Skeletal muscle electrical stimulation improves baroreflex sensitivity and heart rate variability in heart failure rats

Rucatti, Ananda Lazzarotto; Jaenisch, Rodrigo Boemo; Rossato, Douglas Dalcin; Bonetto, Jéssica Hellen Poletto; Ferreira, Janaina Barcellos; Xavier, Léder Leal; Sonza, Anelise; Lago, Pedro Dal

doi:10.1016/j.autneu.2015.08.008

Cited by 13 publications

(7 citation statements)

References 35 publications

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“…Such ANS stimulation might explain the partial restoration of the organ function. According to several studies, ANS stimulation reduces sepsis-related mortality (6,23,39). We showed that WJ-MSCs attenuated ANS dysfunction by exerting a neuroprotective effect, even when the CAP was blocked.…”

Section: Discussionmentioning

confidence: 88%

Wharton’s jelly-derived mesenchymal stem cells attenuate sepsis-induced organ injury partially via cholinergic anti-inflammatory pathway activation

Capcha

Rodrigues

Moreira

et al. 2020

American Journal of Physiology-Regulatory, Integrative and Comp

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Sepsis induces organ dysfunction due to overexpression of the inflammatory host response, resulting in cardiopulmonary and autonomic dysfunction, thus increasing the associated morbidity and mortality. Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs) express genes and secrete factors with anti-inflammatory properties, neurological and immunological protection, as well as improve survival in experimental sepsis. The cholinergic anti-inflammatory pathway (CAP) is mediated by α7-nicotinic acetylcholine receptors (α7nAChRs), which play an important role in the control of systemic inflammation. We hypothesized that WJ-MSCs attenuate sepsis-induced organ injury in the presence of an activated CAP pathway. To confirm our hypothesis, we evaluated the effects of WJ-MSCs as a treatment for cardiopulmonary injury and on neuroimmunomodulation. Male Wistar rats were randomly divided into four groups: control (sham-operated); cecal ligation and puncture (CLP) alone; CLP+WJ-MSCs (1 × 106 cells, at 6 h post-CLP); and CLP+methyllycaconitine (MLA)+WJ-MSCs (5 mg/kg body wt, at 5.5 h post-CLP, and 1 × 106 cells, at 6 h post-CLP, respectively). All experiments, including the assessment of echocardiographic parameters and heart rate variability, were performed 24 h after CLP. WJ-MSC treatment attenuated diastolic dysfunction and restored baroreflex sensitivity. WJ-MSCs also increased cardiac sympathetic and cardiovagal activity. WJ-MSCs reduced leukocyte infiltration and proinflammatory cytokines, effects that were abolished by administration of a selective α7nAChR antagonist (MLA). In addition, WJ-MSC treatment also diminished apoptosis in the lungs and spleen. In cardiac and splenic tissue, WJ-MSCs downregulated α7nAChR expression, as well as reduced the phospho-STAT3-to-total STAT3 ratio in the spleen. WJ-MSCs appear to protect against sepsis-induced organ injury by reducing systemic inflammation, at least in part, via a mechanism that is dependent on an activated CAP.

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Section: Discussionmentioning

confidence: 88%

Wharton’s jelly-derived mesenchymal stem cells attenuate sepsis-induced organ injury partially via cholinergic anti-inflammatory pathway activation

Capcha

Rodrigues

Moreira

et al. 2020

American Journal of Physiology-Regulatory, Integrative and Comp

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“…), intubated and artificially ventilated. For MI, ligation of the left coronary artery was performed, as well as sham operations as previously described [7,10,11] . After the surgery, the rats received a single injection of monofenew (0.05 ml/100 g) and gentamicin (0.05 ml/100 g).…”

Section: Methodsmentioning

confidence: 99%

“…Then, the catheter was positioned inside the left ventricle (LV), and the pulse wave was monitored using the typical graphic registration of ventricular pressure and recorded for 5 min. These data were used to determine mean arterial pressure (MAP), heart rate (HR), left ventricular systolic pressure (LVSP), left ventricular maximum change in pressure over time (+dP/dt max ), left ventricular minimum change in pressure over time (-dP/dt max ), and left ventricular end-diastolic pressure (LVEDP) [7,11] .…”

Section: Methodsmentioning

confidence: 99%

Respiratory Muscle Training Improves Diaphragm Citrate Synthase Activity and Hemodynamic Function in Rats with Heart Failure

Jaenisch¹,

Bertagnolli²,

Borghi‐Silva³

et al. 2017

Braz J Cardiovasc Surg

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Introduction Enhanced respiratory muscle strength in patients with heart failure positively alters the clinical trajectory of heart failure. In an experimental model, respiratory muscle training in rats with heart failure has been shown to improve cardiopulmonary function through mechanisms yet to be entirely elucidated.ObjectiveThe present report aimed to evaluate the respiratory muscle training effects in diaphragm citrate synthase activity and hemodynamic function in rats with heart failure.MethodsWistar rats were divided into four experimental groups: sedentary sham (Sed-Sham, n=8), trained sham (RMT-Sham, n=8), sedentary heart failure (Sed-HF, n=7) and trained heart failure (RMT-HF, n=7). The animals were submitted to a RMT protocol performed 30 minutes a day, 5 days/week, for 6 weeks.ResultsIn rats with heart failure, respiratory muscle training decreased pulmonary congestion and right ventricular hypertrophy. Deleterious alterations in left ventricular pressures, as well as left ventricular contractility and relaxation, were assuaged by respiratory muscle training in heart failure rats. Citrate synthase activity, which was significantly reduced in heart failure rats, was preserved by respiratory muscle training. Additionally, a negative correlation was found between citrate synthase and left ventricular end diastolic pressure and positive correlation was found between citrate synthase and left ventricular systolic pressure.ConclusionRespiratory muscle training produces beneficial adaptations in the diaphragmatic musculature, which is linked to improvements in left ventricular hemodynamics and blood pressure in heart failure rats. The RMT-induced improvements in cardiac architecture and the oxidative capacity of the diaphragm may improve the clinical trajectory of patients with heart failure.

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“…The lipid droplet area was calculated using a stereological tool and the point counting method (Weibel 1979[ 32 ]; Zacharová and Kubínová, 1995[ 34 ]; Ilha et al, 2008[ 15 ]; Lazzarotto Rucatti et al, 2015[ 19 ]; Fernandes et al, 2016[ 13 ]). A grid mask containing an area/point value of 6518.5 nm 2 was placed over the lipid droplet image (13500×).…”

Section: Methodsmentioning

confidence: 99%

Octyl gallate induces hepatic steatosis in HepG2 cells through the regulation of SREBP-1c and PPAR-γ gene expression

Lima

Levorse

Garcia

et al. 2020

EXCLI Journal; 19:Doc962; ISSN 1611-2156

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Skeletal muscle electrical stimulation improves baroreflex sensitivity and heart rate variability in heart failure rats

Cited by 13 publications

References 35 publications

Wharton’s jelly-derived mesenchymal stem cells attenuate sepsis-induced organ injury partially via cholinergic anti-inflammatory pathway activation

Wharton’s jelly-derived mesenchymal stem cells attenuate sepsis-induced organ injury partially via cholinergic anti-inflammatory pathway activation

Respiratory Muscle Training Improves Diaphragm Citrate Synthase Activity and Hemodynamic Function in Rats with Heart Failure

Octyl gallate induces hepatic steatosis in HepG2 cells through the regulation of SREBP-1c and PPAR-γ gene expression

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