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Background: The aim of this study was to investigate the effects of chronic treatment with carvedilol in blood pressure (BPV) and heart rate (HRV) variability of rats with myocardial infarction (MI)., Methods: MI was produced in male rats by ligature of anterior interventricular branch of left coronary artery. Control rats were submitted to a sham surgery (SO). MI and SO rats were randomized to receive for 30 days placebo (Plac 0.5% metilcelulose) or carvedilol (Carv, 2mg/Kg body weight/day, drinking water): SO-Plac (N = 10), SO-Carv (N = 10), MI-Plac (N = 12), MI-Carv (N = 13). Blood pressure (BP) was directly recorded in the awake animals and BPV was determined, in time (variance, mmhg(2)) and frequency domains by the autoregressive method. Statistical significance was set in P<0.05. Data are median and interquartile range., Results: No significant changes in HRV was observed in MI rats, while BPV showed significant decreasing of blood pressure variance (SO-Plac = 42.08 (39.21) mmHg(2) vs. MI-Plac = 21.67 (12.58) mmHg(2), P<0.05), reversed by the Carv treatment (MI-Plac = 21.67 (12.58) vs. MI-Carv = 38.64 (29.25), P<0.05). In the frequency domain analyses, MI reduced absolute and normalized LF component (LF (mmHg(2)): SO-Plac = 8.98 (14.84) vs. MI-Plac = 2.08 (4.84), P<0.05; LF(nu): SO-Plac = 79.48 (45.03) nu vs. MI-Plac = 24.25 (40.67) nu, P<0.05) and increased the normalized HF component of the BPV (SO-Plac = 20.51 (39.18) vs. MI-Plac = 60.51 (39.73). Carv treatment significantly attenuated the LF component fall., Conclusion: Chronic treatment with carvedilol restored the variance of BPV altered by the MI., (Copyright © 2013 Elsevier B.V. All rights reserved.)

A high salt diet is a known risk factor for cardiovascular diseases that leads to cardiac hypertrophy and creates a substrate for arrhythmias and sudden death. However, acute arrhythmogenesis after infarction has not been studied. Male Wistar rats (21 days) received drinking water (MI) or 1% NaCl solution (MI-Salt-C) for 4 weeks. Water was given to another group for 4 weeks, and on the day before surgery, animals received a 1% NaCl solution (MI-Salt-A). Non-invasive systolic blood pressure (SBP) was obtained before surgery. Myocardial infarction (MI) was produced by permanent occlusion of the left coronary artery. Electrocardiogram was monitored during the first 30 min post-occlusion to evaluate arrhythmias. Although SBP was not altered by salt intake (SHAM: 114±2, MI: 112±2, MI-Salt-C: 115±2, MI-Salt-A: 116±4 mm Hg), ventricular hypertrophy was observed in the animals receiving chronic salt diet (SHAM: 0.22±0.008, MI: 0.23±0.007, MI-Salt-C: 0.28±0.01; MI-Salt-A: 0.23±0.01 g/cm; P<0.05). Ventricular premature beats increased in both salt-loaded groups compared to MI group (MI: 805±81, MI-Salt-C: 1145±98; MI-Salt-A: 1023±77; P<0.05). Atrioventricular blockade was only observed in animals subjected to high salt intake (MI-Salt-C: 38.9%; MI-Salt-A: 42.1%). High salt intake was associated with increased post-infarct arrhythmias; however, this effect was unrelated to ventricular hypertrophy., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Objectives: To evaluate the acute effects of colony-stimulating factor (G-CSF) on ventricular arrhythmias after coronary occlusion in rats. Materials and Methods: Male Wistar rats (10 weeks) received G-CSF (100 μg.kg-1) or vehicle. Thirty minutes later, animals were infarcted by coronary occlusion under artificial respiration. Electrocardiogram was monitored for 30 min to evaluate ventricular arrhythmias. Results: G-CSF treatment reduced the number of premature ventricular beats and the number and duration of ventricular tachycardia. The incidence of ventricular fibrillation was significantly reduced by G-CSF (MI-Cont: 11.2 ± 2.4 vs. MI-GCSF: 5.4 ± 1 events; P < 0.05). However, total duration of ventricular fibrillation was not altered (MI-Cont: 84 ± 16 vs. MI-GCSF: 76 ± 13 sec). Conclusions: Acute administration of G-CSF before coronary ligature in rats reduces the incidence of ventricular premature beats and ventricular tachycardia, suggesting a possible direct electrophysiological effect of this cytokine independently of its genomic effects. However, the data suggest that G-CSF treatment may affect the spontaneous recovery from ventricular fibrillation. Acute G-CSF administration acts directly on cardiac electrophysiology, different from chronic treatment. [ABSTRACT FROM AUTHOR]

Background/Aim. Granulocyte colony-stimulating factor (G-CSF) reduces myocardial injury and improves cardiac function after myocardial infarction (MI). We investigated the early alterations provided by G-CSF and the chronic repercussions in infarcted rats. Methods. Male Wistar rats (200-250g) received vehicle (MI) or G-CSF (MI-GCSF) (50 μg/kg, sc) at 7, 3 and 1 days before MI surgery. Afterwards MI was produced and infarct size was measured 1 and 15 days after surgery. Expression of anti- and proapoptotic proteins was evaluated immediately before surgery. 24 hours after surgery, apoptotic nuclei were evaluated. Two weeks after MI, left ventricular (LV) function was evaluated, followed by in situ LV diastolic pressure-volume evaluation. Results. Infarct size was decreased by 1 day pre-treatment before occlusion (36±2.8 vs. 44±2.1% in MI; P<0.05) and remained reduced at 15 days after infarction (28±2.2 vs. 36±1.4% in MI; P<0.05). G-CSF pretreatment increased Bcl-2 and Bcl-xL protein expression, but did not alter Bax in LV. Apoptotic nuclei were reduced by treatment (Sham: 0.46±0.42, MI: 15.5±2.43, MI-GCSF: 5.34±3.34%; P<0.05). Fifteen days after MI, cardiac function remained preserved in G-CSF pretreated rats. The LV dilation was reduced in MI-G-CSF group as compared to MI rats, being closely associated with infarct size. Conclusion. The early beneficial effects of G-CSF were essentials to preserve cardiac function at a chronic stage of myocardial infarction. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]