Calcium ; metabolism ; Calcium Signaling ; Epinephrine ; pharmacology ; Hepatocytes ; drug effects ; metabolism ; Humans

The effect of dexamethasone (10(-5)M) and epinephrine (10(-6)M) on the biosynthesis of metallothionein (MT) in the perfused rat liver was investigated. MT synthesis was determined by measuring the incorporation of 14C-L-aspartic acid into liver MT fraction after the perfusion for five hours of isolated liver by artificial blood containing 14C-L-U-aspartic acid (0.2uci) with dexamethasone or epinephrine. MT was isolated by Sephadex G-75 column chromatography and DEAE Sephadex column chromatography. Incorporation of radioactive 14C into the MT fraction of perfused liver cytosol (9.0grams of liver) from dexamethasone treated, epinephrine treated and control groups were, respective1y, 0.72, 0.34 and 0.33% of total radioactivity infused. Total protein content in the MT fraction of liver perfused with dexamethasone and epinephrine were 0.80, 0.64mg/g liver compared to 0.52mg/g liver in the control. MT, a protein having a high content of cystein and metals is synthesized in the perfused rat liver and its induction is stimulated by dexamethasone, while epinephrine increased the accumulation of Zn in the MT fraction of the perfused rat liver. The present experiment confirms that MT synthesis and degradation are somewhat regulated by glucocorticoid hormone and epinephrine.
Animal ; Dexamethasone/pharmacology* ; Epinephrine/pharmacology* ; Female ; In Vitro ; Liver/drug effects ; Liver/metabolism* ; Metalloproteins/metabolism* ; Metallothionein/metabolism* ; Perfusion ; Rats ; Zinc/metabolism

The influence of thyroxine upon n the cardiac uptake of catecholamines was investigated in rabbits. A single injection of thyroxine(1.0m/kg) into rabbits did not affect the concentration of myocardial catecholamines. However, this dose of thyroxine greatly increased the cardiac uptake of catecholamine following injection of 2.0mg of norepinephrine as compared to that of untreated normal animals and it remained elevated for several hours. Similarly thyroxine also enhanced the accumulation of myocardial catecholamines following administration of dopa(60-80mg/kg) and epinephrine(1.0-1.5mg/kg).
Animal ; Catecholamines/metabolism* ; Epinephrine/metabolism ; Heart/drug effects* ; Male ; Myocardium/metabolism* ; Norepinephrine/metabolism ; Rabbits ; Thyroxine/pharmacology* ; Tritium

AIMTo elucidate the mechanism of depression induced by chronic unpredictable mild stress (CUMS), the effects of CUMS on serotonin (5-HT), tryptophan, stress hormones and behaviour were investigated in rats.

METHODSDepression was induced by for 8 weeks CUMS and confirmed by behavioral tests, the brain and plasma levels of monoamine neurotransmitters were analyzed by HPLC-ECD techniques, the content of plasma corticosterone was evaluated by I125 cortisol radioactivity immunoassay and the serum tryptophan content was measured by HTTACHI L-8800 amino acid analyzer.

RESULTS(1) Rats exposed to a series of mild, unpredictable stressors for 8 weeks displayed the decreased body weight, reduced scores of open-field test and preference of sucrose solution (P < 0.05). (2) Plasma and brain 5-HT contents in rats after exposure to CUMS 8 weeks decreased significantly (P < 0.05). While serum tryptophan content increased at the same time (P < 0.05). (3) Plasma norepinephrine and epinephrine in rats were increased after CUMS 8 weeks, but there was no difference between control and CUMS group in plasma corticosterone.

CONCLUSIONThe behavioral changes induced by CUMS for 8 weeks are similar to the features of human depression, which may be related to the disturbances of tryptophan metabolism induced by increased norepinephrine and epinephrine in CUMS rat.

Animals ; Depression ; metabolism ; Epinephrine ; metabolism ; Hippocampus ; metabolism ; Male ; Neurosecretory Systems ; metabolism ; Norepinephrine ; metabolism ; Rats ; Rats, Wistar ; Serotonin ; metabolism ; Stress, Psychological ; metabolism

