Isoproterenol‐Induced Hypertrophy May Result In Distinct Left Ventricular Changes

Murad, Neif; Tucci, Paulo José Ferreira

doi:10.1046/j.1440-1681.2000.03254.x

Cited by 15 publications

(15 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Non-trained ISO-treated rats (Group I) had significantly smaller LV chamber diameter and increased free wall thickness (Table 1) characterizing the occurrence of LV concentric hypertrophy, which corroborates previous findings in our lab [20]. The ISO-treated rats showed significantly increased nuclear volume in LV (Table 1), multiple foci of subendocardial necrosis, subendocardial fibrosis, and increased myocardial collagen.…”

Section: Optical Microscopysupporting

confidence: 89%

Exercise training prevents β‐adrenergic hyperactivity‐induced myocardial hypertrophy and lesions

Serra

Higuchi

Ihara

et al. 2008

European J of Heart Fail

View full text Add to dashboard Cite

Background: Sustained β-adrenoreceptor activation promotes cardiac hypertrophy and cellular injury. Aims: To evaluate the cardioprotective effect of exercise on damage induced by β-adrenergic hyperactivity. Methods: Male Wistar rats were randomised into four groups (n = 8 per group): sedentary non-treated control (C), sedentary treated with isoproterenol 0.3 mg/kg/day administered subcutaneously for 8 days (I), exercised non-treated (E) and exercised plus isoproterenol administered during the last eight days of exercise (IE). Exercised animals ran on a treadmill for 1 h daily 6 times a week for 13 weeks. Results: Isoproterenol caused increases in left ventricle (LV) wet and dry weight/body weight ratio, LV water content and cardiomyocyte transverse diameter. Additionally, isoproterenol induced severe cellular lesions, necrosis, and apoptosis, increased collagen content and reduced capillary and fibre fractional areas. Notably, all of these abnormalities were completely prevented by exercise. Conclusion: Our data have demonstrated that complete cardioprotection is possible through exercise training; by preventing β-adrenergic hyperactivity-induced cardiac hypertrophy and structural injury.

show abstract

Section: Optical Microscopysupporting

confidence: 89%

Exercise training prevents β‐adrenergic hyperactivity‐induced myocardial hypertrophy and lesions

Serra

Higuchi

Ihara

et al. 2008

European J of Heart Fail

View full text Add to dashboard Cite

show abstract

“…Similar findings of little or no change in cardiac function have been reported in rats treated with low doses (0.2-0.4 mg/kg body mass) of isoproterenol (24,433), although it has been suggested that in rats, the changes to the heart during isoproterenolinduced cardiac hypertrophy are not homogeneous and that myocardial mass, myocardial relaxation, left ventricular stiffness, and systolic function can differ between subgroups of animals (318).…”

Section: A Effects Of ␤-Agonists On Cardiac Muscle Structure and Funsupporting

confidence: 72%

Role of β-Adrenoceptor Signaling in Skeletal Muscle: Implications for Muscle Wasting and Disease

Lynch¹,

Ryall²

2008

Physiological Reviews

363

356

View full text Add to dashboard Cite

The importance of beta-adrenergic signaling in the heart has been well documented, but it is only more recently that we have begun to understand the importance of this signaling pathway in skeletal muscle. There is considerable evidence regarding the stimulation of the beta-adrenergic system with beta-adrenoceptor agonists (beta-agonists). Although traditionally used for treating bronchospasm, it became apparent that some beta-agonists could increase skeletal muscle mass and decrease body fat. These so-called "repartitioning effects" proved desirable for the livestock industry trying to improve feed efficiency and meat quality. Studying beta-agonist effects on skeletal muscle has identified potential therapeutic applications for muscle wasting conditions such as sarcopenia, cancer cachexia, denervation, and neuromuscular diseases, aiming to attenuate (or potentially reverse) the muscle wasting and associated muscle weakness, and to enhance muscle growth and repair after injury. Some undesirable cardiovascular side effects of beta-agonists have so far limited their therapeutic potential. This review describes the physiological significance of beta-adrenergic signaling in skeletal muscle and examines the effects of beta-agonists on skeletal muscle structure and function. In addition, we examine the proposed beneficial effects of beta-agonist administration on skeletal muscle along with some of the less desirable cardiovascular effects. Understanding beta-adrenergic signaling in skeletal muscle is important for identifying new therapeutic targets and identifying novel approaches to attenuate the muscle wasting concomitant with many diseases.

