Myocardial Necroses Produced in Domesticated Rats and in Wild Rats by Sensory and Emotional Stresses.

Raab, W.; Chaplin, James Patrick; Bajusz, E

doi:10.3181/00379727-116-29338

Cited by 50 publications

(21 citation statements)

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“…Values are means Ϯ SE of 8-12 animals per group. Significant differences were determined by 1-way ANOVA, and Tukey's post hoc test was used to determine significance of differences vs. control: *P Ͻ 0.05; **P Ͻ 0.01; ***P Ͻ 0.001. myocytes in the left ventricle wall and hemorrhage in papillary muscles in this ventricle, coincide with other reports in rats (45), pigs (29), and rabbits (13). The appearance of mononucleate cells, similar to those observed after 24 h of the stressful stimulus, has been interpreted as part of the healing process (19).…”

Section: Discussionsupporting

confidence: 89%

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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: Discussionsupporting

confidence: 89%

“…Thus immobilization or restraint, alone or in combination with other stimuli, induces myocardial necrotic lesions in several species (13,29,35,45). Stress-induced injury results in the release of cytosolic enzymes to the blood (3,36).…”

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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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“…Immobilization or restraint, alone or in combination with other stimuli, induce myocardial necrotic lesions in several species (Raab et al 1964;Jö nsson and Johansson 1974;Downing and Chen 1985;Matsuoka et al 1998). Stress-induced injury results in the release of cytosolic enzymes into the blood (Meltzer 1971;Arakawa et al 1997).…”

Section: Introductionmentioning

confidence: 97%

ErbB receptors protect the perfused heart against injury induced by epinephrine combined with low-flow ischemia

et al. 2009

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ErbB receptor tyrosine kinases are important in maintaining the long-term structural integrity of the heart and in the induction of hypertrophy. In addition, in vivo activation of ErbB1 by epidermal growth factor (EGF) protects the heart against acute stress-induced damage. We examined here whether the ErbB sytem acutely protects the isolated heart in which stress was induced in vitro by ischemia combined with epinephrine infusion (EPI). In perfused mouse hearts, EGF induced Tyr-phosphorylation of ErbB1 but not ErbB2. Neuregulin-1beta (NRG-1beta) induced Tyr-phosphorylation of both ErbB4 and ErbB2. We also found differences in the signaling cascades activated by each growth factor. To stress the perfused mouse heart, we combined EPI with low-flow ischemia. This resulted in (i) loss of left ventricle contraction force ( + dP/dt(max)) and developed pressure (LVDP) after a short period of hypercontractility, (ii) enhanced anaerobic metabolism (lactate production), and (iii) myocyte injury (lactate dehydrogenase (LDH) release). EGF and NRG-1beta had different effects on stressed-heart contractility. EGF reduced to a half the loss of both + dP/dt(max) and LVDP. In contrast, NRG-1beta exacerbated the hypercontractility soon after reperfusion. This is coincident with a transient increase in coronary flow after reperfusion. In spite of these differences in contraction, both EGF and NRG-1beta induced similar early protection as shown by the reduction of LDH release. Our results show that the ErbB system protects the perfused heart against damage induced by acute stress. They reinforce the relevance of ErbB receptors and ligands in cardiac physiology.

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“…The rat is normally not prone to develop atherosclerotic disease, although stress 14 or intensive breeding 15 lead to myocardial lesions. However, Koletsky 1617 isolated a mutant gene that has been designated corpulent (cp) that led to obesity, hyperiipidemia, and a fulminant atherosclerosis.…”

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Effects of chronic ethanol consumption in atherosclerosis-prone JCR:LA-corpulent rat.

et al. 1989

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Rats of the atherosclerosis-prone JCR:LA-corpulent strain were subjected to long-term low (0.5% wt/vol) or high (4% wt/vol) consumption of ethanol from 1 to 12 months of age. The corpulent rats are hyperphaglc, obese, and Insulin-resistant; exhibit a marked very low density lipoproteln hyperlipldemla; and develop both vascular and myocardlal lesions while eating a normal rat chow. The total lipld profile of the rat sera showed only limited changes with ethanol consumption. There were also no significant effects on high density lipoproteln llplds. Ethanol consumption was associated with elevated fasting glucose concentrations in both lean and corpulent rats and a strong decrease In fasting Insulin levels and pancreatic B-cell volume density In the hyperlnsullnemlc corpulent rats. The relative frequency of myocardlal nodules of chronic Inflammatory cells was Increased In the ethanolconsuming rats, both lean and corpulent. In contrast, old organized lesions (scars) were absent in the ethanol-consumlng corpulent rats. Thus, ethanol consumption had no major effect on serum llplds or lipoprotelns in the corpulent rat but was associated with a reduction In insulin resistance and Islet cell hyperplasla, with an associated decreased Incidence of myocardlal lesions. (Arteriosclerosis 9:122-128, January/February 1989) E pidemiologic studies in man have established that a wide range of risk factors are associated with the development of atherosclerotic disease and its sequelae.

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Myocardial Necroses Produced in Domesticated Rats and in Wild Rats by Sensory and Emotional Stresses.

Cited by 50 publications

References 0 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

ErbB receptors protect the perfused heart against injury induced by epinephrine combined with low-flow ischemia

Effects of chronic ethanol consumption in atherosclerosis-prone JCR:LA-corpulent rat.

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