Effects of vagal denervation on cerebral blood flow regulation immediately after the onset of ventricular pacing in anesthetized rats

Figures

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  Fig. 1. Representative cardiorespiratory and CBF responses caused by ventricular pacing in a vagotomized rat. CBF was measured in the motor cortex. The gray area indicates the period of ventricular pacing at 600, 650, 700, 750, and 800 beats/min, respectively (from left to right). HR, heart rate; CBF, cerebral blood flow; AP, arterial pressure; CVP, central venous pressure; ICP, intracranial pressure; PetCO2, partial pressure of end-tidal carbon dioxide; bpm, beats/min.

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  Fig. 2. Averaged cardiorespiratory responses to ventricular pacing in the sham (□) and vagotomy groups (). The amber and dark orange areas indicate moderate and severe hypotension, respectively. The number of sham-operated rats was previously described6, except 800 bpm (ΔMAP, n = 10; ΔCVP, n = 5; ΔICP, n = 9; ΔPetCO2, n = 7). The number of vagotomized rats was as follows: ΔMAP, n = 16, 21, 21, 21, 21, and 18, respectively (from 550 to 800 bpm); ΔCVP, n = 11, 15, 14, 16, 14, and 13, respectively; ΔICP, n = 12, 17, 17, 17, 17, and 16, respectively; ΔPetCO2, n = 12, 17, 17, 17, 17, and 14, respectively. Bars are shown as mean with SD. P-values were obtained from a linear mixed model with covariates of baseline values and are in bold when statistically significant (P < 0.05). MAP, mean arterial pressure.

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  Fig. 3. Time courses of regional CBF (a) and CVC responses (b) to ventricular pacing in the vagotomy group. The gray area indicates the period of ventricular pacing at each pacing rate. The number of rats for CBF and CVC was as follows: MC, n = 7, 13, 13, 13, 13, and 11, respectively (from 550 to 800 bpm); mPFC, n = 9, 17, 17, 17, 16, and 13, respectively; amygdala, n = 7, 12, 12, 12, 11, and 9, respectively; DH, n = 9, 14, 14, 14, 14, and 8, respectively; thalamus, n = 7, 13, 13, 13, 13, and 8, respectively; HC, n = 9, 15, 15, 15, 15, and 14, respectively; VTA, n = 8, 11, 11, 11, 10, and 6, respectively; dlPAG, n = 5, 7, 7, 7, 7, and 3, respectively; PB, n = 4, 6, 6, 6, 6, and 4, respectively. Data are shown as mean ± SD. CBF, cerebral blood flow; CVC, cerebrovascular conductance; MC, motor cortex; mPFC, medial prefrontal cortex; DH, dorsal hypothalamus; HC, hippocampus; VTA, ventral tegmental area; dlPAG, dorsolateral periaqueductal gray; PB, parabrachial nucleus.

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  Fig. 4. Effects of vagotomy on regional CBF responses depending on the degree of hypotension caused by ventricular pacing. The number of sham-operated rats (□) was previously described6. The number of vagotomized rats () was as follows: moderate hypotension, n = 13, 17, 12, 14, 13, 15, 11, 7, and 6, respectively (from left to right column); severe hypotension, n = 4, 10, 4, 7, 7, 9, 5, 2, and 3, respectively. Bars are shown as mean with SD. P-values were obtained from a linear mixed model with covariates of baseline MAP and ΔMAP.

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  Fig. 5. Averaged cardiorespiratory (a) and cerebrovascular responses (b) to 5% CO2 exposure in the sham (□) and vagotomy groups (). (a) The number of rats was as follows: ΔPetCO2, 16 sham-operated rats and 18 vagotomized rats; ΔHR, 19 and 22 rats, respectively; ΔMAP, 19 and 22 rats, respectively; ΔCVP, 11 and 15 rats, respectively; ΔICP, 15 and 18 rats, respectively. Bars are shown as mean with SD. (b) The number of sham-operated rats was previously described6. The number of vagotomized rats was as follows: response time, n = 9, 7, 12, 11, 12, 12, 11, 7, and 6, respectively (from left to right column); CO2 reactivity, n = 11, 14, 12, 10, 10, 12, 10, 6, and 5, respectively. Bars are shown as mean with SD. P-values were obtained from a linear mixed model with/without a covariate of PetCO2 responses.

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  Fig. 6. Effect of vagotomy on the cardiac arterial baroreflex caused by phenylephrine. The sham group (□) and the vagotomy group () comprised 17 and 21 rats, respectively. Bars are shown as mean with SD. P-values < 0.05 are in bold.