Abstract
In congestive heart failure (CHF), while resting parasympathetic activity becomes reduced, parasympathetically-mediated responses to stressors have not been described. This study aimed to (1) elucidate the effect of CHF on fear bradycardia, a parasympathetically-mediated response, and (2) examine if brain oxidative stress of CHF mediates fear bradycardia. White noise sound (WNS) exposure to conscious rats induced freezing behavior and elicited bradycardia. WNS exposure-elicited bradycardia was greater in rats with CHF than in controls. Superoxide dismutase mimetics administered in the lateral/ventrolateral midbrain periaqueductal gray (l/vlPAG), a region that contributes to the generation of fear bradycardia, had no effect on the bradycardia response in control and CHF rats. Dihydroethidium staining in situ showed that superoxide generation in the l/vlPAG of CHF rats was increased as compared to controls. These results demonstrate that CHF leads to the augmentation of fear bradycardia. Moreover, oxidative stress in the l/vlPAG of CHF unlikely mediates the augmented fear bradycardia.