Differential Effects of Sympatholytic Agents on the Power Spectrum of Rats during the Cooling-Induced Hemodynamic Perturbations

Abstract

Cold stress-elicited hemodynamic perturbations (CEHP) its underlying mechanisms still not clear. We examined the difference of two effector arms of sympathetic outflows, the sympathoadrenal system, and postganglionic sympathetic neurons, their role in CEHP genesis by using two sympatholytic agents, fusaric acid (FA, dopamine-β-hydroxylase inhibitor) and guanethidine (GUA, norepinephrine-depleting drug). Adult male Sprague-Dawley rats were divided into three groups (n = 6, each), an intraperitoneal injection of control vehicle saline or FA or GUA and then all rats were subjected to a 10-min CS trial. Systolic blood pressure (SBP), heart rate (HR), dicrotic notch (Dn), power spectrum of blood pressure variability and HR variability (BPV, HRV), and coherence spectrum at very-low, low, and high frequency regions (VLF: 0.02–0.2 Hz, LF: 0.2–0.6 Hz, and HF: 0.6–3.0 Hz) were monitored using telemetry throughout the experiment course. We observed both FA and GUA attenuated SBP and HR and the spectral powers of BPV at VLF, LF, and HF in both baseline (PreCS) and cold stimuli (CS) conditions, but apparently, FA exerted stronger effects than GUA did. Both FA and GUA generally attenuated the responses of CS-induced pressor and tachycardia and the CS-increased VLFBPV, LFBPV, and HFBPV, but different effects between FA and GUA, when compared with control vehicle under CS. FA reduced the CS-reduced VLFHRV and the CS-increased LFBPV and HFBPV more than GUA did. We further observed in both PreCS and CS, GUA but not FA increased HFHRV; FA reduced but apparently, GUA increased the occurrence of Dn. Finally, we observed FA weakened, but GUA strengthened the coherence between BPV and HRV at both LF and HF regions. Taken together, the different effects between FA and GUA on CEHP indicate a role of the sympathoadrenal mechanism in response to CS.

Heart rate variability in male rats

“…In control group, HRV was measured telemetrically before the experiment itself in awake and freely moving male animals (Carll et al, 2012; Choudhary et al, 2018; Couderc et al, 2002; Fazan Jr. et al, 2015; Hazari et al, 2021; Imai et al, 2008; Koizumi et al, 2011; Lamb et al, 2012; Lin et al, 2016; Mamalyga, 2013; Mangin et al, 1998; Pereira‐Junior et al, 2006, 2010; Saalfield & Spear, 2014; Shi et al, 2017; Soler et al, 2018; Towa et al, 2004; Tsai et al, 2020; Yang et al, 2019; Zajączkowski et al, 2014). If we assume that the location of implantation (subcutaneous on the back or intra‐abdominal) and the length of recovery do not play a role, then theoretically we can assume that these values could approach the “missing” reference values, although unfortunately, only for males and at the given time of measurement.…”