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cardiotoxicity/hypoxie
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Hypoxia as a risk factor for doxorubicin-induced cardiotoxicity: a NMR evaluation.
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Previous studies suggested that one possible mechanism of doxorubicin (DXR)-induced cardiomyopathy involves the depletion of high-energy phosphate stores. In this study, we used 31P nuclear magnetic resonance to assess the high-energy phosphate content in Langendorff perfused rat hearts. Hearts were
Anionic currents in hypoxia-mediated cardiac toxicity: a computer study.
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Hypoxia-caused modulation of cardiac electrophysiology was modeled by computer simulation. Emphasis was on the effect of activation of anionic channels on the electrical state of the tissue. The model includes implicitly the effect of the presence of reactive oxygen species (ROS) and nitrogen oxide
Further observations on the cardiotoxicity of isoprenaline during hypoxia.
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1 In dogs respired with 10% oxygen: 90% nitrogen, only five out of 16 dogs survived repeated intravenous doses of isoprenaline (either 0.5 or 1.0 mug/kg) and only one out of six dogs survived repeated isoprenaline inhalations from a pressurized aerosol.2 In dogs respired with 15% oxygen: 85%
Molecular biomarkers of cantharidin-induced cardiotoxicity in Sprague-Dawley rats: Troponin T, vascular endothelial growth factor and hypoxia inducible factor-1α.
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Early diagnosis of cantharidin-induced myocardial injury is the key to reduce the fatality rate in clinical practice. The purpose of the present study was to explore biomarkers that can be used for the prediction and diagnosis of cantharidin-induced myocardial injury. Of 65 male Sprague-Dawley rats
Effects of respiratory and metabolic pH changes and hypoxia on ropivacaine-induced cardiotoxicity in dogs.
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We have studied the effects of acute changes in acid-base status and hypoxia on the cardiotoxic effects of intracoronary injection of ropivacaine in anaesthetized dogs. The effects of intracoronary ropivacaine were compared when ropivacaine was administered during eucapnia and during each of another
The influence of hypoxia and hypercapnia on the cardiotoxicity of isoprenaline in dogs [proceedings].
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Animal model of cardiotoxicity: carbon monoxide induced ECG hypoxia masked in light narcosis.
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Inhalation exposure of restrained conscious rats to carbon monoxide (1000 ppm, 120 min.) led to a peak carboxyhaemoglobine concentration of 40-45%. At this concentrations spontaneous motor activity was not affected significantly but the physical capacity at endurance run was depressed by 70%. From
Cardiotoxicities of paclitaxel in African Americans.
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OBJECTIVE
To assess the cardiac disturbances in African-American patients treated with paclitaxel.
METHODS
One-hundred-nineteen African-American patients received paclitaxel for various cancers at Howard University Hospital during the years 1993-2001. Medical records of 100 patients were available
Role of hypoxia-inducible factors in the dexrazoxane-mediated protection of cardiomyocytes from doxorubicin-induced toxicity.
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OBJECTIVE
Iron aggravates the cardiotoxicity of doxorubicin, a widely used anticancer anthracycline, and the iron chelator dexrazoxane is the only agent protecting against doxorubicin cardiotoxicity; however, the mechanisms underlying the role of iron in doxorubicin-mediated cardiotoxicity and the
Hypoglycemia enhances bupivacaine-induced cardiotoxicity in the rat.
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The effect of blood glucose concentration on bupivacaine-induced cardiotoxicity was investigated in normoglycemic and hypoglycemic adult rats and compared to that of equipotent doses of lidocaine. The anesthetic agents were injected intraperitoneally into tracheostomized animals anesthetized with
Styrene maleic acid copolymer-pirarubicin induces tumor-selective oxidative stress and decreases tumor hypoxia as possible treatment of colorectal cancer liver metastases.
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BACKGROUND
Pirarubicin, a derivative of doxorubicin, induces tumor destruction via the production of reactive oxygen species (ROS) but is associated with cardiotoxicity. As a macromolecule (conjugated to styrene-maleic acid [SMA]), SMA-pirarubicin is selective to tumors resulting in improved
Repression of hypoxia-reoxygenation injury in the catalase-overexpressing heart of transgenic mice.
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Hypoxia-reoxygenation injury results at least in part from reactive oxygen free radicals. Catalase is a major enzyme involved in detoxification of hydrogen peroxide. The activity of catalase per gram of tissue in the heart is very low, being only about 2% that of liver in rodents and humans, which
Distinct mechanisms of cardiomyocyte apoptosis induced by doxorubicin and hypoxia converge on mitochondria and are inhibited by Bcl-xL.
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Hypoxia and doxorubicin can cause cardiotoxicity and loss of myocardial function. These effects are due, in part, to an induction of apoptosis. Herein we identify the apoptotic pathways activated in H9c2 cells in response to hypoxia (O(2)/N(2)/CO(2), 0.5:94.5:5) and doxorubicin (0.5 muM). Although
Drug-induced cardiotoxicity due to aminophylline treatment: a case report.
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BACKGROUND
Aminophylline, a theophylline compound that contains ethylenediamine, has untoward side effects on many organ systems.
OBJECTIVE
The goal of this case report was to illustrate the occurrence of acute adverse events (ie, chest discomfort and myocardial enzyme elevation) that may be
On-chip monitoring of skeletal myoblast transplantation for the treatment of hypoxia-induced myocardial injury.
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A comprehensive elucidation of the unexpected adverse events that occur in skeletal myoblast transplantation is fundamental for the optimization of myocardial therapeutic effects. However, a well-defined method to study the interactions between skeletal myoblasts and cardiomyocytes during the
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