scholarly journals Obesity-Induced Heart Rate Variability Impairment and Decreased Systolic Function in Obese Male Dogs

Animals ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 1383
Author(s):  
Wanpitak Pongkan ◽  
Wannida Jitnapakarn ◽  
Warunee Phetnoi ◽  
Veerasak Punyapornwithaya ◽  
Chavalit Boonyapakorn

Obesity can induce cardiovascular diseases in both humans and animals. Heart rate variability (HRV) is an indicator of sympathovagal balance and is used to identify cardiovascular diseases in humans. However, HRV and cardiac function have rarely been investigated in obese dogs. This study investigated the effect of obesity on oxidative stress, HRV, and cardiac function in obese and non-obese dogs. The nine-scale body condition score (BCS) system was used to determine obesity. Thirty small breed dogs were divided into a normal weight group (n = 15) and an obese group (n = 15). All dogs underwent physical examination, plasma malondialdehyde (MDA) measurement, electrocardiography, echocardiography, and two hours of Holter monitoring. This study found that obese dogs had increased plasma MDA and sympathovagal imbalance, which was indicated by impaired time and frequency domains compared to normal weight dogs. Although cardiac function was within normal limits, the echocardiographic study found that the obese dogs had reduced cardiac wall thickness and lower systolic function, as indicated by a reduction in %ejection fraction, %fractional shortening, increased left ventricular (LV) internal diameter during systole, and LV end-systolic volume compared to normal weight dogs. This study concluded that obesity in dogs can induce increased plasma oxidative stress, impaired HRV, and reduced cardiac systolic function compared to non-obese dogs.

2005 ◽  
Vol 289 (6) ◽  
pp. H2616-H2623 ◽  
Author(s):  
Yun-He Liu ◽  
Oscar A. Carretero ◽  
Oscar H. Cingolani ◽  
Tang-Dong Liao ◽  
Ying Sun ◽  
...  

Using inducible nitric oxide (NO) synthase (iNOS) knockout mice (iNOS−/−), we tested the hypotheses that 1) lack of iNOS attenuates cardiac remodeling and dysfunction and improves cardiac reserve postmyocardial infarction (MI), an effect that is partially mediated by reduction of oxidative stress due to reduced interaction between NO and reactive oxygen species (ROS); and 2) the cardioprotection afforded by iNOS deletion is eliminated by Nω-nitro-l-arginine methyl ester (l-NAME) due to inhibition of endothelial NOS (eNOS) and neuronal NOS (nNOS). MI was induced by ligating the left anterior descending coronary artery. Male iNOS−/− mice and wild-type controls (WT, C57BL/6J) were divided into sham MI, MI+vehicle, and MI+l-NAME (100 mg·kg−1·day−1 in drinking water for 8 wk). Cardiac function was evaluated by echocardiography. Left ventricular (LV) maximum rate of rise of ventricular pressure divided by pressure at the moment such maximum occurs (dP/d t/instant pressure) in response to isoproterenol (100 ng·kg−1·min−1 iv) was measured with a Millar catheter. Collagen deposition, myocyte cross-sectional area, and expression of nitrotyrosine and 4-hydroxy-2-nonenal (4-HNE), markers for ROS, were determined by histopathological and immunohistochemical staining. We found that the MI-induced increase in LV chamber dimension and the decrease in ejection fraction, an index of systolic function, were less severe in iNOS−/− compared with WT mice. l-NAME worsened LV remodeling and dysfunction further, and these detrimental effects were also attenuated in iNOS−/− mice, associated with better preservation of cardiac function. Lack of iNOS also reduced nitrotyrosine and 4-HNE expression after MI, indicating reduced oxidative stress. We conclude that iNOS does not seem to be a pathological mediator of heart failure; however, the lack of iNOS improves cardiac reserve post-MI, particularly when constitutive NOS isoforms are blocked. Decreased oxidative stress and other adaptive mechanisms independent of NOS may be partially responsible for such an effect, which needs to be studied further.


2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Markus Wallner ◽  
Jason M Duran ◽  
Sarah Koller ◽  
Sadia Mohsin ◽  
Steffen Lis ◽  
...  

