Jaenisch RB, Hentschke VS, Quagliotto E, Cavinato PR, Schmeing LA, Xavier LL, Dal Lago P. Respiratory muscle training improves hemodynamics, autonomic function, baroreceptor sensitivity, and respiratory mechanics in rats with heart failure. J Appl Physiol 111: 1664 -1670, 2011. First published September 8, 2011 doi:10.1152/japplphysiol.01245.2010.-Respiratory muscle training (RMT) improves functional capacity in chronic heart-failure (HF) patients, but the basis for this improvement remains unclear. We evaluate the effects of RMT on the hemodynamic and autonomic function, arterial baroreflex sensitivity (BRS), and respiratory mechanics in rats with HF. Rats were assigned to one of four groups: sedentary sham (n ϭ 8), trained sham (n ϭ 8), sedentary HF (n ϭ 8), or trained HF (n ϭ 8). Trained animals underwent a RMT protocol (30 min/day, 5 day/wk, 6 wk of breathing through a resistor), whereas sedentary animals did not. In HF rats, RMT had significant effects on several parameters. It reduced left ventricular (LV) end-diastolic pressure (P Ͻ 0.01), increased LV systolic pressure (P Ͻ 0.01), and reduced right ventricular hypertrophy (P Ͻ 0.01) and pulmonary (P Ͻ 0.001) and hepatic (P Ͻ 0.001) congestion. It also decreased resting heart rate (HR; P Ͻ 0.05), indicating a decrease in the sympathetic and an increase in the vagal modulation of HR. There was also an increase in baroreflex gain (P Ͻ 0.05). The respiratory system resistance was reduced (P Ͻ 0.001), which was associated with the reduction in tissue resistance after RMT (P Ͻ 0.01). The respiratory system and tissue elastance (Est) were also reduced by RMT (P Ͻ 0.01 and P Ͻ 0.05, respectively). Additionally, the quasistatic Est was reduced after RMT (P Ͻ 0.01). These findings show that a 6-wk RMT protocol in HF rats promotes an improvement in hemodynamic function, sympathetic and vagal heart modulation, arterial BRS, and respiratory mechanics, all of which are benefits associated with improvements in cardiopulmonary interaction. myocardial infarction; cardiovascular control; diaphragm; cardiopulmonary interaction THE HALLMARK SYMPTOMS OF heart failure (HF) subsequent to myocardial infarction (MI) are dyspnea and early fatigue, leading to reduced exercise tolerance and functional capacity (1). Furthermore, after MI, the neurohumoral excitation, which initially helps to preserve the cardiac output of patients who have systolic dysfunction, becomes deleterious with the persistence of cardiac dysfunction (12). In HF, the neurohumoral excitation is characterized by sympathetic hyperactivity and the attenuation of parasympathetic activity (12), which is associated with blunted baroreflex sensitivity (BRS) (30). In this context, impaired short-term control of arterial pressure (AP) and decreased heart-rate variability (HRV) (30) have been associated with an increased risk of sudden death of cardiac origin (45) and postinfarct mortality, regardless of the ejection fraction or ventricular arrhythmias (30).Together with the cardiovascular alterations, changes in the r...

Glutamate and γ-aminobutyric acid (GABA) participate in central cardiovascular control, and are found in the rat posterodorsal medial amygdala (MePD), an area of the forebrain that modulates emotional/social behaviors. Here we tested whether these neurotransmitters in the MePD could change the basal activity, chemoreflex, and baroreflex cardiovascular responses in awake rats. Power spectral analysis and symbolic analysis were used to evaluate these responses. Microinjections of saline, glutamate (2 µg), or GABA (61 ng or 100 µg; n = 5-7 rats per group) did not affect basal parameters or chemoreflex responses. However, baroreflex responses showed marked changes. Glutamate increased power spectral and symbolic sympathetic indexes related to both cardiac and vascular modulations (P < 0.05). In turn, the displacement of the baroreflex half-maximal heart rate (HR) response was associated with a GABA (61 ng) mediated decrease in the upper plateau (P < 0.05). Administration of GABA (61 ng, but not 100 µg) also increased HR variability (P < 0.05), in association with parasympathetic activation. These data add novel evidence that the MePD can promote selective responses in the central regulation of the cardiovascular system, i.e., glutamate in the MePD evoked activation of a central sympathetic reflex adjustment, whereas GABA activated a central parasympathetic one.

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The posterodorsal medial amygdala (MePD) is responsive to androgens and participates in the integration of olfactory/vomeronasal stimuli for the display of sexual behavior in rats. Adult gonadectomy (GDX) affects the MePD structural integrity at the same time that impairs male mating behavior. At the cellular level, dendritic spines modulate excitatory synaptic transmission, strength, and plasticity. Here, we describe the effect of GDX on the number and shape of dendritic spines in the right and left MePD using confocal microscopy and 3D image reconstruction. Age-matched adult rats were intact (n = 6), submitted to a sham procedure (n = 4) or castrated and studied 90 days after GDX (n = 5). The MePD neurons have a density of 1.1 spines/dendritic μm composed of thin, mushroom-like, stubby/wide, and few ramified or atypical spines. Irrespective of brain hemisphere, GDX decreased the dendritic spine density in the MePD, but induced different effects on each spine type. That is, compared to control groups, GDX reduced (i) the number (up to 50%) of thin, mushroom-like, and ramified spines, and (ii) the size and the neck length of thin spines as well as the head diameter of ramified spines. Besides, GDX increased the number of stubby/wide and atypical spines (up to 140% and 400%, respectively). These data show that GDX promotes a cellular and synaptic reorganization in a spine-specific manner in the MePD. By altering the number and shape of these connectional elements, GDX can affect the neural transmission and hinder the function of integrated brain circuitries in the male brain.

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