End tidal carbon dioxide tension (ETCO2), the partial pressure of exhaled CO2 obtained at the end of tidal breath measured by capnometer, can enable PaCO2 estimation and the monitoring of adequate ventilation. However, there are many factors that may affect ETCO2. Recently, we experienced a patient that developed an abrupt increase of ETCO2 of over 10 mmHg following the subcutaneous infiltration of a high dose of epinephrine for intraoperative hemostasis. This increase in ETCO2 may have been caused by an increased cardiac output and an increase in CO2 production due to increased tissue metabolism. Therefore, when we use ETCO2 to monitor a patient's ventilation, we should bear in mind that three factors - ventilation, hemodynamics and metabolism, may affect the the determined ETCO2 level.
Carbon Dioxide ; Cardiac Output ; Epinephrine* ; Hemodynamics ; Hemostasis* ; Humans ; Metabolism ; Partial Pressure ; Ventilation

Acetylcholine ; metabolism ; Animals ; Arcuate Nucleus of Hypothalamus ; metabolism ; Dopamine ; metabolism ; Epinephrine ; metabolism ; Female ; Neurotransmitter Agents ; metabolism ; Norepinephrine ; metabolism ; Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission

OBJECTIVETo investigate the influence of adrenaline on the expression of TGFbeta1, bFGF and procollagen for human normal and hypertrophic scar dermal fibroblasts cultured in vitro.

METHODSHuman normal and hypertrophic scar dermal fibroblasts were propagated in a serum-free in vitro model with adrenaline for 24 hours. The human mRNA levels of bFGF, TGF-beta1 and I procollagen in fibroblasts were determined by RT-PCR. Levels of bFGF and TGF-beta1 in the supernatants of fibroblasts cultured in vitro were determined by enzyme-linked immunosorbent assay (ELISA).

RESULTSIn our study, adrenaline caused statistically significant increase in the peak levels of bFGF for normal and hypertrophic scar fibroblast cell lines (P < 0.01). It also caused statistically significant decrease in the level of TGF-beta1 for normal and hypertrophic scar fibroblast cell lines. Modulation of normal fibroblasts with 0.05, 0.10 and 0.20 micromol/L adrenaline resulted in a statistically significant (P < 0.01) decrease in the expression of I procollagen mRNA. However, only 0.20 micromol/L adrenaline can decreased the mRNA expression of I procollagen in the hypertrophic scar fibroblasts.

CONCLUSIONSWe conclude from these results that adrenaline can increase the production of bFGF and decrease production of TGF-beta1 and I procollagen in human normal dermal and hypertrophic scar fibroblasts cultured in vitro.

Cells, Cultured ; Cicatrix, Hypertrophic ; metabolism ; Collagen Type I ; metabolism ; Epinephrine ; pharmacology ; Fibroblast Growth Factor 2 ; metabolism ; Fibroblasts ; drug effects ; metabolism ; Humans ; Procollagen ; metabolism ; RNA, Messenger ; metabolism ; Transforming Growth Factor beta1 ; metabolism

OBJECTIVETo investigate the role of protein kinase C (PKC) in the down-regulation of fibroblast proliferation in normal skin (NFb) and hyperplastic scar (SFb) by adrenaline.

METHODSHuman NFb and SFb cells were cultured in vitro. Phentolamine (in final concentrations of 0 and 3 x 10(-6) micromol/L) was added to the culture medium. One hour later, adrenaline in different final concentrations (0.00, 0.05, 0.10, 0.20 micromol/L) was added to the culture medium and incubated for 24 hours. The cellular proliferation activity and cell viability rate were determined with MTT. The cell culture supernatant was harvested for the determination of LDH activity to assess the toxicity of phentolamine and adrenaline. The phosph-PKC activity was determined with Western-blotting and was semiquantitatively analyzed.

RESULTS(1) After stimulation with adrenaline alone, or combined 0.20 micromol/L adrenaline with 3 x 10(-6) micromol/L phentolamine, the cell viability of both NFb and SFb decreased significantly (P < 0.05 or 0.01). (2) There was no difference in the LDH activity between the cells either stimulated by adrenaline in all concentrations or by combination of adrenaline and phentolamine (P > 0.05). (3) The phosphorylation of PKC in NFb and SFb cells stimulated by 0.05, 0.10, 0.20 micromol/L adrenaline was obviously higher than that before stimulation (P < 0.01). When phentolamine in the concentration of 3 x 10(-6) micromol/L was used alone for stimulation, the phosphorylation of PKC in NFb cells (123 +/- 5) was also evidently higher than that before stimulation (80 +/- 5, P < 0.01). But there was no such effect on SFb cells (P > 0.05). When adrenaline in the concentration of 0.05, 0.10 or 0.20 micromol/L was separately added together with phentolamine in the dose of 3 x 10(6) micromol/L for the stimulation, the phosphorylation of PKC in NFb and SFb cells was evidently lower than that when 3 different concentrations of adrenaline was used alone for stimulation (P < 0.01).

