We previously reported that cholinergic stimulation with pyridostigmine (PY) induces anti-inflammatory cell recruitment soon after myocardial infarction (MI). In this study, we evaluated the anti-inflammatory effects of PY during the proliferative phase of cardiac repair by analyzing the infiltration of macrophages, Treg lymphocytes, oxidative stress and inflammatory cytokines. Wistar rats underwent control sham surgery or ligation of the left coronary artery and were randomly allocated to remain untreated (untreated infarcted group, I) or to receive PY (30 mg·kg(−1)·day(−1)) in the supplied water (infarcted treated group, I + PY). Blood pressure and heart rate variability were registered at day 5 post-MI. The animals were euthanized 7 days after thoracotomy, when the hearts were removed and processed for immunohistochemistry (CD68, CD206, FOXP3), cytokines (IL-1β, IL-6, IL-10, TNF-α) and oxidative stress (superoxide dismutase, catalase, glutathione peroxidase, lipidic and protein peroxidation). PY treatment increased parasympathetic modulation, M2 macrophages and the anti-oxidant enzyme activity but reduced protein oxidation (carbonyls) and the concentration of IL-1β, IL-6, TNF-α and IL-10. Cholinergic stimulation induces parasympathetic neuro-immune modulation and anti-inflammatory cell enrollment as well as prevents oxidative stress and cytokine production after MI.
Our data are the first to show that isolated HC is characterized by an increase in cardiac and vasomotor sympathetic drive, a decrease in cardiac vagal modulation and baroreflex impairment during normoxia and hypoxia. In addition, our data suggest that statin treatment has a potential role in restoring the physiological cardiovascular autonomic control at baseline and during cardiovascular challenge.
The aim of this study is to evaluate the activity of sympathetic nerve sistem by microneurography in asymptomatic patients with aortic insufficiency (AoI) chronic important.Were included 10 asymptomatic patients with anatomically important AoI of rheumatic etiology with normal left ventricular function (ejection fraction>; 55%) by echocardiogram.Exclusion criteriadiabetes mellitus, renal failure, neuropathy, or beta‐blockers. A control group of normotensive volunteers (control group, n=11) with age, sex and body mass index‐ matched was included. MNSA by microneuragraphy, and blood pressure (BP) by FINOMETER® were evaluated in supine rest position. Continuous variables are described as mean ± SD and categorical variables as relative frequencies. Student t test and a multivariate analysis model were used, p <0.05 was considered statistically significant.AoI group and control group showed no statistically significant regarding age, sex and BMI. Systolic BP in AoI group was 148 +16 mmHg vs. 120±4 mmHg in control group (p = 0.0001), Diastolic BP was 60±6 mmHg in AoI and 73±3 mmHg in control group (p = 0.0001). The MSNA was in the AoI group 25±3 vs. 15±2 in the control group (p <0.001). Aortic insufficiency was associated independently with a higher MSNA (p = 0.02).AoI important chronic and asymptomatic is associated with increased MSNA.
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