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epinephrine/cáncer
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Microvascular mechanisms of change in tumor blood flow due to angiotensin II, epinephrine, and methoxamine: a functional morphometric study.
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To elucidate the microvascular mechanisms of change in tumor blood flow elicited by vasopressors, a functional morphometric study of the s.c. microcirculation within a rat transparent chamber was performed. Arteriolar vessels were classified centripetally (a2-a5) according to Strahler's method.
The blood supply of experimental liver metastases. VIII. Increased capillary blood flow within liver tumors with administration of epinephrine.
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Capillary blood flow has been studied with a laser doppler probe in normal liver tissue and within Walker carcinosarcoma tumors implanted in the livers of rats. Epinephrine, in doses from 1 to 100 micrograms injected as a bolus into the portal system caused immediate significant rises in tumor
Epinephrine attenuates down-regulation of monocyte tumor necrosis factor receptors during human endotoxemia.
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Epinephrine inhibits lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF) production by increasing intracellular cAMP concentrations. Because agents that increase cAMP levels can enhance TNF receptor expression in vitro, granulocyte and monocyte TNF receptors were determined by FACS-analysis
Epinephrine inhibits endotoxin-induced IL-1 beta production: roles of tumor necrosis factor-alpha and IL-10.
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Epinephrine has been found to inhibit the production of the proinflammatory cytokine tumor necrosis factor (TNF)-alpha and to enhance the production of anti-inflammatory cytokine interleukin (IL)-10. To determine the effect of epinephrine on IL-1 beta production, the following experiments were
Epinephrine or peplomycin combined with hyperthermia in irradiated Lewis lung carcinoma: effects on tumor growth, skin reaction, and lung metastasis.
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Although hyperthermia potentiates the effect of radiation, the combined effect decreases as the time between irradiation and hyperthermia increases. The purpose of this study was to prevent the rapid loss of efficacy by the local injection of epinephrine or peplomycin(PEP), two agents known as
The blood supply of experimental liver metastases. VII. Further studies on increased tumor vascularity caused by epinephrine.
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The effects of epinephrine on the vascularity of tumors within the liver of rats were studied by simultaneous injection of Microfil into the arterial and portal systems. A marked increase in perfusion of capillary-sized vessels within the central portions of the tumor was observed in both induced
Phase 2 study of intratumoral cisplatin and epinephrine treatment for locally recurrent head and neck tumors.
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Local relapses of head and neck tumors are not often eligible for surgical and/or radiotherapy retreatment, and the efficacy of systemic chemotherapy is poor. A greater accumulation and efficacy of anticancer drugs with lower systemic toxicity is theoretically obtained with intratumoral
Intraoperative chemotherapy with cisplatin and epinephrine after cytoreductive surgery in patients with recurrent ovarian cancer: a phase I study.
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BACKGROUND
Intraperitoneal (i.p.) epinephrine was shown to increase the accumulation of i.p. cisplatin in tumours, and thus its antitumour effect in a model of peritoneal carcinomatosis in rats.
METHODS
To determine the tolerance to i.p. epinephrine with cisplatin, 18 patients with recurrent ovarian
Epinephrine enhances penetration and anti-cancer activity of local cisplatin on rat sub-cutaneous and peritoneal tumors.
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Despite the theoretical advantages of a high local concentration of anti-cancer drugs, local chemotherapy often fails to produce complete and lasting responses in experimental and human solid tumors. Experiments using Patent Blue dye showed that fluids diffused poorly into tumor mass when injected
Epinephrine protects cancer cells from apoptosis via activation of cAMP-dependent protein kinase and BAD phosphorylation.
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The stress hormone epinephrine is known to elicit multiple systemic effects that include changes in cardiovascular parameters and immune responses. However, information about its direct action on cancer cells is limited. Here we provide evidence that epinephrine reduces sensitivity of cancer cells
Stress-induced epinephrine enhances lactate dehydrogenase A and promotes breast cancer stem-like cells.
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Chronic stress triggers activation of the sympathetic nervous system and drives malignancy. Using an immunodeficient murine system, we showed that chronic stress-induced epinephrine promoted breast cancer stem-like properties via lactate dehydrogenase A-dependent (LDHA-dependent) metabolic rewiring.
Voluntary Running Suppresses Tumor Growth through Epinephrine- and IL-6-Dependent NK Cell Mobilization and Redistribution.
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Regular exercise reduces the risk of cancer and disease recurrence. Yet the mechanisms behind this protection remain to be elucidated. In this study, tumor-bearing mice randomized to voluntary wheel running showed over 60% reduction in tumor incidence and growth across five different tumor models.
Effects of epinephrine and amrinone on contractility and cyclic adenosine monophosphate generation of tumor necrosis factor alpha-exposed cardiac myocytes.
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OBJECTIVE
This study utilized an in vitro neonatal rat cardiac myocyte assay to evaluate potential differences in the response of TNF-alpha-exposed myocytes to stimulation with the adrenergic agent, epinephrine, and the phosphodiesterase III inhibitor, amrinone.
METHODS
Contractility was assessed by
Epinephrine inhibits tumor necrosis factor-alpha and potentiates interleukin 10 production during human endotoxemia.
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Short-term preexposure of mononuclear cells to epinephrine inhibits LPS-induced production of TNF, whereas preexposure for 24 h results in increased TNF production. To assess the effects of epinephrine infusions of varying duration on in vivo responses to LPS, the following experiments were
Cancer stressors and protective factors: predictors of stress experienced during treatment for childhood cancer.
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Perceptions of cancer stressors and protective factors are predictors of stress experienced during treatment for childhood cancer were assessed in this study. Cancer stressors were the type of treatment received during two clinic visits and the child's perception of the cancer experience. Protective
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