Distinction between atropine-sensitive control of microvascular and cardiac oscillatory activity

This study tested whether "high frequency" oscillations (HF; >0.12 cycles/s) in microvascular flow during a vasoconstrictive challenge constitute a homeostatic cholinergic response at the level of the microvasculature or simply represent oscillations that originate at the heart and are transmitted to passive microvascular beds. Heart rate, blood pressure, respiratory rate, and laser Doppler flowmetry of the forehead and finger were monitored in healthy volunteers at baseline, during systemic infusion of phenylephrine (0.4-0.6 microg/kg/min), and during subsequent addition of intravenous atropine (< or = 2.0 mg/70 kg). Spectral-domain analysis documented that atropine-sensitive oscillatory power of the R-wave to R-wave intervals of the electrocardiogram was predominant at the respiratory frequency (0.20 Hz) at baseline and during phenylephrine infusion. In contrast, arteriolar-capillary networks of the forehead developed a prominent atropine-sensitive oscillatory peak at 0.14 +/- 0.02 Hz during phenylephrine infusion (P < 0.05 for differences in oscillatory magnitude and frequency between forehead flow and R-R intervals). The cross-power spectral density confirmed the lack of common power between forehead flow and R-R oscillations. Post hoc assessments showed that---similar to heart rate---systemic pressure and systemic flow also had persistent power at 0.20 Hz and did not develop a peak at the forehead oscillatory frequency; phenylephrine likewise did not induce atropine-sensitive oscillations in the finger, a finding attributable to adrenergic predominance in this region. We conclude that atropine-sensitive oscillatory activity in the forehead microvasculature in response to a vasoconstrictive challenge constitutes a local response that is not due to, nor associated with, mechanical transmission from the heart and proximal vasculature.