show abstract

“…The structural changes in rat myocardium following chronic ISO administration are not uniform, with myocardial necrosis and reparative fibrosis prevailing over stimulation of the myocyte growth in some animals [118]. Importantly, the accumulation of collagen fibers in LV subendocardium tends to extend outwards from intermuscular spaces and encircle the ventricular fibers [99,100,118,119].…”

Section: Morphological Changes In Heart Tissuementioning

confidence: 99%

“…Importantly, the accumulation of collagen fibers in LV subendocardium tends to extend outwards from intermuscular spaces and encircle the ventricular fibers [99,100,118,119]. This effect contributes to increased myocardial stiffness and impaired diastolic relaxation.…”

Section: Morphological Changes In Heart Tissuementioning

confidence: 99%

Cardiac hypertrophy induced by sustained β-adrenoreceptor activation: pathophysiological aspects

2007

View full text Add to dashboard Cite

Cardiac hypertrophy is promoted by adrenergic over-activation and represents an independent risk factor for cardiovascular morbidity and mortality. The basic knowledge about mechanisms by which sustained adrenergic activation promotes myocardial growth, as well as understanding how structural changes in hypertrophied myocardium could affect myocardial function has been acquired from studies using an animal model of chronic systemic beta-adrenoreceptor agonist administration. Sustained beta-adrenoreceptor activation was shown to enhance the synthesis of myocardial proteins, an effect mediated via stimulation of myocardial growth factors, up-regulation of nuclear proto-oncogenes, induction of cardiac oxidative stress, as well as activation of mitogen-activated protein kinases and phosphatidylinositol 3-kinase. Sustained beta-adrenoreceptor activation contributes to impaired cardiac autonomic regulation as evidenced by blunted parasympathetically-mediated cardiovascular reflexes as well as abnormal storage of myocardial catecholamines. Catecholamine-induced cardiac hypertrophy is associated with reduced contractile responses to adrenergic agonists, an effect attributed to downregulation of myocardial beta-adrenoreceptors, uncoupling of beta-adrenoreceptors and adenylate cyclase, as well as modifications of downstream cAMP-mediated signaling. In compensated cardiac hypertrophy, these changes are associated with preserved or even enhanced basal ventricular systolic function due to increased sarcoplasmic reticulum Ca(2+) content and Ca(2+)-induced sarcoplasmic reticulum Ca(2+) release. The increased availability of Ca(2+) to maintain cardiomyocyte contraction is attributed to prolongation of the action potential due to inhibition of the transient outward potassium current as well as stimulation of the reverse mode of the Na(+)-Ca(2+) exchange. Further progression of cardiac hypertrophy towards heart failure is due to abnormalities in Ca(2+) handling, necrotic myocardial injury, and increased myocardial stiffness due to interstitial fibrosis.

show abstract

Isoproterenol‐Induced Hypertrophy May Result In Distinct Left Ventricular Changes

Cited by 15 publications

References 25 publications

Exercise training prevents β‐adrenergic hyperactivity‐induced myocardial hypertrophy and lesions

Exercise training prevents β‐adrenergic hyperactivity‐induced myocardial hypertrophy and lesions

Role of β-Adrenoceptor Signaling in Skeletal Muscle: Implications for Muscle Wasting and Disease

Cardiac hypertrophy induced by sustained β-adrenoreceptor activation: pathophysiological aspects

Contact Info

Product

Resources

About