Prolonged paradoxical sleep deprivation (PSD) and cold stress (CS) are known to cause sympathoexcitation and increase the risk of cardiovascular disease. The present study examined the effect of PSD with CS on hemodynamic perturbations by investigating blood pressure and heart rate variability (BPV and HRV) in conscious rats. Adult male Sprague-Dawley rats were divided into three groups (n = 10, each): normal sleep (NS), PSD of 72 h, and recovery sleep of 7 days after PSD. When compared with NS, PSD increased systolic blood pressure in all three conditions: before CS (PreCS), CS, and after CS (PostCS). The PSD also increased heart rate in both PreCS and PostCS. Furthermore, spectral power changes were observed throughout the experiment. The PSD increased very-low-frequency BPV in PreCS, decreased very-low-frequency HRV in CS, and increased low-frequency BPV in all three conditions. The PSD increased low-frequency HRV in PreCS, increased high-frequency BPV in both CS and PostCS, and also increased high-frequency HRV in both PreCS and CS but decreased that in PostCS. On the other hand, when compared with PSD, recovery sleep has reversed most cardiovascular changes in PSD toward the NS level. However, when compared with NS, spectral powers of very-low-frequency BPV in the recovery phase showed a lower level. These results showed that in the resting condition, PSD might evoke sympathoexcitation with a tendency to increase both very-low-frequency BPV and very-low-frequency HRV, as the intensified myogenic oscillations. However, in the CS condition, PSD evoked the sympathoexcitation yet might attenuate such myogenic oscillations.

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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