Autonomic neuroscience : basic & clinical
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We examined the Hurst exponent of heart rate time series and its relation with the subjective measures of valence and arousal in two groups of subjects. The electrocardiogram (ECG) and the subjective valence and arousal were measured during the administration of emotional film stimuli (happiness, sadness, anger and fear). The results showed that there is a difference in the Hurst exponent for the happiness and sadness conditions but not between the negative emotion conditions (sadness, anger and fear). This seems to indicate that the Hurst exponent is an indicator of subjective valence.
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Obesity is associated with reduced heart rate variability (HRV), reflecting detrimental changes in cardiac regulation by the autonomic nervous system (ANS). Weight loss reverses this change and ANS dysfunction is thought to have a role in obesity-related cardiac pathology. Few studies have examined the influence of weight-reduction (bariatric) surgery on cardiac autonomic control. This study therefore sought to assess longitudinal changes in indices of cardiac autonomic control following two types of bariatric procedure, laparascopic gastric banding (LGB) and biliopancreatic diversion (BPD). ⋯ This pilot study suggests that the mechanism responsible for improving cardiac regulation following bariatric surgery might be the weight loss itself. Furthermore, post-surgery improvement in QTVI implies that weight loss reduces the risk of ventricular arrhythmic events.
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The present study has investigated the effect of blockade of nitric oxide synthesis on cardiovascular autonomic adaptations induced by aerobic physical training using different approaches: 1) double blockade with methylatropine and propranolol; 2) systolic arterial pressure (SAP) and heart rate variability (HRV) by means of spectral analysis; and 3) baroreflex sensitivity. ⋯ Our results showed that nitric oxide synthesis blockade impaired the cardiovascular autonomic adaptations induced by previous aerobic physical training in rats that might be, at least in part, ascribed to a decreased baroreflex sensitivity.
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Studies have shown that the dorsomedial hypothalamus (DMH) is a key region in the descending pathways mediating the cardiovascular response to emotional stress. We have recently demonstrated that the lateral/dorsolateral periaqueductal gray (l/dlPAG) is an important synaptic relay in mediating the tachycardic effect produced by activation of DMH neurons. This synaptic relay is mediated via NMDA excitatory amino acid receptors. ⋯ The tachycardic and pressor responses evoked by air jet stress paradigm were also attenuated after treatment with 8-OH-DPAT in the l/dlPAG. The increases in heart rate and arterial pressure produced by microinjection of the excitatory amino acid receptor agonist, NMDA, into the l/dlPAG were largely reduced (by 94% and 73%, respectively) after treatment in the same region with 8-OH-DPAT. Taken together, our findings indicate that 5-HT(1A) receptors at the lateral dorsolateral PAG play a significant role in modulating the descending cardiovascular pathways from the dorsomedial hypothalamus and consequently the cardiovascular response to emotional stress.
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Sympathetic adrenergic nerves originating in the superior cervical ganglia innervate cerebral blood vessels. The present study aimed to characterize olfactory bulb blood flow changes in response to cervical sympathetic trunk (CST) stimulation. Further, we compared the sympathetic control of olfactory bulb blood flow in adult (4-6 mo) and aged (18-21 mo) Wistar rats. ⋯ Blood flow was significantly decreased from pre-stimulus flow in both adult and aged rats, and the stimulus-induced changes in flow were larger in adult compared with aged rats. Blood flow responses were abolished by i.v. administration of the alpha-adrenergic blocker phenoxybenzamine, in both age groups. These results indicate that blood vessels in the rat olfactory bulb are constricted by sympathetic nerve fibers via activation of alpha-adrenergic receptors, and the effectiveness of this regulation declines in aged rats.