Susceptibility to life-threatening ventricular arrhythmias in an animal model of paradoxical sleep deprivation

Joukar, Siyavash; Ghorbani-Shahrbabaki, Soodabe; Hajali, Vahid; Sheibani, Vahid; Naghsh, Nooshin

doi:10.1016/j.sleep.2013.07.008

Cited by 41 publications

(33 citation statements)

References 33 publications

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“…The other study demonstrated that OSAS is the most common secondary etiology in patients with resistant hypertension [22]. Consistent with the present study, previous experimental studies also reported that acute REM sleep deprivation is associated with arterial hypertension [23,24]. Increase of sympathetic nervous system (SNS) activity, increase of vascular resistance, activation of the renin-angiotensin-aldosterone system, and increase of arterial stiffness following sleep loss and hypoxemia are some involving factors in this type of hypertension [25][26][27].…”

Section: Discussionsupporting

confidence: 92%

“…In addition, patients that suffer from OSA have some degrees of endothelial dysfunction [28] that may be another predisposing factor for hypertension. However, this effect cannot be attributed to the hyperactivity of hypothalamic-pituitary-adrenal (HPA) axis [24,29]. HRV, a physiological phenomenon, is characterized by variation in the time interval between heartbeats.…”

Section: Discussionmentioning

confidence: 99%

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Does experimental paradoxical sleep deprivation (EPSD) is an appropriate model for evaluation of cardiovascular complications of obstructive sleep apnea?

Joukar

Ghorbani-Shahrbabaki

2015

Sleep Breath

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Purpose Some of the previous studies have used animal model of paradoxical sleep deprivation for investigation of sleep loss complications. The present study is designed to examine the effectiveness and reliability of this model for investigation and assessment of some cardiovascular complications of obstructive sleep apnea syndrome. Methods The Wistar rat groups were divided into the control group, the Test48 and Test72 groups, who experienced paradoxical sleep deprivation for 48 and 72 h, and the Sham48 and Sham72 groups, who were exposed to environmental conditions same to test groups but without sleep deprivation, respectively. At the end of the experiment, blood pressure and heart rate variability were assessed. ResultsThe results showed that 72 h rapid eye movements sleep deprivation significantly increased the systolic blood pressure compared to the control (p < 0.01), Sham48 and Test48 groups (p < 0.05). The comparison of the heart rate and heart rate variability parameters such as time domain indices (RR interval, SDNN, RMSSD, SD1, SD2, and SD1/ SD2) as well as frequency-domain variables (total power, LF and HF power, and LF/HF) had no significant difference among animal groups. Conclusions These findings suggest that rat paradoxical sleep deprivation may be a suitable model for induction and investigation of hemodynamic alterations which occurs in obstructive sleep apnea syndrome; however, it cannot be an alternative model to induce heart rate variability alterations similar to those reported in patient with obstructive sleep apnea.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Does experimental paradoxical sleep deprivation (EPSD) is an appropriate model for evaluation of cardiovascular complications of obstructive sleep apnea?

Joukar

Ghorbani-Shahrbabaki

2015

Sleep Breath

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“…Hemodynamic and electrocardiogram (ECG) recording and arrhythmia induction were performed as described previously (16). A day after the completion of the training session, the animals were anesthetized with intraperitoneal sodium thiopental (50 mg/kg).…”

Section: Blood Pressure and Electrocardiogram Recording And Arrhythmimentioning

confidence: 99%

“…Where RR is R-R interval and f = 150 msec (16)(17)(18). The premature ventricular contraction (PVC), ventricular tachycardia (VT), and ventricular fibrillation (VF) were counted during the 15 minutes of the experiment, and the latency and duration of PVC, VT, and VF was measured in seconds.…”

Section: Measured and Calculated Parametersmentioning

confidence: 99%

Nandrolone plus moderate exercise increases the susceptibility to lethal arrhythmias

