Low-dose atropine amplifies cardiac vagal modulation and increases dynamic baroreflex function in humans.
Auton Neurosci. 2005; 118(1-2):108-15 (ISSN: 1566-0702)
Cho SK; Hwang GS; Kim YK; Huh IY; Hahm KD; Han SM
Department of Anesthesiology and Pain Management, Asan Medical Center, College of Medicine, University of Ulsan, 388-1 Pungnap-dong, Songpa-gu, Seoul, 138-736, South Korea.
It has been previously known that low-dose atropine (LDA) enhances vagal outflow to the heart. To demonstrate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability, we evaluated the effect of vagal cardiac stimulation with administration of LDA on ABP fluctuation during dynamic hypertensive and hypotensive stimuli. We assessed changes in RR interval (RRI), ABP, power spectral densities of heart rate variability (HRV) and ABP variability, and spontaneous baroreflex sensitivity (BRS) in 16 healthy volunteers before and after administration of LDA (2 microg/kg). Transient hypertension was induced by phenylephrine (2 microg/kg), whereas hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. LDA elicited bradycardia and significantly increased high-frequency (HF, 0.15-0.4 Hz) power of HRV and spontaneous BRS, as determined by transfer function analysis. The increase in systolic blood pressure (SBP) after phenylephrine administration was significantly attenuated by LDA (16+/-2 to 11+/-3 mmHg, P<0.005) and was associated with the augmented reflex bradycardia, whereas the decrease in SBP after cuff deflation was not affected (14+/-5 to 13+/-5 mmHg) with the augmented reflex tachycardia. Increases of HF HRV were correlated significantly and negatively with the increased SBP induced by phenylephrine before and after LDA (r=-0.502, P<0.05). These data suggest that the increased vagal cardiac function induced by LDA augments HR buffering effects, and is important in minimizing arterial pressure fluctuation during dynamic hypertensive stimuli.