Faculty Bibliography

BACKGROUND:Autonomic arousal-responses to emotional stimuli change with age. Age-dependent autonomic responses to music-onset are undetermined. OBJECTIVE:To determine whether cardiovascular-autonomic responses to "relaxing" or "aggressive" music differ between young and older healthy listeners. METHODS:In ten young (22.8±1.7 years) and 10 older volunteers (61.7±7.7 years), we monitored respiration (RESP), RR-intervals (RRI), and systolic and diastolic blood pressure (BPsys, BPdia) during silence and 180second presentations of two "relaxing" and two "aggressive" classical-music excerpts. Between both groups, we compared RESP, RRI, BPs, spectral-powers of mainly sympathetic low-frequency (LF: 0.04-0.15Hz) and parasympathetic high-frequency (HF: 0.15-0.5Hz) RRI-oscillations, RRI-LF/HF-ratios, RRI-total-powers (TP-RRI), and BP-LF-powers during 30s of silence, 30s of music-onset, and the remaining 150s of music presentation (analysis-of-variance and post-hoc analysis; significance: p<0.05). RESULTS:During silence, both groups had similar RRI, LF/HF-ratios and LF-BPs; RESP, LF-RRI, HF-RRI, and TP-RRI were lower, but BPs were higher in older than younger participants. During music-onset, "relaxing" music decreased RRI in older and increased BPsys in younger participants, while "aggressive" music decreased RRI and increased BPsys, LF-RRI, LF/HF-ratios, and TP-RRI in older, but increased BPsys and RESP and decreased HF-RRI and TP-RRI in younger participants. Signals did not differ between groups during the last 150s of music presentation. CONCLUSIONS:During silence, autonomic modulation was lower - but showed sympathetic predominance - in older than younger persons. Responses to music-onset, particularly "aggressive" music, reflect more of an arousal- than an emotional-response to music valence, with age-specific shifts of sympathetic-parasympathetic balance mediated by parasympathetic withdrawal in younger and by sympathetic activation in older participants.

BACKGROUND AND PURPOSE: Pharmacological blockade showed sympathetic origin of 0.03 to 0.15 Hz blood pressure (BP) oscillations and parasympathetic origin of 0.15 to 0.5 Hz RR-interval (RRI) oscillations, but has not been used to determine origin of cerebral blood flow velocity (CBFV) oscillations at these frequencies. This study evaluated by pharmacological blockade whether 0.1 Hz CBFV oscillations are related to sympathetic and 0.2 Hz CBFV oscillations to parasympathetic modulation. METHODS: In 11 volunteers (24.6 +/- 2.3 years), we monitored RRIs, BP, and proximal middle cerebral artery CBFV, at rest, during 180 s sympathetic BP activation by 0.1 Hz sinusoidal neck suction (NS), and during 180 s parasympathetic RRI activation by 0.2 Hz NS. We repeated recordings after 25 mg carvedilol, and after 0.04 mg/kg atropine. Autoregressive analysis quantified RRI-, BP-, and CBFV-spectral powers at 0.1 Hz and 0.2 Hz. We compared parameters at rest, during 0.1 Hz, or 0.2 Hz NS, with and without carvedilol or atropine (analysis of variance, post hoc testing; significance, P<0.05). RESULTS: Carvedilol significantly increased RRIs and lowered BP, CBFV, and 0.1 Hz RRI-, BP-, and CBFV-powers at baseline (P=0.041 for CBFV-powers), and during 0.1 Hz NS-induced sympathetic activation (P<0.05). At baseline and during 0.2 Hz NS-induced parasympathetic activation, atropine lowered RRIs and 0.2 Hz RRI-powers, but did not change BP, CBFV, and 0.2 Hz BP- and CBFV-powers. CONCLUSIONS: Attenuation of both 0.1 Hz CBFV and BP oscillations after carvedilol indicates a direct relation between 0.1 Hz CBFV oscillations and sympathetic modulation. Absent effects of atropine on BP, CBFV, and 0.2 Hz BP and CBFV oscillations suggest that there is no direct parasympathetic influence on 0.2 Hz BP and CBFV modulation.