Rationale: Myocardial injury after repeated or continuous administration of isoproterenol (ISO) in preclinical models has been widely described in the literature by our lab and others. Recent controversial reports using a one-time dose of ISO, to mimic a Takotsubo-like cardiomyopathy, demonstrated pronounced and reversible depression of cardiac function at one-week post injection with widespread myocyte death followed by robust myocardial regeneration and recovery of cardiac function. Hypothesis: Single-dose ISO does not produce depression of cardiac function Methods and Results: C57Bl/6 mice were given a single subcutaneous injection of vehicle (saline) or 5, 200, or 300 mg/kg of ISO. Cardiac function was measured using transthoracic echocardiography with cardiac strain analysis at baseline prior to ISO injection and after 1, 7, 14, and 28 days post-injection. Animals were sacrificed after 1, 7, and 28 days post-injection for evaluation of gross heart weight (HW), HW/body weight (BW) and HW/tibia length (TL). Left ventricular (LV) functional measurements revealed no significant differences in global systolic function (ejection fraction and fractional shortening) between vehicle- or ISO-treated animals at any concentration. Additionally, no significant differences were detected between vehicle- or ISO-treated animals in any cardiac dimensions measured by echocardiography (LV cross-sectional area, internal diameter, end-diastolic or end-systolic volumes) or in gross HW, HW/BW or HW/TL. LV global cardiac strain was also not significantly different between vehicle and ISO-treated animals at any time point. When apical regions of the LV endocardium (the area most predominantly affected by Takotsubo cardiomyopathy) were specifically examined using strain analysis, no significant differences could be detected between vehicle and ISO-treated animals at any time point. Conclusion: Single-dose ISO injury in a mouse model does not produce any depression of cardiac function at 1 week post injection.


2017 ◽  
Vol 232 (2) ◽  
pp. 189-204 ◽  
Author(s):  
Pongpan Tanajak ◽  
Hiranya Pintana ◽  
Natthaphat Siri-Angkul ◽  
Juthamas Khamseekaew ◽  
Nattayaporn Apaijai ◽  
...  

Long-term high-fat diet (HFD) consumption causes cardiac dysfunction. Although calorie restriction (CR) has been shown to be useful in obesity, we hypothesized that combined CR with dipeptidyl peptidase-4 (DPP-4) inhibitor provides greater efficacy than monotherapy in attenuating cardiac dysfunction and metabolic impairment in HFD-induced obese-insulin resistant rats. Thirty male Wistar rats were divided into 2 groups to be fed on either a normal diet (ND, n = 6) or a HFD (n = 24) for 12 weeks. Then, HFD rats were divided into 4 subgroups (n = 6/subgroup) to receive just the vehicle, CR diet (60% of mean energy intake and changed to ND), vildagliptin (3 mg/kg/day) or combined CR and vildagliptin for 4 weeks. Metabolic parameters, heart rate variability (HRV), cardiac mitochondrial function, left ventricular (LV) and fibroblast growth factor (FGF) 21 signaling pathway were determined. Rats on a HFD developed insulin and FGF21 resistance, oxidative stress, cardiac mitochondrial dysfunction and impaired LV function. Rats on CR alone showed both decreased body weight and visceral fat accumulation, whereas vildagliptin did not alter these parameters. Rats in CR, vildagliptin and CR plus vildagliptin subgroups had improved insulin sensitivity and oxidative stress. However, vildagliptin improved heart rate variability (HRV), cardiac mitochondrial function and LV function better than the CR. Chronic HFD consumption leads to obese-insulin resistance and FGF21 resistance. Although CR is effective in improving metabolic regulation, vildagliptin provides greater efficacy in preventing cardiac dysfunction by improving anti-apoptosis and FGF21 signaling pathways and attenuating cardiac mitochondrial dysfunction in obese-insulin-resistant rats.


2015 ◽  
Vol 40 (1) ◽  
pp. 99-108 ◽  
Author(s):  
Manuela Ferrario ◽  
Jochen G. Raimann ◽  
Brett Larive ◽  
Andreas Pierratos ◽  
Stephan Thijssen ◽  
...  

