We examined whether the improvement of impaired NO-dependent vasorelaxation by exercise training could be mediated through a BH4-dependent mechanism. Male spontaneously hypertensive rats (SHR, n = 20) and Wistar-Kyoto rats (WKY, n = 20) were trained (Tr) for 9 weeks on a treadmill and compared to age-matched sedentary animals (Sed). Endothelium-dependent vasorelaxation (EDV) was assessed with acetylcholine by measuring isometric tension in rings of femoral artery precontracted with 10(-5) M phenylephrine. EDV was impaired in SHR-Sed as compared to WKY-Sed (p = 0.02). Training alone improved EDV in both WKY (p = 0.01) and SHR (p = 0.0001). Moreover, EDV was not different in trained SHR than in trained WKY (p = 0.934). Pretreatment of rings with L-NAME (50 μM) cancelled the difference in ACh-induced relaxation between all groups, suggesting that NO pathway is involved in these differences. The presence of 10(-5) M BH4 in the organ bath significantly improved EDV for sedentary SHR (p = 0.030) but not WKY group (p = 0.815). Exercise training turned the beneficial effect of BH4 on SHR to impairment of ACh-induced vasorelaxation in both SHR-Tr (p = 0.01) and WKY-Tr groups (p = 0.04). These results suggest that beneficial effect of exercise training on endothelial function is due partly to a BH4-dependent mechanism in established hypertension.

We examined whether the improvement of impaired NO-dependent vasorelaxation by exercise training could be mediated through a BH4-dependent mechanism. Male spontaneously hypertensive rats (SHR, n = 20) and Wistar-Kyoto rats (WKY, n = 20) were trained (Tr) for 9 weeks on a treadmill and compared to age-matched sedentary animals (Sed). Endothelium-dependent vasorelaxation (EDV) was assessed with acetylcholine by measuring isometric tension in rings of femoral artery precontracted with 10(-5) M phenylephrine. EDV was impaired in SHR-Sed as compared to WKY-Sed (p = 0.02).

In our previous research, a deep 5-min stop at 15 msw (50 fsw), in addition to the typical 3-5 min shallow stop, significantly reduced precordial Doppler detectable bubbles (PDDB) and "fast" tissue compartment gas tensions during decompression from a 25 msw (82 fsw) dive; the optimal ascent rate was 10 msw (30 fsw/min). Since publication of these results, several recreational diving agencies have recommended empirical stop times shorter than the 5 min stops that we used, stops of as little as 1 min (deep) and 2 min (shallow). In our present study, we clarified the optimal time for stops by measuring PDDB with several combinations of deep and shallow stop times following single and repetitive open-water dives to 25 msw (82 fsw) for 25 mins and 20 minutes respectively; ascent rate was 10 msw/min (33 fsw). Among 15 profiles, stop time ranged from 1 to 10 min for both the deep stops (15 msw/50 fsw) and the shallow stops (6 msw/20 fsw). Dives with 2 1/2 min deep stops yielded the lowest PDDB scores--shorter or longer deep stops were less effective in reducing PDDB. The results confirm that a deep stop of 1 min is too short--it produced the highest PDDB scores of all the dives. We also evaluated shallow stop times of 5, 4, 3, 2 and 1 min while keeping a fixed time of 2.5 min for the deep stop; increased times up to 10 min at the shallow stop did not further reduce PDDB. While our findings cannot be extrapolated beyond these dive profiles without further study, we recommend a deep stop of at least 2 1/2 mins at 15 msw (50 fsw) in addition to the customary 6 msw (20 fsw) for 3-5 mins for 25 meter dives of 20 to 25 minutes to reduce PDDB.

Backround: Nitrogen narcosis impairs cognitive function, a fact relevant during SCUBA-diving. Oxygen-enriched air (nitrox) became popular in recreational diving, while evidence of its advantages over air is limited. AIM: Compare effects of nitrox28 and air on two psychometric tests.

ntroduction: The effects of scuba diving on the vessel wall have been studied mainly at the level of large conduit arteries. Data regarding the microcirculation are scarce and indicate that these two vascular beds are affected differently by diving. Methods: We assessed the changes in cutaneous microcirculation before an air scuba dive, then 30 min and 24 h after surfacing. Endothelium-dependent and independent vasomotion were successively elicited by iontophoretic administration of acetylcholine and sodium nitroprusside respectively, and cutaneous blood flux was monitored by laser Doppler flowmetry.