Baroreflex Sensitivity Impairment Is Associated With Cardiac Diastolic Dysfunction in Rats

Mostarda, Cristiano Teixeira; Moraes‐Silva, Ivana C.; Moreira, Edson Dias; Medeiros, Alessandra; Piratello, Aline Cristina; Consolim‐Colombo, Fernanda Marciano; Caldini, Élia Garcia; Brum, Patrícia Chakur; Krieger, Eduardo Moacyr; Irigoyen, Maria Cláudia

doi:10.1016/j.cardfail.2011.02.007

Cited by 28 publications

(29 citation statements)

References 30 publications

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“…The rats were anesthetized (80 mg/kg ketamine and 12 mg/kg xylazine ip), and images were obtained with a 10 -14-MHz linear transducer in a SEQUOIA 512 (ACUSON, Mountain View, CA) for measurements of LV ejection fraction (LVEF), LV fractional shortening, left atria diameter, and isovolumetric relaxation time (IVRT), as described previously (5,8,22). MI was defined by echocardiography as any abnormal segmental wall motion, including hypokinesis, akinesis, and dyskinesis.…”

Section: Methodsmentioning

confidence: 99%

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Increase in cholinergic modulation with pyridostigmine induces anti-inflammatory cell recruitment soon after acute myocardial infarction in rats

Rocha

Ribeiro

França

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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-We tested the hypothesis that an increase in the anti-inflammatory cholinergic pathway, when induced by pyridostigmine (PY), may modulate subtypes of lymphocytes (CD4ϩ, CD8ϩ, FOXP3ϩ) and macrophages (M1/M2) soon after myocardial infarction (MI) in rats. Wistar rats, randomly allocated to receive PY (40 mg·kg Ϫ1 ·day Ϫ1 ) in drinking water or to stay without treatment, were followed for 4 days and then were subjected to ligation of the left coronary artery. The groupsdenominated as the pyridostigmine-treated infarcted (IP) and infarcted control (I) groups-were submitted to euthanasia 3 days after MI; the heart was removed for immunohistochemistry, and the peripheral blood and spleen were collected for flow cytometry analysis. Noninfarcted and untreated rats were used as controls (C Group). Echocardiographic measurements were registered on the second day after MI, and heart rate variability was measured on the third day after MI. The infarcted groups had similar MI areas, degrees of systolic dysfunction, blood pressures, and heart rates. Compared with the I Group, the IP Group showed a significant higher parasympathetic modulation and a lower sympathetic modulation, which were associated with a small, but significant, increase in diastolic function. The IP Group showed a significant increase in M2 macrophages and FOXP3 ϩ cells in the infarcted and peri-infarcted areas, a significantly higher frequency of circulating Treg cells (CD4 ϩ CD25 ϩ FOXP3 ϩ ), and a less extreme decrease in conventional T cells (CD25 ϩ FOXP3 Ϫ ) compared with the I Group. Therefore, increasing cholinergic modulation with PY induces greater anti-inflammatory cell recruitment soon after MY in rats. myocardial infarction; T lymphocytes; macrophage activation; anticholinesterase drugs; cholinergic anti-inflammatory reflex

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Section: Methodsmentioning

confidence: 99%

“…After echocardiographic evaluation, while the rats were still under anesthesia, a catheter filled with 0.06 ml of saline solution was implanted into the femoral artery of the rats, as described in another article (8,22).…”

Section: Methodsmentioning

confidence: 99%

Increase in cholinergic modulation with pyridostigmine induces anti-inflammatory cell recruitment soon after acute myocardial infarction in rats

Rocha

Ribeiro

França

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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“…2, 19) Patients with heart failure and preserved ejection fraction (HFpEF) are supersensitive to volume overload, and flash pulmonary edema often occurs transiently which is rapidly resolved by intravascular volume reduction. 20) The stressed blood volume and systemic blood pressure are controlled by several systems.…”

Section: 14-17)mentioning

confidence: 99%

Heart Failure as a Disruption of Dynamic Circulatory Homeostasis Mediated by the Brain

Kishi

2016

Int. Heart J.

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SummaryCirculatory homeostasis is associated with interactions between multiple organs, and the disruption of dynamic circulatory homeostasis could be considered as heart failure. The brain is the central unit integrating neural and neurohormonal information from peripheral organs and controlling peripheral organs using the autonomic nervous system. Heart failure is worsened by abnormal sympathoexcitation associated with baroreflex failure and/or chemoreflex activation, and by vagal withdrawal, and autonomic modulation therapies have benefits for heart failure. Recently, we showed that baroreflex failure induces striking volume intolerance independent of left ventricular dysfunction. Many studies have indicated that an overactive renin-angiotensin system, excess oxidative stress and excess inflammation, and/or decreased nitric oxide in the brain cause sympathoexcitation in heart failure. We have demonstrated that angiotensin II type 1 receptor (AT 1 R)-induced oxidative stress in the rostral ventrolateral medulla (RVLM), which is known as a vasomotor center, causes prominent sympathoexcitation in heart failure model rats. Interestingly, systemic infusion of angiotensin II directly affects brain AT 1 R with sympathoexcitation and left ventricular diastolic dysfunction. Moreover, we have demonstrated that targeted deletion of AT 1 R in astrocytes strikingly improved survival with prevention of left ventricular remodeling and sympathoinhibition in myocardial infarction-induced heart failure. From these results, we believe it is possible that AT 1 R in astrocytes, not in neurons, have a key role in the pathophysiology of heart failure. We would like to propose a novel concept that the brain works as a central processing unit integrating neural and hormonal input, and that the disruption of dynamic circulatory homeostasis mediated by the brain causes heart failure. (Int Heart J 2016; 57: 145-149)

