Past strong experiences determine acute cardiovascular autonomic responses to acoustic stress.

BACKGROUND: Stress is a major risk factor for cardiovascular (CV) disease. We hypothesized that past strong experiences might modulate acute CV autonomic responses to an unexpected acoustic stimulus. A i m: The study's aim was to compare acute CV autonomic responses to acoustic stress between students with and without a past strong experience associated with the acoustic stimulus. MATERIALS AND METHODS: Twenty five healthy young volunteers - medical and non-medical students - were included in the study. CV hemodynamic parameters, heart rate (HR), and blood pressure (BP) variability were assessed for 10 min at rest and for 10 min after two different acoustic stimuli: a standard sound signal and a specific sound signal used during a practical anatomy exam (so-called "pins"). RESULTS: Both sounds stimulated the autonomic nervous system. The "pins" signal caused a stronger increase in HR in medical students (69 ± 10 vs. 73 ± 13 bpm, p = 0.004) when compared to non-medical students (69 ± 6 vs. 70 ± 10, p = 0.695). Rises in diastolic BP, observed 15 seconds after sound stressors, were more pronounced after the "pins" sound than after the standard sound signal only in medical students (3.1% and 1.4% vs. 3% and 4.4%), which was also reflected by low-frequency diastolic BP variability (medical students: 6.2 ± 1.6 vs. 4.1 ± 0.8 ms2, p = 0.04; non-medical students: 6.0 ± 4.3 vs. 4.1 ± 2.6 ms2, p = 0.06). CONCLUSIONS: The "pins" sound, which medical students remembered from their anatomy practical exam, provoked greater sympathetic activity in the medical student group than in their non-medical peers. Thus, past strong experiences modulate CV autonomic responses to acute acoustic stress.

Oral L-arginine improves endothelial function in healthy individuals older than 70 years.

Ageing is associated with progressive endothelial dysfunction in normal humans. Flow-mediated dilation (FMD) of the brachial artery is impaired in elderly individuals with cardiovascular disease and vascular nitric oxide (NO) bioavailability is reduced. We investigated whether oral L-arginine, the substrate for NO synthesis, can improve impaired FMD in healthy very old people. In a prospective, double-blind, randomized crossover trial, 12 healthy old subjects (age 73.8 +/- 2.7 years) took L-arginine (8 g p.o. two times daily) or placebo for 14 days each, separated by a wash-out period of 14 days. FMD was determined by high-resolution ultrasound in the brachial artery during reactive hyperaemia. Baseline artery diameter was 3.88 +/- 0.18 mm. L-Arginine significantly improved FMD (to 5.7 +/- 1.2%, p < 0.0001), whereas placebo had no effect (-0.25 +/- 0.7%; n.s.). After L-arginine, plasma levels of L-arginine increased significantly (114.9 +/- 11.6 versus 57.4 +/- 5.0 micromol/l), but placebo had no effect. As NO synthesis can be antagonized by its endogenous inhibitor asymmetric dimethyl L-arginine (ADMA), we determined ADMA plasma concentrations, which were elevated at baseline in comparison to healthy middle-aged individuals (3.9 +/- 0.2 versus 1.0 +/- 0.1 micromol/l; p < 0.0001). ADMA remained unchanged during treatment, but L-arginine supplementation normalized the L-arginine/ADMA ratio (p < 0.05). We conclude that in healthy very old age endothelial function is impaired and may be improved by oral L-arginine supplementation, probably due to normalization of the L-arginine/ADMA ratio.