studied CBFV with both-sided transcranial Doppler with fixed transducer-position and heart rate under increasing hyperoxic conditions in nine professional military oxygen divers. The divers performed dynamic exercise on a bicycle-ergometer in a hyperbaric chamber (ergometries I-III, 21kPa, 100kPa, 150kPa pO2), with continuous blood pressure (ergometries I, II), end-tidal CO2 (PetCO2; ergometry I) being measured. RESULTS: Systolic (CBFVsyst) and diastolic CBFV (CBFVdiast) readings at rest decreased with increasing pO2. During exercise, CBFVsyst and CBFVdiast significantly increased in parallel with increasing pO2, despite reduced flow velocities at rest. ERGOMETRY I: CBFVsyst increased from 65.0 +/- 11.3 cm/second at rest to 80.2 +/- 23.4cm/s during maximum workload (n.s.), diastolic from 14.5 +/- 4.1 cm/second to 15.6 +/- 7.5 cm/s (n.s.). PetCO2 increased from 43.4 +/- 7.8mmHg to 50.0 +/- 7.5mmHg. ERGOMETRY II: CBFVsyst increased from 58.2 +/- 16.5 cm/second to 99.7 +/- 17.0 cm/s (p<0.001), diastolic from 14.0 +/- 10.7 cm/second to 29.4 +/- 11.1 cm/second (p<0.01). ERGOMETRY III: CBFVsyst increased from 54.4 +/-15.0cm/second to 109.4 +/- 22.3cm/s (p<0.001), diastolic from 14.7 +/- 10.4 cm/second to 35.5 +/- 9.3 cm/second (p<0.01). INTERPRETATION: Physical exercise overrules the decrease in CBFV during hyperoxia and leads to even higher CBFV-increases with increasing pO2. A tendency towards CO2 retainment with elevated PetCOz may be causative and thus heighten the risk of oxygen-induced neurotoxicity.