Joukar¹,

Baravati²,

Fathpour³

et al. 2015

Res Cardiovasc Med

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Background: Until now, no experimental study has directly assessed the arrhythmogenesis of chronic consumption of anabolic androgenic steroids along with moderate-intensity endurance exercise. Objectives: We evaluated the influence of integration of anabolic androgenic steroids along with moderate-intensity endurance exercise on susceptibility to lethal ventricular arrhythmias in rat. Materials and Methods:The animal groups were as follows: control group (CTL); exercise group (EX) which were under 6 weeks of treadmill exercise; nandrolone group (Nan) which received 5 mg/kg of nandrolone decanoate twice a week; vehicle group (Arach) which received Arachis oil (solvent of nandrolone); trained vehicle group (Arach + Ex); and trained nandrolone group (Nan + Ex). One day after ending of the intervention period, arrhythmia was inducted by intravenous infusion of aconitine and ventricular arrhythmias were recorded. Then malondialdehyde (MDA) and glutathione peroxidase (GPX) of heart tissue were measured. Results: Nandrolone, exercise, and their combination were associated with heart hypertrophy. Exercise could prevent the incremental effect of nandrolone on MDA/GPX ratio. Chronic administration of nandrolone with moderate-intensity endurance exercise had no significant effect on blood pressure, heart rate, and basal electrocardiographic parameters. Combination of nandrolone and exercise significantly increased the incidence of ventricular fibrillation (VF) and reduced the VF latency (P < 0.05). Conclusions:The findings suggest that chronic coadministration of nandrolone with moderate-intensity endurance exercise facilitates the VF occurrence in rat. Complementary studies are needed to elucidate the involved mechanisms of this abnormality.

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“…Despite studies showing the impact of sleep debt on cardiovascular health, 4,12 little is known about its effects on cardiac contractile machinery and the role of resistance training as a preventive tool. Therefore, the aim of this study was to evaluate the effect of high-intensity resistance training on myocardial contractility in rats subsequently subjected to paradoxical sleep deprivation.…”

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confidence: 99%

Effect Of Resistance Training On Myocardial Contractility In Vitro After Sleep Deprivation

Giampá

Mônico‐Neto

Souza

et al. 2017

International Journal of Cardiovascular Sciences

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Background: Resistance training promotes cardiovascular health benefits that may affected by sleep deprivation. Objective:To evaluate the effect of high-intensity resistance training on myocardial contractility in rats subsequently subjected to paradoxical sleep deprivation. Methods:Forty male Wistar rats were distributed into control group (CTRL), resistance training (REST), 96-hour paradoxical sleep deprivation (PSD96) and resistance training followed by 96-hour paradoxical sleep deprivation (REST/PSD96). The animals underwent high-intensity resistance training for 8 weeks, 5x/week. Twenty-four hours after the last training session, the PSD96 and REST/PSD96 groups were submitted to paradoxical sleep deprivation, which was followed by the in vitro study of isolated papillary muscle contractile mechanics. Results:In comparison with the CTRL group, a lower papillary muscle length and increased cross sectional area were found in PSD96 and RETS/PSD96, which were associated with decreased temporal parameters of contraction force and relaxation. Decreased resting tension and slowing of relaxation time were found in the PSD96 group only. This effect was attenuated by previous resistance training. Conclusion:Resistance training partially prevented contractile changes induced by PSD, minimizing the slowing in relaxation time. Thus, high-intensity exercise seems to not fully protect the cardiac tissue from PSD-induced effects. (Int J Cardiovasc Sci. 2017;30(1):20-31)

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Susceptibility to life-threatening ventricular arrhythmias in an animal model of paradoxical sleep deprivation

Cited by 41 publications

References 33 publications

Does experimental paradoxical sleep deprivation (EPSD) is an appropriate model for evaluation of cardiovascular complications of obstructive sleep apnea?

Does experimental paradoxical sleep deprivation (EPSD) is an appropriate model for evaluation of cardiovascular complications of obstructive sleep apnea?

Nandrolone plus moderate exercise increases the susceptibility to lethal arrhythmias

Effect Of Resistance Training On Myocardial Contractility In Vitro After Sleep Deprivation

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