Role of Catecholamines in Stress-Induced Heart Disease

Antalóczy, Z

doi:10.1007/978-1-4613-2589-5_18

Cited by 3 publications

(2 citation statements)

References 2 publications

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“…First, catecholamine administration induces necrotic lesions similar to those induced by stress (1,13,47,54). Second, adrenergic, but not cholinergic, blockers reduce the extent of stress-induced heart injury as measured by enzyme activities in plasma (3).…”

Section: Discussionmentioning

confidence: 99%

Activated epidermal growth factor receptor (ErbB1) protects the heart against stress-induced injury in mice

Pareja

Sánchez

Lorita

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Acute, high-intensity stress induces necrotic lesions in the heart. We found that restraint-and-cold (4°C) exposure (RCE) raises plasma lactate dehydrogenase (LDH), creatine kinase (CK), and transaminase activity in a time-dependent manner, with a peak value 7 h after stimulus cessation. At 24 h, signs of necrotic lesions were observed in paraffin sections stained with hematoxylineosin: focal accumulation of mononuclear cells in subendocardial areas of the left ventricle wall and focal hemorrhage in papillary muscles. In contrast, intermale fighting (IF) did not increase plasma CK activity, although LDH and transaminase activities did increase. In IF, no histological evidence of heart injury was observed. Because IF, but not RCE, increased plasma epidermal growth factor (EGF) concentration by ∼1,000-fold, we hypothesized that EGF receptor (ErbB1) activation may protect the heart against stress-induced injury. To examine this hypothesis, we injected the ErbB1 tyrosine kinase inhibitor tyrphostin AG-1478 (25 mg/kg ip) immediately before mice were exposed to IF. After 3 h, plasma activities of LDH-1 and CK increased. Plasma enzyme activities were as low in control mice (injected with vehicle alone) as in nonfighting mice. In the last experiment, we injected EGF (0.25 mg/kg ip) 20 min before exposing mice to RCE. After 7 h, plasma LDH-1 and CK activities were significantly lower in these animals than in mice injected with vehicle. The effect required ErbB1 activation, because simultaneous administration of AG-1478 completely abolished the effect of exogenous EGF. We conclude that activated ErbB1, by endogenous or exogenous ligands, may protect the heart against stress-induced injury.

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Section: Discussionmentioning

confidence: 99%

Activated epidermal growth factor receptor (ErbB1) protects the heart against stress-induced injury in mice

Pareja

Sánchez

Lorita

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…It is known that the sympathetic nervous system is involved in arrhythmogenesis associated with ischemic heart disease (18) and that a high dose of epinephrine may induce arrhythmias in nonischemic hearts (1). To study the effect of EGF on the arrhythmogenic effect of epinephrine, we ran new experiments in which epinephrine infusion lasted for 10 min.…”

Section: Effect Of Egf On Cardiac Myocytes and Perfusedmentioning

confidence: 99%

Effects of epidermal growth factor on epinephrine-stimulated heart function in rodents

Lorita

Escalona

Faraudo

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Epidermal growth factor (EGF) interferes with beta-adrenergic receptor (beta-AR) signaling in adipocytes and hepatocytes, which leads to decreased lipolytic and glycogenolytic responses, respectively. We studied the effect of EGF on the heart. EGF interfered with the cAMP signal generated by beta-AR agonists in cardiac myocytes. In perfused hearts, EGF decreased inotropic and chronotropic responses to epinephrine but not to 8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphate. Sustained epinephrine infusion induced heart contracture, which resulted in altered heart function as demonstrated by decreased inotropy and increased heart rate variability. EGF prevented all these alterations. In the whole animal (anesthetized mice), EGF administration reduced the rise in heart rate induced by a single epinephrine dose and the occurrence of Bezold-Jarisch reflex episodes induced by repeated doses. Sialoadenectomy enhanced the response to epinephrine, and EGF administration restored normal response. All these results suggest that, by interfering with beta-AR signaling, EGF protects the heart against the harmful effects of epinephrine.

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A Moderate Carnitine Deficiency Exacerbates Isoproterenol-Induced Myocardial Injury in Rats

Giudice

Bonomini²,

Arduini

2016

Cardiovasc Drugs Ther

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Role of Catecholamines in Stress-Induced Heart Disease

Cited by 3 publications

References 2 publications

Activated epidermal growth factor receptor (ErbB1) protects the heart against stress-induced injury in mice

Activated epidermal growth factor receptor (ErbB1) protects the heart against stress-induced injury in mice

Effects of epidermal growth factor on epinephrine-stimulated heart function in rodents

A Moderate Carnitine Deficiency Exacerbates Isoproterenol-Induced Myocardial Injury in Rats

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