Echocardiographic assessment of cardiac structure and function in rats

Brown, Lindsay; Fenning, Andrew; Chan, Vincent; Loch, D. S.; Wilson, Kristin; Anderson, Bonita; Burstow, Darryl J.

doi:10.1046/j.1444-2892.2002.00148.x

Cited by 68 publications

(55 citation statements)

References 19 publications

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“…Our findings showed an increased left ventricular end-diastolic pressure and an increased central venous pressure, both of which are signs of heart failure. Echocardiography is commonly used as a noninvasive method to assess cardiac function during heart disease (5,7,12,39). Our 2D and 2D-guided M-mode images demonstrated an increased left ventricular internal diameter, endocardial area, and left ventricular volume in the heart failure rats compared with the control rats.…”

Section: L490mentioning

confidence: 69%

β-Adrenoceptor stimulation of alveolar fluid clearance is increased in rats with heart failure

Maron

Luther²,

Pilati³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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We thus hypothesized that its function might be upregulated in rats with heart failure, a condition that severely challenges the lung's ability to maintain fluid balance. Heart failure was induced by left coronary artery ligation. Echocardiographic and cardiovascular hemodynamics confirmed its development at 16 wk postligation. At that time, alveolar fluid clearance was measured by an increase in protein concentration over 1 h of a 5% albumin solution instilled into the lungs. Baseline alveolar fluid clearance was similar in heart failure and age-matched control rats. Terbutaline was added to the instillate to determine whether heart failure rats responded to ␤-adrenoceptor stimulation. Alveolar fluid clearance in heart failure rats was increased by 194% after terbutaline stimulation compared with a 153% increase by terbutaline in control rats. To determine the mechanisms responsible for this accelerated alveolar fluid clearance, we measured ion transporter expression (ENaC, Na-KATPase, CFTR). No significant upregulation was observed for these ion transporters in the heart failure rats. Lung morphology showed significant alveolar epithelial type II cell hyperplasia in heart failure rats. Thus, alveolar epithelial type II cell hyperplasia is the likely explanation for the increased terbutaline-stimulated alveolar fluid clearance in heart failure rats. These data provide evidence for previously unrecognized mechanisms that can protect against or hasten resolution of alveolar edema in heart failure. albumin; terbutaline APPROXIMATELY FIVE MILLION Americans are living with heart failure, with 400,000 new cases diagnosed annually (18). A major clinical problem in heart failure is the development of pulmonary venous (and consequently, pulmonary capillary) hypertension, which ultimately may lead to pulmonary edema and impaired blood oxygenation. Recent studies have demonstrated that excess pulmonary edema fluid is cleared from the alveoli secondary to active transepithelial Na transport (14, 31). The alveolar epithelium plays a critical role during pulmonary edema recovery by actively absorbing Na (14, 31). ␤-adrenoceptor and dopamine receptor agonists increase Na transport and thus hasten the resolution of pulmonary edema (2, 6, 31). These observations have important clinical significance because they suggest that ␤-adrenoceptor-or dopamine receptor-agonist therapy might help patients to recover more rapidly from pulmonary edema (2, 16).Lungs of heart failure patients undergo extensive remodeling (18,25,26), resulting in architectural changes such as pulmonary artery and vein wall thickening, pulmonary arteriole muscularization, and capillary endothelial and alveolar epithelial basement membrane thickening (18). Collectively, such remodeling results in increased alveolocapillary barrier thickness, correlating with reduced microvascular fluid and protein permeabilities (11,20,45). In addition to the aforementioned changes, alveolar epithelial type II cell proliferation may occur in these lungs (25,26). Hence, the hypot...

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Section: L490mentioning

confidence: 69%

β-Adrenoceptor stimulation of alveolar fluid clearance is increased in rats with heart failure

Maron

Luther²,

Pilati³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The LV responds by increasing its internal diameter. 23,24 Therefore, the aerobic-trained heart develops eccentric hypertrophy. 25 The results of the present study show that in rats submitted to endurance training, the diameter of the axon and of the myelin sheath of the vagus nerve fibers increases.…”

Section: Discussionmentioning

confidence: 99%

Endurance training induces structural and morphoquantitative changes in rat vagus nerve

