| ORIGINAL ARTICLE |
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| Year : 2019 | Volume
: 62
| Issue : 2 | Page : 86-92 |
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Differential effects of sympatholytic agents on the power spectrum of rats during the cooling-induced hemodynamic perturbations
Yung-Nien Yang1, Hsien-Lung Tsai2, Yu-Chieh Lin3, Yia-Ping Liu4, Che-Se Tung3
1 Heart Center, Cheng Hsin General Hospital, Taipei, Taiwan
2 Department of Emergency, Cheng Hsin General Hospital, Taipei, Taiwan
3 Department of Medical Research and Education, Cheng Hsin General Hospital, Taipei, Taiwan
4 Department of Physiology, National Defense Medical Center; Department of Psychiatry, Cheng Hsin General Hospital, Taipei, Taiwan
Correspondence Address:
Prof. Che-Se Tung
Division of Medical Research and Education, Cheng Hsin General Hospital, No. 45, Cheng Hsin St., Beitou, Taipei 11280
Taiwan
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/CJP.CJP_7_18
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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.
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