Baroreceptor denervation reduces inflammatory status but worsens cardiovascular collapse during systemic inflammation

Figures

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  Figure 1. Effects of sino-aortic denervation (SAD) on mean arterial pressure (MAP), and heart rate (HR) of saline (Sal)-treated rats (panel A) and rats with SI (panel B, LPS, 1.5 mg.kg−1). Bradycardic gain during stimulation of the arterial baroreceptors (panel C) and maximal hypotensive response to LPS-induced SI (panel D). Representative recordings showing PAP, MAP (white line; top) and HR responses to i.v. injection of phenylephrine (Phe; panel E). Δ Tb (panel F) and thermal indexes (panel G). Results are presented as and mean ± SEM. *,#p < 0.05 compared with time zero and ***p < 0.0001 difference between groups using the two-way ANOVA with Tukey’s post hoc test (panel A and B). *p < 0.05 using the unpaired t test (panel C and D). **p < 0.01 using the one-way ANOVA with Tukey’s post hoc test (panel G). Control + Sal (n = 5–7), Control + LPS (n = 7–9), SAD + Sal (n = 5–9), and SAD + LPS (n = 8–9).

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  Figure 2. Variability in heart rate (HR) and in systolic arterial pressure (SAP) in the time-domain during LPS-induced SI. Standard deviation (SDNN, panel A) and root mean square of the successive differences (RMSSD, panel B) from PI series. Standard deviation (SD) from series (panel C). Control + Sal, Control + LPS, SAD + Sal, and SAD + LPS groups were evaluated 180 min after LPS administration. Results are presented as individual values and mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0,001, ****p < 0.0001 using the one-way ANOVA with Tukey’s post hoc test. Control + Sal (n = 9), Control + LPS (n = 8), SAD + Sal (n = 9), and SAD + LPS (n = 7).

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  Figure 3. Power spectral analyses of pulse interval (PI) and systolic arterial pressure (SAP) from Control + Sal, Control + LPS, SAD + Sal, and SAD + LPS groups. Representative tracings from each experimental group (panel A and B). Magnitude of low frequency (LF, panel C) and high frequency (HF, panel D) components of PI. Magnitude of HF component of LF component of PI (panel E). Results are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0,001, and ****p < 0.0001 using the one-way ANOVA with Tukey’s post hoc test. Control + Sal (n = 8), Control + LPS (n = 8), SAD + Sal (n = 9), and SAD + LPS (n = 8).

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  Figure 4. Detrended fluctuation analysis (DFA) from Control + Sal, Control + LPS, SAD + Sal, and SAD + LPS groups that where evaluated 180 min after LPS administration. Average values of α1 (panel A), α2 (panel B) and α3 (panel C) are shown. Results are presented mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0,001, ****p < 0.0001 using the one-way ANOVA with Tukey’s post hoc test. Control + Sal (n = 9), Control + LPS (n = 9), SAD + Sal (n = 8), and SAD + LPS (n = 9).

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  Figure 5. Multiscale entropy (MSE) from Control + Sal, Control + LPS, SAD + Sal and, SAD + LPS groups that where evaluated 180 min after LPS administration. Mean MSE profiles obtained from Control + Sal, SAD + Sal (panel A), Control + LPS, and SAD + LPS (panel B). Average values of entropy calculated for scales 1 and 2, 3 to 7 and 8 to 20 are shown (panel C). Results are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0,001, ****p < 0.0001 compared using the one-way ANOVA with Tukey’s post hoc test. Control + Sal (n = 9), Control + LPS (n = 9), SAD + Sal (n = 9), and SAD + LPS (n = 9).

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  Figure 6. Cumulative concentration-response curves to the α-1 adrenergic agonist [phenylephrine (Phe) panel A], Phe in presence of L-NAME, non-selective inhibitor of nitric oxide synthase, (10−4 M, panel B), Acetylcholine (ACh), endothelium-dependent vasodilator (panel C), sodium nitroprusside (SNP) endothelium-independent vasodilator (panel D). Electrical-field stimulation (EFS, panel E) from Control + Sal, Control + LPS, SAD + Sal and, SAD + LPS groups. EFS in presence of L-NAME (10−4 M, panel F) in resistance mesenteric arteries. Results are presented as mean ± SEM. *p < 0.05 using the one-way ANOVA Tukey’s post hoc test. Control + Sal (n = 4–5), Control + LPS (n = 5), SAD + Sal (n = 4), and SAD + LPS (n = 5).

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  Figure 7. Plasma (panel A, B, C, and D) and splenic levels (E–H) of pro-inflammatory and anti-inflammatory cytokines from Control + Sal, Control + LPS, SAD + Sal and SAD + LPS groups. Results are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0,001, ****p < 0.0001 using the one-way ANOVA with Tukey’s post hoc test. Control + Sal (n = 8–12), Control + LPS (n = 9–10), SAD + Sal (n = 5), and SAD + LPS (n = 7–13).

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  Figure 8. Plasma levels of corticosterone (panel A), NOx (nitrate, panel B), and norepinephrine (panel C) from Control + Sal, Control + LPS, SAD + Sal and SAD + LPS groups. Results are presented as mean values ± SEM. ****p < 0.0001 using the one-way ANOVA with Tukey’s post hoc test. Control + Sal (n = 9), Control + LPS (n = 8–9), SAD + Sal (n = 5–6), and SAD + LPS (n = 5–9).