Pianca

Neto

Pithon‐Curi

et al. 2015

Rev Bras Med Esporte

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Introduction: Many nervous system tissues and cells suffers positive changes when faced to exercise training. However, data on vagus nerve adaptation from exercise-induced study is absent. Objective: To analyze the effect of an endurance training on the vagus nerve morphology of rats. Methods: Wistar rats (6 months of age) were divided into two groups: control group (CG, n=8), and aerobic trained group (AT, n=8). AT was submitted to a treadmill training program of five times per week during 12 weeks. The maximum speed stipulated in the training protocol corresponded to 60% of the mean maximum intensity achieved by the group in the test of maximum effort. Results: Twelve weeks of treadmill training resulted in left ventricular hypertrophy in the AT group compared to CG. There was a significant increase in the area of both the myelinated and unmyelinated axons, and in the area of myelin sheath with training. The number of neurotubules and neurofilaments in myelinated fibers of aerobic trained group was significantly greater than CG (p≤0.05). Conclusion: Endurance training promoted significant increase in morphometric parameters of the vagus nerve in the same way it affect somatic nerves.

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“…At 32 wk, rats were anesthetized using intraperitoneal Zoletil, as previously described (6,30), and echocardiographic examination (Hewlett Packard Sonos 5500, 12-MHz transducer) was performed, in accordance with the guidelines of the American Society of Echocardiography, using the leading-edge method (34).…”

Section: Rats and Dietsmentioning

confidence: 99%

Chronic high-carbohydrate, high-fat feeding in rats induces reversible metabolic, cardiovascular, and liver changes

Poudyal

Panchal

Ward

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Poudyal H, Panchal SK, Ward LC, Waanders J, Brown L. Chronic high-carbohydrate, high-fat feeding in rats induces reversible metabolic, cardiovascular, and liver changes. Am J Physiol Endocrinol Metab 302: E1472-E1482, 2012. First published March 20, 2012 doi:10.1152/ajpendo.00102.2012.-Age-related physiological changes develop at the same time as the increase in metabolic syndrome in humans after young adulthood. There is a paucity of data in models mimicking chronic diet-induced changes in human middle age and interventions to reverse these changes. This study measured the changes during chronic consumption of a high-carbohydrate (as cornstarch), low-fat (C) diet and a high-carbohydrate (as fructose and sucrose), high-fat (H) diet in rats for 32 wk. C diet feeding induced changes without metabolic syndrome, such as disproportionate increases in total body lean and fat mass, reduced bone mineral content, cardiovascular remodeling with increased systolic blood pressure, left ventricular and arterial stiffness, and increased plasma markers of liver injury. H diet feeding induced visceral adiposity with reduced lean mass, increased lipid infiltration in the skeletal muscle, impaired glucose and insulin tolerance, cardiovascular remodeling, hepatic steatosis, and increased infiltration of inflammatory cells in the heart and the liver. Chia seed supplementation for 24 wk attenuated most structural and functional modifications induced by age or H diet, including increased whole body lean mass and lipid redistribution from the abdominal area, and normalized the chronic low-grade inflammation induced by H diet feeding; these effects may be mediated by increased metabolism of anti-inflammatory n-3 fatty acids from chia seed. These results suggest that chronic H diet feeding for 32 wk mimics the diet-induced cardiovascular and metabolic changes in middle age and that chia seed may serve as an alternative dietary strategy in the management of these changes. obesity; chia seed; omega-3 fatty acids; metabolic syndrome METABOLIC SYNDROME is defined as a cluster of risk factors, including type 2 diabetes mellitus, hypertension, dyslipidemia, and central obesity, leading to cardiovascular diseases (3). The worldwide pandemic of metabolic syndrome and, particularly, central obesity, has been attributed to increased consumption of lipogenic sugars, such as fructose, together with saturated fats (1, 37). The Western diet, characterized by excessive intake of saturated and trans fatty acids and a low n-3-to-n-6 polyunsaturated fatty acid (PUFA) ratio, has been associated with chronic diseases such as metabolic syndrome, renal diseases, and arthritis (2,12,24,36).Early onset of obesity is a key predictor of type 2 diabetes, dyslipidemia, hypertension, and obesity in young adulthood and middle age (9,13,19,20). Childhood or adolescent obesity is a direct cause of cardiovascular disease in young, middleaged, and elderly populations and increased all-cause mortality (25). The progression from childhood through middle age to old age is...

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Echocardiographic assessment of cardiac structure and function in rats

Cited by 68 publications

References 19 publications

β-Adrenoceptor stimulation of alveolar fluid clearance is increased in rats with heart failure

β-Adrenoceptor stimulation of alveolar fluid clearance is increased in rats with heart failure

Endurance training induces structural and morphoquantitative changes in rat vagus nerve

Chronic high-carbohydrate, high-fat feeding in rats induces reversible metabolic, cardiovascular, and liver changes

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