Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos

Bruder‐Nascimento, Thiago; Campos, Dijon Henrique Salomé de; Leopoldo, André Soares; Okoshi, Katashi; Cordellini, Sandra; Cicogna, Antônio Carlos

doi:10.1590/s0066-782x2012005000082

Cited by 9 publications

(10 citation statements)

References 35 publications

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“…Myocardial function was evaluated by studying isolated papillary muscles from the LV. This procedure has been utilized by various authors 9 , 17 , 29 . This preparation allows us to measure the capacity of cardiac muscle to shorten and develop force independently of influences that can modify in vivo mechanical performance of the myocardium, such as heart rate, preload, and afterload.…”

Section: Methodsmentioning

confidence: 99%

Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway

Campos

Leopoldo

Nascimento

et al. 2014

Arquivos Brasileiros De Cardiologia

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BackgroundObesity is defined by excessive accumulation of body fat relative to lean tissue. Studies during the last few years indicate that cardiac function in obese animals may be preserved, increased or diminished.ObjectiveStudy the energy balance of the myocardium with the hypothesis that the increase in fatty acid oxidation and reduced glucose leads to cardiac dysfunction in obesity.Methods30-day-old male Wistar rats were fed standard and hypercaloric diet for 30 weeks. Cardiac function and morphology were assessed. In this paper was viewed the general characteristics and comorbities associated to obesity. The structure cardiac was determined by weights of the heart and left ventricle (LV). Myocardial function was evaluated by studying isolated papillary muscles from the LV, under the baseline condition and after inotropic and lusitropic maneuvers: myocardial stiffness; postrest contraction; increase in extracellular Ca2+ concentration; change in heart rate and inhibitor of glycolytic pathway.ResultsCompared with control group, the obese rats had increased body fat and co-morbities associated with obesity. Functional assessment after blocking iodoacetate shows no difference in the linear regression of DT, however, the RT showed a statistically significant difference in behavior between the control and the obese group, most notable being the slope in group C.ConclusionThe energy imbalance on obesity did not cause cardiac dysfunction. On the contrary, the prioritization of fatty acids utilization provides protection to cardiac muscle during the inhibition of glycolysis, suggesting that this pathway is fewer used by obese cardiac muscle.

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Section: Methodsmentioning

confidence: 99%

Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway

Campos

Leopoldo

Nascimento

et al. 2014

Arquivos Brasileiros De Cardiologia

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“…The glands and LV were removed, dissected and weighed. Cardiac hypertrophy was assessed by using the LV/tibia (mm) ratio and, on echocardiography, the LV (g)/final body weight (FBW) ratio, according to our previous study 7 , 8 , 13 .…”

Section: Methodsmentioning

confidence: 99%

“…The literature and previous data from our laboratory have shown that stress induces cardiac alterations, such as fibrosis, systolic and diastolic left ventricle (LV) dysfunction and Ca 2+ transit alteration 6 , 9 - 13 . Moreover, cardiovascular changes are not restricted only to the heart, some evidence implicates that different types of acute stress induce modulated vascular response to different agonists, such as increased acetylcholine response and decreased contractile effect of noradrenaline, which are nitric oxide (NO) and endothelium-dependent 7 , 14 - 16 .…”

Section: Introductionmentioning

confidence: 99%

Chronic Stress Improves NO- and Ca2+ Flux-Dependent Vascular Function: A Pharmacological Study

Bruder‐Nascimento¹,

Campos²,

Cicogna³

et al. 2014

Arquivos Brasileiros De Cardiologia

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BackgroundStress is associated with cardiovascular diseases.ObjectiveThis study aimed at assessing whether chronic stress induces vascular alterations, and whether these modulations are nitric oxide (NO) and Ca2+ dependent.MethodsWistar rats, 30 days of age, were separated into 2 groups: control (C) and Stress (St). Chronic stress consisted of immobilization for 1 hour/day, 5 days/week, 15 weeks. Systolic blood pressure was assessed. Vascular studies on aortic rings were performed. Concentration-effect curves were built for noradrenaline, in the presence of L-NAME or prazosin, acetylcholine, sodium nitroprusside and KCl. In addition, Ca2+ flux was also evaluated.ResultsChronic stress induced hypertension, decreased the vascular response to KCl and to noradrenaline, and increased the vascular response to acetylcholine. L-NAME blunted the difference observed in noradrenaline curves. Furthermore, contractile response to Ca2+ was decreased in the aorta of stressed rats.ConclusionOur data suggest that the vascular response to chronic stress is an adaptation to its deleterious effects, such as hypertension. In addition, this adaptation is NO- and Ca2+-dependent. These data help to clarify the contribution of stress to cardiovascular abnormalities. However, further studies are necessary to better elucidate the mechanisms involved in the cardiovascular dysfunction associated with stressors. (Arq Bras Cardiol. 2014; [online].ahead print, PP.0-0)

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“…Similarly, the number of patients suffering from moderate to high levels of stress has been increasing. Evidence suggests that chronic stress may induce hypertension 1) , although the underlying mechanisms remain unclear. The amygdala in the limbic system induces emotion, and the central nucleus of the amygdala (CeA) is associated with the induction of negative emotions due to mental stress 2) .…”

Section: Introductionmentioning

confidence: 99%

Effects of bilateral lesions in the central amygdala on spontaneous baroreceptor reflex in conscious rats

Tsukioka

Yamanaka

Waki

2019

JPFSM

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The amygdala induces emotion and controls the cardiovascular system. We previously found that lesions in the central nucleus of amygdala (CeA), which is associated with negative emotion, chronically increase the arterial pressure (AP); however, the mechanism involved in this process remains unclear. In this study we compared the heart rate (HR), high frequency (HF) component of HR variability as an index of cardiac vagal outflow, and spontaneous baroreceptor reflex gain (sBRG) before and after the occurrence of bilateral lesions in CeA for further understanding of cardiovascular regulation by CeA. The results showed that CeA lesions induced a chronic decrease in HR and increase in sBRG, suggesting that CeA regulates the autonomic nervous system. Taken together with our previous results, CeA was shown to control AP and HR as well as baroreflex gain; however, the mechanisms controlling basal AP through CeA are likely to be independent of mechanisms for baroreflex gain control. These contradictory findings may partially explain the known diverse hemodynamic patterns of the amygdala in response to a variety of stress conditions.

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Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos

Abstract: Background: Chronic stress is associated with cardiac remodeling; however the mechanisms have yet to be clarified.

Cited by 9 publications

References 35 publications

Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway

Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway

Chronic Stress Improves NO- and Ca2+ Flux-Dependent Vascular Function: A Pharmacological Study

Effects of bilateral lesions in the central amygdala on spontaneous baroreceptor reflex in conscious rats

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