A comparative study of myocardial function and morphology during fasting/refeeding and food restriction in rats

Pinotti, M.; Leopoldo, André Soares; Dal-Pai-Silva, Maeli; Sugizaki, Mário Mateus; Nascimento, André Ferreira do; Aragon, Flávio Ferrari; Padovani, Carlos Roberto; Cicogna, Antônio Carlos

doi:10.1016/j.carpath.2009.08.001

Cited by 12 publications

(16 citation statements)

References 41 publications

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“…In the present study we have also observed that animals under food restriction presented a significantly lower baseline MAP and HR, corroborating previous data from different research groups, both in rats and in humans [18,35]. However, the foundation of these changes can be multifactorial since hypovolemia [6], cardiac dysfunctions [10] or dysfunctions in the reflexes that control the blood pressure (BP) [19] could lead to both bradycardia and hypotension.…”

Section: Discussionsupporting

confidence: 93%

“…Other cardiovascular disorders such as electrocardiographic abnormalities, left ventricular hypertrophy, systolic dysfunction, ventricular remodelling, diastolic myocardial dysfunction, decreased cardiac contraction and decrease of lateral ventricle relaxation [10,35] are also related to severe reduction in food intake.…”

Section: Introductionmentioning

confidence: 98%

“…In another study, a severe restriction, a reduction of forty percent (40%), for 8 weeks, in spontaneously hypertensive rats, induced a reduction in blood pressure [32]. Furthermore, in humans, reduction in food intake is very common among patients with anorexia nervosa who also present bradycardia and hypotension [15].Other cardiovascular disorders such as electrocardiographic abnormalities, left ventricular hypertrophy, systolic dysfunction, ventricular remodelling, diastolic myocardial dysfunction, decreased cardiac contraction and decrease of lateral ventricle relaxation [10,35] are also related to severe reduction in food intake.Considering that severe acute FR can cause cardiovascular diseases, the regulatory mechanisms involved in the regulation of the cardiovascular function could be compromised, leading to the pathological conditions cited above. Remarkably, other dietary challenges can also disrupt the cardiovascular regulatory mechanisms.…”

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confidence: 96%

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Increased α1-adrenoreceptor activity is required to sustain blood pressure in female rats under food restriction

et al. 2015

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 98%

mentioning

confidence: 96%

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Increased α1-adrenoreceptor activity is required to sustain blood pressure in female rats under food restriction

et al. 2015

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“…a reduction of 60% in the dietary protein for 35 days, after weaning are characterized mainly by increased levels of baseline mean blood pressure, increased sympathetic efferent activity directed to the heart and increased heart rate [Oliveira et al, 2004;Penitente et al, 2007;Martins et al, 2011]. Different models of malnutrition such as protein/calorie restriction or food restriction applied to rats have been shown to depress left ventricular (LV) mechanical function [Okoshi et al, 2002;Gut et al, 2003;Pinotti et al, 2010], despite some contrasting results [Nutter et al, 1979;Cicogna et al, 2001]. The main mechanical changes observed when using isolated heart or papillary muscle preparations are the reduced contractility and prolonged time courses of contraction and relaxation [Cicogna et al, 2000[Cicogna et al, , 2001Pinotti et al, 2010].…”

Section: Introductionmentioning

confidence: 99%

Protein Restriction after Weaning Modifies the Calcium Kinetics and Induces Cardiomyocyte Contractile Dysfunction in Rats

Penitente¹,

Novaes²,

Chianca

et al. 2013

Cells Tissues Organs

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Protein restriction (PR) is associated with cardiovascular diseases. The purpose of this study was to investigate the effects on single ventricular cardiomyocyte contractile function of a short-term PR after weaning. Male Fischer rats that were 28 days old were randomly divided into a control group (CG, n = 16) and a protein-restricted group (PRG, n = 16). After weaning, CG and PRG animals received isocaloric diets containing 15 and 6% protein, respectively, for 35 days. Biometric parameters were then measured, and the hearts were removed for the analysis of contractile function and calcium transient in isolated cardiomyocytes of the left ventricule (LV), and the quantification of calcium and collagen fibers in LV myocardium. PRG animals had lower body weight (BW) and LV weight (LVW), an increased LVW to BW ratio and a higher proportion of collagen fibers than CG animals. PRG animals exhibited reduced tissue levels of calcium, reduced the length, width and volume of cardiomyocytes and their sarcomere length compared to CG animals. Cardiomyocytes from PRG animals had a lower amplitude of shortening, a slower time to the peak of shortening and a longer time to half-relaxation than those from the CG. Cardiomyocytes from PRG animals also presented a lower peak of calcium transient and a longer calcium transient decay time than CG animals. Taken together, the results indicate that short-term PR after weaning induces a marked structural remodeling of the myocardium parenchyma and stroma that coexists with contractile dysfunctions in single LV cardiomyocytes of rats, which is probably associated with pathological changes of the intracellular calcium kinetics, rather than inadequate available amounts of this mineral in cardiac tissue.

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“…In vitro starvation results in mitochondrial depletion (Carreira et al, 2010). This mitochondrial depletion may contribute to the observed myocardial dysfunction after food restriction (Pinotti et al, 2010). If depletion of mitochondria is not followed by an induction of mitochondrial biogenesis (Hancock et al, 2011), this will be detrimental for the heart.…”

Section: Mitophagy and Mitobiogenesismentioning

confidence: 99%

Impact of caloric restriction on myocardial ischaemia/reperfusion injury and new therapeutic options to mimic its effects

Rohrbach

Aslam

Niemann

et al. 2014

British J Pharmacology

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Caloric restriction (CR) is the most reliable intervention to extend lifespan and prevent age‐related disorders in various species from yeast to rodents. Short‐ and long‐term CR confers cardio protection against ischaemia/reperfusion injury in young and even in aged rodents. A few human trials suggest that CR has the potential to mediate improvement of cardiac or vascular function and induce retardation of cardiac senescence also in humans. The underlying mechanisms are diverse and have not yet been clearly defined. Among the known mediators for the benefits of CR are NO, the AMP‐activated PK, sirtuins and adiponectin. Mitochondria, which play a central role in such complex processes within the cell as apoptosis, ATP‐production or oxidative stress, are centrally involved in many aspects of CR‐induced protection against ischaemic injury. Here, we discuss the relevant literature regarding the protection against myocardial ischaemia/reperfusion injury conferred by CR. Furthermore, we will discuss drug targets to mimic CR and the possible role of calorie restriction in preserving cardiovascular function in humans.

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A comparative study of myocardial function and morphology during fasting/refeeding and food restriction in rats

Cited by 12 publications

References 41 publications

Increased α1-adrenoreceptor activity is required to sustain blood pressure in female rats under food restriction

Increased α1-adrenoreceptor activity is required to sustain blood pressure in female rats under food restriction

Protein Restriction after Weaning Modifies the Calcium Kinetics and Induces Cardiomyocyte Contractile Dysfunction in Rats

Impact of caloric restriction on myocardial ischaemia/reperfusion injury and new therapeutic options to mimic its effects

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