Background: Non-linear heart rate variability (HRV) indices were hypothesized to correlate with cardiac function, fluid overload and physical performance in hemodialysis patients. Methods: Twenty-four-hour Holter electrocardiograms were recorded in patients enrolled in the Frequent Hemodialysis Network (FHN) Daily Dialysis Trial. Correlations between non-linear HRV indices and left ventricular ejection fraction (LVEF), left ventricular end-diastolic volume (LVEDV), extracellular volume (ECV)/total body water (TBW) ratio, the SF-36 Physical Health Composite (PHC) and Physical Functioning (PF) scores were tested. Results: We studied 210 subjects (average age 49.8 ± 13.5 years, 62% men, 42% diabetics). In non-diabetic patients, multiscale entropy (MSE) slope sample entropy (SampEn) and approximate entropy (ApEn) correlated positively with LVEF, PF and PHC and inversely with LVEDV and ECV/TBW. Spectral power slope correlated positively with ECV/TBW (r = 0.27). Irregularity measures (MSE ApEn and MSE SampEn) correlated positively with LVEDV (r = 0.19 and 0.20). Conclusion: Non-linear HRV indices indicated an association between a deteriorated heart rate regulatory system and impaired cardiac function, fluid accumulation and poor physical condition.


2016 ◽  
Vol 51 (1) ◽  
pp. 89-92 ◽  
Author(s):  
Grayson A Doss ◽  
Christoph Mans ◽  
Rebecca L Stepien

Alpha2-agonist anesthetic combinations are often used in rodent anesthesia but no information about their effects on cardiac function in chinchillas exists. The purpose of this study was to utilize echocardiography to evaluate the cardiovascular effects of dexmedetomidine–ketamine anesthesia in chinchillas. Echocardiographic examinations were performed in eight adult chinchillas under manual restraint and following dexmedetomidine (0.015 mg/kg) and ketamine (4 mg/kg) administration. Dexmedetomidine–ketamine anesthesia resulted in a significantly decreased heart rate, fractional shortening, cardiac output, and flow velocity across the aortic and pulmonic valves, and significantly increased left ventricular internal diameter in systole. The observed changes in echocardiographic parameters are similar to those previously reported in chinchillas anesthetized with isoflurane.


2013 ◽  
Vol 36 (5) ◽  
pp. 255 ◽  
Author(s):  
Andrée-Anne Gagnon-Audet ◽  
Paul Poirier ◽  
Hélène Turcotte ◽  
Julie Martin ◽  
Marjorie Bastien ◽  
...  

Purpose: Obesity is associated with left ventricular diastolic dysfunction and altered heart rate variability, as well as pulmonary dysfunction. The relationship between asthma and cardiac dysfunction in severely obese subjects is unknown, although it has been hypothesized that cardiac dysfunction may contribute to increase airway hyper-responsiveness (AHR). This study aimed to determine if AHR is associated with left ventricular diastolic dysfunction and heart rate variability in severely obese subjects. Methods: Sixty-one subjects with severe obesity (BMI ≥35 kg/m2 with comorbidities) completed this study. All subjects completed respiratory questionnaires, spirometry, lung volume measurements, methacholine inhalation test, 24hour Holter monitoring and a complete echocardiography evaluation. Blood samples were obtained for measurement of metabolic markers. Subjects with AHR, defined by a provocative concentration of methacholine inducing a 20% fall in FEV1 (PC20) < 8 mg/ml, were compared with those with no AHR (PC20 ≥8 mg/ml). Results: According to these criteria, 32 subjects had AHR and 29 had no AHR(mean PC201.70 mg/ml and 15.3 mg/ml respectively, p < 0.001). The groups were similar for anthropometric data and comorbidities. Fasting glucose, Hb1Ac, total cholesterol, LDL, triglycerides, Apo-B, C-reactive protein (CRP) and pro-BNP levels were also comparable between groups (p > 0.05). CRP level correlated with PC20 (AHR, r=0.38, p=0.03). Indices of heart rate variability and overall cardiac function were similar in subjects with or without AHR but grade 2 left ventricular diastolic dysfunction was more prevalent in subjects with AHR (p=0.037). Conclusions: Altered cardiac function, dysglycemia and dyslipidemia do not seem to be significantly associated with AHR in severely obese subjects in contrast to systemic inflammation.


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