BACKGROUND: In patients with familial dysautonomia (FD), prominent orthostatic hypotension (OH) endangers cerebral perfusion. Supine repositioning or abdominal compression improves systolic and diastolic blood pressure (BPsys and BPdia). OBJECTIVE: To determine whether OH recovers faster with combined supine repositioning and abdominal compression than with supine repositioning alone. METHODS: In 9 patients with FD (17.8 +/- 3.9 years) and 10 healthy controls (18.8 +/- 5 years), we assessed 2-min averages of BPsys, BPdia, and heart rate (HR) during supine rest, standing, supine repositioning, another supine rest, second standing, and supine repositioning with abdominal compression by leg elevation and flexion. We determined BPsys- and BPdia-recovery-times as intervals from return to supine until BP reached values equivalent to each participant's 2-min average at supine rest minus two standard deviations. Differences in signal values and BP-recovery-times between groups and positions were assessed by ANOVA and post hoc testing (significance: P < 0.05). RESULTS: Patients with FD had pronounced OH that improved with supine repositioning. However, BP only reached supine rest values with additional abdominal compression. In controls, BP was stable during positional changes. Without abdominal compression, BP-recovery-times were longer in patients with FD than those in controls, but similar to control values with compression (BPsys: 83.7 +/- 64.1 vs 36.6 +/- 49.5 s; P = 0.013; BPdia: 84.6 +/- 65.2 vs 35.3 +/- 48.9 s; P = 0.009). CONCLUSION: Combining supine repositioning with abdominal compression significantly accelerates recovery from OH and thus lowers the risk of hypotension-induced cerebral hypoperfusion.

BACKGROUND AND PURPOSE: Localized head and neck cooling might be suited to induce therapeutic hypothermia in acute brain injury such as stroke. Safety issues of head and neck cooling are undetermined and may include cardiovascular autonomic side effects that were identified in this study. METHODS: Ten healthy men (age 35+/-13 years) underwent 120 minutes of combined head and neck cooling (Sovika, HVM Medical). Before and after onset of cooling, after 60 and 120 minutes, we determined rectal, tympanic, and forehead skin temperatures, RR intervals, systolic and diastolic blood pressures (BP), laser-Doppler skin blood flow at the index finger and cheek, and spectral powers of mainly sympathetic low-frequency (0.04-0.15 Hz) and parasympathetic high-frequency (0.15-0.5 Hz) RR interval oscillations and sympathetic low-frequency oscillations of BP. We compared values before and during cooling using analysis of variance with post hoc analysis; (significance, P<0.05). RESULTS: Forehead skin temperature dropped by 5.5+/-2.2 degrees C with cooling onset and by 12.4+/-3.2 degrees C after 20 minutes. Tympanic temperature decreased by 4.7+/-0.7 degrees C within 40 minutes, and rectal temperature by only 0.3+/-0.3 degrees C after 120 minutes. Systolic and diastolic BP increased immediately on cooling onset and rose by 15.3+/-20.8 mm Hg and 16.5+/-13.4 mm Hg (P=0.004) after 120 minutes, whereas skin blood flow fell significantly during cooling. RR intervals and parasympathetic RR interval high-frequency powers increased with cooling onset and were significantly higher after 60 and 120 minutes than they were before cooling. CONCLUSIONS: Head and neck cooling prominently reduced tympanic temperature and thus might also induce intracerebral hypothermia; however, it did not significantly lower body core temperature. Profound skin temperature decrease induced sympathetically mediated peripheral vasoconstriction and prominent BP increases that are not offset by simultaneous parasympathetic heart rate slowing. Prominent peripheral vasoconstriction and BP increase must be considered as possibly harmful during head and neck cooling.