Myocardial and Plasma Lactate Changes in Arteriosclerotic and Non-Arteriosclerotic Rats During Isoproterenol-Induced Infarction

Bc, Wexler; Rf, Lutmer

doi:10.1177/000331977202300106

Cited by 7 publications

(6 citation statements)

References 25 publications

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“…The results confirm the observations of others d., Wexler and Judd, 1970;Csapo, Dusek and Rona, 1972) that isoprenaline produces widespread myocardial necrosis in the rat albeit at dose levels which would be fatal in humans. We have to record that our experiments have shown that there may be considerable variations in the cardiotoxicity of different samples of isoprenaline.…”

Section: Discussionsupporting

confidence: 91%

Experiences with isoprenaline induced myocardial necrosis in the rat

Woolf

Davies

Shaw

et al. 1976

The Journal of Pathology

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An attempt has been made to quantify myocardial lesions produced in the rat by isoprenaline for use as a model to assess possible incremental effects of environmental and dietary factors. This was initially made difficult by variation in the cardiotoxicity of different samples of isoprenaline. Investigation of these samples failed to reveal the basis for the differences. Active preparations have, however, produced profound changes both clinically and pathologically. The earliest light-microscopic changes both clinically and pathologically. The earliest light-microscopic change was loss of fuchsinophilia of fibres in sections stained by the picro-Mallory technique. By 24 hr obvious necrosis, fragmentation and lysis of the fibres had occurred. Treatment of frozen sections to demonstrate succinate dehydrogenase showed early changes in the character of formazan, suggesting the possibility of a transient alteration in the hydrogen transport system. By 48 hr, this is reversed except in those fibres undergoing necrosis where there is a complete loss of formazan. This contrast in staining between normal and necrotic fibres constitutes the basis for quantification which has been carried out by point counting. The results show some differences in the amount of myocardial necrosis between different batches of animals but relatively small differences within individual batches, suggesting that the introduction of additional variants into the system should be capable of producing clear cut results.

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Section: Discussionsupporting

confidence: 91%

Experiences with isoprenaline induced myocardial necrosis in the rat

Woolf

Davies

Shaw

et al. 1976

The Journal of Pathology

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“…It causes cardiac tissue (cardiomyocytes) oxidative stress due to catecholamine auto-oxidation, which stimulates lipid peroxidation, an irreversible myocardial membrane damage ( Zhou et al, 2008 ; Octavia et al, 2012 ). Isoproterenol is widely employed in cardiovascular research as an adrenergic stimulation inducer in the study of protective and preventive effects against severe cardiac dysfunctions ( Wexler and Judd, 1970 ; Wexler, 1978 ; Zhang et al, 2009 ). Sun et al, Zhang et al and Liu et al developed LC-MS methods for the analyses of metabolites in rat blood samples following isoproterenol treatment ( Zhang et al, 2009 ; Liu et al, 2014 ; Sun et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Untargeted Metabolomics Studies of H9c2 Cardiac Cells Submitted to Oxidative Stress, β-Adrenergic Stimulation and Doxorubicin Treatment: Investigation of Cardiac Biomarkers

Lima

Amaral²,

Moretto³

et al. 2022

Front. Mol. Biosci.

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One of the biggest challenges in the search for more effective treatments for diseases is understanding their etiology. Cardiovascular diseases (CVD) are an important example of this, given the high number of deaths annually. Oxidative stress (the imbalance between oxidant and antioxidant species in biological system) is one of the factors responsible for CVD occurrence, demanding extensive investigation. Excess of reactive oxygen species (ROS) are primarily responsible for this condition, and clinical and scientific literature have reported a significant increase in ROS when therapeutic drugs, such as doxorubicin and isoproterenol, are administered. In this context, the aim of this study is the investigation of potential biomarkers that might be associated with oxidative stress in cardiomyocytes. For this purpose, H9c2 cardiomyocytes were submitted to oxidative stress conditions by treatment with doxorubicin (DOX), isoproterenol (ISO) and hydrogen peroxide (PER). Metabolomics analyses of the cell extract and the supernatant obtained from the culture medium were then evaluated by CE-ESI(+)-TOF-MS. Following signal processing, statistical analyses, and molecular features annotations, the results indicate changes in the aspartate, serine, pantothenic acid, glycerophosphocholine and glutathione metabolism in the cell extract.

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“…The observations that plasma lipids increase with age in the rat and are elevated in repeatedly bred rats are not new (8,9). Boberg et at?.…”

mentioning

confidence: 99%

Reduction of Plasma Cholesterol Levels in Male Retired Breeder Rats by an Anabolic Steroid, Oxandrolone

Mills¹,

Kriz²,

Jones³

1973

Experimental Biology and Medicine

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Myocardial and Plasma Lactate Changes in Arteriosclerotic and Non-Arteriosclerotic Rats During Isoproterenol-Induced Infarction

Cited by 7 publications

References 25 publications

Experiences with isoprenaline induced myocardial necrosis in the rat

Experiences with isoprenaline induced myocardial necrosis in the rat

Untargeted Metabolomics Studies of H9c2 Cardiac Cells Submitted to Oxidative Stress, β-Adrenergic Stimulation and Doxorubicin Treatment: Investigation of Cardiac Biomarkers

Reduction of Plasma Cholesterol Levels in Male Retired Breeder Rats by an Anabolic Steroid, Oxandrolone

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