CONCLUSIONAdrenaline can inhibit the proliferation of NFb and SFb by activating PKC through binding alpha adrenaline receptor.

Cell Proliferation ; drug effects ; Cells, Cultured ; Cicatrix, Hypertrophic ; metabolism ; Down-Regulation ; Epinephrine ; adverse effects ; Fibroblasts ; cytology ; Humans ; Phentolamine ; adverse effects ; Phosphorylation ; Protein Kinase C ; metabolism ; Skin ; drug effects

Sleep-disordered breathing (SDB) is associated with increased cardiovascular and cerebrovascular morbidity. Epidemiological and clinic-based studies have shown that SDB is related to impaired glucose tolerance and increased insulin resistance, independent of obesity. Despite of a consistent association between SDB and impaired glucose-insulin metabolism, the mechanism underlying this relationship has not been fully elucidated. It is recognized that hypoxemia and hypercapnia that occur in SDB provoke sympathetic nervous activity and catecholamine, epinephrine and norepinephrine, and cortisol are released. Sympathetic hyperactivity and increased catecholamines can impair glucose homeostasis by increasing glycogenolysis and gluconeogenesis, which can result in increased circulating insulin levels and increased risk of insulin resistance. A prospective study is needed to investigate the causal relationship between SDB and impaired glucose-insulin metabolism in a healthy population without diabetes, hypertension and obesity as etiologic risk factors.
Anoxia ; Catecholamines ; Epinephrine ; Gluconeogenesis ; Glucose ; Glycogenolysis ; Homeostasis ; Hydrocortisone ; Hypercapnia ; Hypertension ; Insulin ; Insulin Resistance ; Metabolism ; Norepinephrine ; Obesity ; Risk Factors ; Sleep Apnea Syndromes* ; Sleep Wake Disorders

BACKGROUND: Epinephrine is frequently administered during cardiac surgery. The vascular response to epinephrine might be altered by ischemia and reperfusion, since altered vascular control has been demonstrated even after a short period of ischemia. To test the hypothesis, the effects of epinephrine on regional myocardial contractility, coronary blood flow (CBF) and myocardial oxygen consumption (MVO2) were investigated before and after ischemia in an open-chest canine myocardium. METHODS: Fifteen dogs were acutely instrumented under enflurane anesthesia to measure aortic and left ventricular pressures, pulmonary and left anterior descending (LAD) blood flows via Doppler flowmeter, and subendocardial segment length in the region supplied by LAD. Incremental doses of epinephrine (4, 10, 20, 30 ng/mL of LAD flow) were infused directly into LAD before (normal) and after a 15 min of LAD occlusion and subsequent 30 min-reperfusion (stunned). Segment shortening (%SS), as an index of regional myocardial contractility was evaluated. Simultaneous arterial and coronary venous contents of oxygen and lactate were measured during epinephrine (0.0, 4, 10, and 30 ng/mL) infusion. Effectiveness of metabolic vasodilation was determined from oxygen extraction ratio (EO2). RESULTS: Epinephrine infusions before ischemia resulted in dose-dependent increases in %SS and MVO2. These changes were accompanied by excessive increases in CBF, resulting in decreased EO2. After the ischemia and reperfusion, %SS was depressed and lactate extraction (Elac) was reduced, but similar mechanical responses to epinephrine were observed. However, in the stunned myocardium, CBF increased in parallel with increases in MVO2, resulting in unaltered EO2. Epinephrine infusion further decreased Elac dose-dependently in stunned myocardium. Heart rate and left ventricular systolic and diastolic pressures were little but similarly affected during epinephrine infusions before and after myocardial ischemia. CONCLUSIONS: The results suggest that epinephrine exerts positive inotropic effects in both normal and stunned myocardium, and that epinephrine causes direct coronary vasodilation in normal myocardium, but this effect is abolished in stunned myocardium in dogs. It is also suggested that epinephrine infusion depresses Elac dose-dependently in stunned myocardium.
Anesthesia ; Animals ; Dogs* ; Enflurane ; Epinephrine* ; Flowmeters ; Heart Rate ; Ischemia ; Lactic Acid ; Metabolism* ; Myocardial Ischemia ; Myocardial Stunning* ; Myocardium ; Oxygen ; Oxygen Consumption ; Reperfusion ; Thoracic Surgery ; Vasodilation ; Ventricular Pressure