Measurement of Mouse Heart Rate Variability using Echocardiographic System.

AIM: We employed an echocardiographic (ECHO) system as the backbone for the collection of electrocardiogram (ECG) and heart rate variability (HRV) data. The system was tested using an exercise model in which C57 male mice were exposed to sham or forced wheel running. METHODS: Peak/peak (RR) interval was recorded over a 3 min period using the ECG platform of the ECHO system. Isoflurane-anesthetized male mice were divided into two groups (n = 8/group): sedentary (S) and forced wheel trained (T). HRV was analyzed in time and frequency domains (Fast Fourier Transform). Exercise training (T) was performed on a motorized wheel at low intensity 1 h/day, 5 days/week, 8 weeks duration. Cardiac morphometry and function were analyzed using ECHO while ECG was the basis to measure HRV. The sampling rate was 8000 Hz. Results show that the trained mice presented a reduction in heart rate as compared to the sedentary group. This was associated with lower cardiac sympathetic and higher parasympathetic modulation leading to an improved sympathetic/parasympathetic ratio (low-frequency band/high-frequency band). The trained group showed a reduction in isovolumetric relaxation time, reduced myocardial performance index, increased relative wall thickness, and left ventricle mass when compared to the sedentary group. CONCLUSION: Results document the utility of combining the ECHO and the ECG platform, allowing for the dual measurement of autonomic and cardiac function in mice.

Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats.

BACKGROUND: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. The aim of the present study was to investigate the association between hyperglycemia and myocardial infarction on cardiovascular autonomic modulation and cardiac oxidative stress profile in rats. Male Wistar rats were divided into: control (C), diabetic (D), myocardial infarcted (MI) and diabetic infarcted rats (DMI). METHODS: Diabetes was induced by streptozotocin (STZ, 50 mg/Kg) at the beginning of the protocol and MI was induced by left coronary occlusion 15 days after STZ. Thirty days after streptozocin-induced diabetes, cardiovascular autonomic modulation was evaluated by spectral analysis, and oxidative stress profile was determined by antioxidant enzyme activities and superoxide anion, together with protein carbonylation and redox balance of glutathione (GSH/GSSG). RESULTS: The diabetic and infarcted groups showed decreased heart rate variability and vagal modulation (p < 0.05); however, sympathetic modulation decreased only in diabetic groups (p < 0.05). Sympatho/vagal balance and vascular sympathetic modulation were increased only in the MI group (p < 0.05). Diabetes promoted an increase in catalase concentration (p < 0.05). Glutathione peroxidase activity was increased only in DMI when compared to the other groups (p < 0.05). Superoxide anion and protein carbonylation were increased only in MI group (p < 0.05). Cardiac redox balance, as evaluated by GSH/GSSG, was lower in the MI group (p < 0.05). CONCLUSIONS: These data suggest that hyperglycemia promotes compensatory mechanisms that may offer protection against ischemia, as demonstrated by increased antioxidants, decreased pro-oxidants and protein damage, possibly related to the improvements in both redox balance and sympathetic modulation to the heart.

Cardioprotection afforded by exercise training prior to myocardial infarction is associated with autonomic function improvement.

BACKGROUND: It has been suggested that exercise training (ET) protects against the pathological remodeling and ventricular dysfunction induced by myocardial infarction (MI). However, it remains unclear whether the positive adjustments on baroreflex and cardiac autonomic modulations promoted by ET may afford a cardioprotective mechanism. The aim of this study was to evaluate the effects of aerobic ET, prior to MI, on cardiac remodeling and function, as well as on baroreflex sensitivity and autonomic modulation in rats. METHODS: Male Wistar rats were divided into 4 groups: sedentary rats submitted to Sham surgery (C); trained rats submitted to Sham surgery (TC); sedentary rats submitted to MI (I), trained rats submitted to MI (TI). Sham and MI were performed after ET period. After surgeries, echocardiographic, hemodynamic and autonomic (baroreflex sensitivity, cardiovascular autonomic modulation) evaluations were conducted. RESULTS: Prior ET prevented an additional decline in exercise capacity in TI group in comparison with I. MI area was not modified by previous ET. ET was able to increase the survival and prevent additional left ventricle dysfunction in TI rats. Although changes in hemodynamic evaluations were not observed, ET prevented the decrease of baroreflex sensitivity, and autonomic dysfunction in TI animals when compared with I animals. Importantly, cardiac improvement was associated with the prevention of cardiac autonomic impairment in studied groups. CONCLUSIONS: Prior ET was effective in changing aerobic capacity, left ventricular morphology and function in rats undergoing MI. Furthermore, these cardioprotective effects were associated with attenuated cardiac autonomic dysfunction observed in trained rats. Although these cause-effect relationships can only be inferred, rather than confirmed, our study suggests that positive adaptations of autonomic function by ET can play a vital role in preventing changes associated with cardiovascular disease, particularly in relation to MI.

Ventricular and autonomic benefits of exercise training persist after detraining in infarcted rats.

We evaluate the effects of detraining (DT, for 1 month) on the left ventricular (LV) remodeling and function, hemodynamic and baroreflex sensitivity (BRS), as well as on mortality rate of infarcted (MI) rats after 3 months of exercise training (ET, 50-70 % of VO2max). Male Wistar rats were divided into five groups: control (C, n = 10), untrained-infarcted (UI, n = 15), trained-infarcted (TI, n = 12), untrained-infarcted plus 1 month (UI-1, n = 15) and detrained-infarcted 1 month (DI-1, n = 15). LV function was evaluated by echocardiography at the initial and final of the protocols. After following, ET and/or DT protocols, hemodynamic and BRS [by tachycardic (TR) and bradycardic (BR) responses] were assessed. TI group displayed increased VO2max in comparison with UI and DI-1 groups; however, DI-1 values remained increased compared to UI-1 group. MI area was reduced by ET and maintained after DT. Ejection fraction (TI = 60 ± 2 and DI-1 = 61 ± 2 % vs. UI = 41 ± 1 and UI-1 = 37 ± 3 %), E/A ratio (TI = 1.6 ± 0.1 and DI-1 = 1.9 ± 0.1 vs. UI = 2.9 ± 0.2 and UI-1 = 2.9 ± 0.3), TR (TI = 3.3 ± 0.3 and DI-1 = 3.3 ± 0.4 vs. UI = 1.7 ± 0.1 and UI-1 = 1.6 ± 0.1 bpm/mmHg) and BR (TI = -2.2 ± 0.1 and DI-1 = -2.0 ± 0.1 vs. UI = -1.3 ± 0.09 and UI-1 = -1.2 ± 0.09 bpm/mmHg) were improved by ET and maintained after DT in comparison with untrained rats. These changes resulted in mortality reduction in the TI (8 %) and DI-1 groups (13 %) compared with the UI (46 %) and UI-1 (53 %) groups. These findings indicate that ET is not only an effective tool in the management of cardiovascular and autonomic MI derangements, but also that these positive changes were maintained even after 1 month of DT in rats.