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“…A DSA crônica está associada à maior lesão de órgãos-alvo na hipertensão arterial (MIAO et al, 2006;MORAES-SILVA, I. et al, 2010), à disfunção diastólica (MOSTARDA et al, 2011) No entanto, também existem evidências de que a disautonomia poderia ser anterior e causadora das alterações metabólicas (ROCCHINI et al, 1999). Há evidencias que em jovens adultos o aumento da atividade simpática está diretamente relacionado com ganho de peso e resistência à insulina (JULIUS et al, 2000).…”

Section: 2)sistema Nervoso Autônomo E Regulação Cardiovascularunclassified

Curso temporal das alterações autonômicas e metabólicas da hipertensão por sobrecarga de frutose: papel do barorreflexo

Santos¹

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Autorizo a reprodução e divulgação total ou parcial deste trabalho, por qualquer meio convencional ou eletrônico, para fins de estudo e pesquisa, desde que citada a fonte. The increased consumption of fructose in recent decades is closely associated with the higher incidence of obesity, metabolic syndrome and associated comorbidities, such as Dyslipidemia, Dysautonomia, and diabetes. However, the literature does not present temporal characterization of the events that occur until the establishment of the diseases. On this basis, this work aims to evaluate the temporal autonomic and metabolic changes in metabolic syndrome model induced by fructose overload, with emphasis on the role of the baroreflex, here tested using sinoaortic denervation. Additionally, we intend to identify in this model, if autonomic changes precede or follow the metabolic changes. Four experimental groups were used (rats), followed by 90 days: control (C), treated with fructose (F), sinoaortic denervated (D) and denervated treated with fructose (DF). Fructose overload was performed using drinking water solution (10%). Blood pressure recording was performed via radio telemetry for 13 weeks. Fructose was able to promote development of metabolic syndrome, causing blood pressure, fasting blood glucose and abdominal fat increase and changing lipid profile (from the seventh week to thirteenth week of treatment). Dados Internacionais de Catalogação na Publicação (CIP)PreparadaAutonomic changes, characterized by increased cardiac and peripheral sympathetic modulation, occurred in the second week of Protocol. Fructose group presented changes of renal function and inflammation. The baroreflex seems to participate in the changes induced by fructose during the development of the metabolic syndrome, since his absence determines changes in various metabolic parameters in addition to the expected hemodynamic. Additionally, fructose treatment induced late functional impairment of blood pressure reflex control. Based on our results we can conclude that the changes in autonomic control precede and probably contribute to the metabolic changes induced by the excessive consumption of fructose.Descriptors: autonomic nervous system diseases; metabolic syndrome X;inflammation; blood pressure; fructose; sympathetic nervous system; baroreflex. (ELLIOTT et al., 2002;STANHOPE et al., 2015). Relação de figuras Relação de tabelasExperimentalmente, um modelo simples para indução de SM é através de ração comercial rica em frutose (60%) (HWANG et al., 1987) ou adicionando frutose na água de beber (10 a 20%) (DAI & MCNEILL, 1995). Animais que são tratados com frutose, independentemente da via de administração, apresentam distúrbios semelhantes aqueles encontrados na SM, como resistência à insulina, aumento dos triglicerídeos e da insulina plasmática e hipertensão (YOSHIDA et al., 2003;BRITO et al., 2008;ARAUJO et al., 2015).Nesse contexto, nosso grupo tem trabalhado com animais tratados com frutose, demonstrando diversas alterações autonômicas, como menor atividade va...

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Baroreflex Sensitivity Impairment Is Associated With Cardiac Diastolic Dysfunction in Rats

Cited by 28 publications

References 30 publications

Increase in cholinergic modulation with pyridostigmine induces anti-inflammatory cell recruitment soon after acute myocardial infarction in rats

Increase in cholinergic modulation with pyridostigmine induces anti-inflammatory cell recruitment soon after acute myocardial infarction in rats

Heart Failure as a Disruption of Dynamic Circulatory Homeostasis Mediated by the Brain

Curso temporal das alterações autonômicas e metabólicas da hipertensão por sobrecarga de frutose: papel do barorreflexo

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