We reported a case of pheochromocytoma with initial presentation of cardiac arrest. The patient underwent implantable cardioverter defibrillator for primary prevention but subsequently experienced repeated implantable cardioverter defibrillator shocks and syncopal episodes. A mass was found in the adrenal gland by CT, which was confirmed by anatomopathological analysis of the surgical specimen.

The benefits of consuming soy and its protein have been reported in many studies. However, its phytoestrogen content raises concerns about consumption during lactation and gestation We therefore examined the effects of soybean or soy protein isolate on the parameters-related cardiovascular pathophysiology in lactating mothers and their offsprings at weaning and adulthood. Lactating rats were divided: casein control (C); soy protein isolate (SPI); and soybean (S). At weaning, half of the litter received commercial ration up to 150 days. The levels of 17-β-estradiol and superoxide dismutase were low in the S mothers. For the SPI mothers, we observed a reduction of thiobarbituric acid reactive substances (TBARS). At weaning, atherogenic indices [1 = total cholesterol (TC)/HDL; 2 = LDL/HDL; 3 = TC-HDL/HDL)] decreased in the S and SPI offsprings compared to the casein control group; TBARS and antioxidant enzymes increased in the S offspring, while reduced/oxidized glutathione ratio increased in the SPI offspring, indicating lower oxidative stress. In adulthood, the SPI offspring showed an increase in liver cholesterol and atherogenic index 1 and 3 (vs. C and S) and 2 (vs. S). In addition, we found a decrease in catecholamines in the adrenal medulla and an increase in caffeine-stimulated secretion, but tyrosine hydroxylase expression remained constant. Maternal consumption of SPI during lactation worsened atherogenic indices of the offsprings in adulthood, which was associated with increased liver cholesterol and decreased catecholamines in the adrenal medulla. Soy consumption had no consistent long-term effects on the evaluated parameters compared to casein consumption. The data suggest that the consumption of SPI during lactation should be done with caution.

Here we focused on the dynamic processes in the snail at different time after short-term hypergravity load (STHL) by monitoring the state of neuroendocrine and immune systems, the nucleic acid synthesis levels in the atrial cells, and the behaviour of the atrial granular cells (GCs). We observed that immediately after centrifugation (14 g for 15 min) in the snail haemolymph concentration of dopamine and noradrenaline (measured by high-performance liquid chromatography) and the number of circulating haemocytes and their proliferative activity (estimated by the direct cell counting and [3H]thymidine incorporation, respectively) increased significantly, whereas the concentration of adrenaline decreased. Twenty-four hours after STHL, the levels of catecholamines and haemocytes returned to their control values. In the atrial epicardial and endothelial cells, a notable drop of transcription activity (evaluated by [3H]uridine autoradiography) from the baseline in the immediate post-STHL period was followed by its gradual increase reaching a maximum at the day 5 and subsequent decrease to control value by the day 10. In endothelial cells, DNA-synthesizing activity (evaluated by [3H]thymidine autoradiography) equal to zero before and just after STHL, increased significantly at the day 5, and decreased by the day 10. The atrial GCs underwent total degranulation. Formed as a result small ungranulated cells exhibited DNA synthesis. Afterwards, most probably, the GCs divided and regranulated. One month after STHL the GC population had been restored. Overall, STHL has triggered an immediate reaction of the neuroendocrine and immune systems and initiated long-lasting processes at a cellular level, which included alterations in activity of nucleic acid syntheses in the epicardial and endothelial cells and remodelling of the GC population in the atrium.

In adipocytes the hydrolysis of TAG to produce fatty acids and glycerol under fasting conditions or times of elevated energy demands is tightly regulated by neuroendocrine signals, resulting in the activation of lipolytic enzymes. Among the classic regulators of lipolysis, adrenergic stimulation and the insulin-mediated control of lipid mobilisation are the best known. Initially, hormone-sensitive lipase (HSL) was thought to be the rate-limiting enzyme of the first lipolytic step, while we now know that adipocyte TAG lipase is the key enzyme for lipolysis initiation. Pivotal, previously unsuspected components have also been identified at the protective interface of the lipid droplet surface and in the signalling pathways that control lipolysis. Perilipin, comparative gene identification-58 (CGI-58) and other proteins of the lipid droplet surface are currently known to be key regulators of the lipolytic machinery, protecting or exposing the TAG core of the droplet to lipases. The neuroendocrine control of lipolysis is prototypically exerted by catecholaminergic stimulation and insulin-induced suppression, both of which affect cyclic AMP levels and hence the protein kinase A-mediated phosphorylation of HSL and perilipin. Interestingly, in recent decades adipose tissue has been shown to secrete a large number of adipokines, which exert direct effects on lipolysis, while adipocytes reportedly express a wide range of receptors for signals involved in lipid mobilisation. Recently recognised mediators of lipolysis include some adipokines, structural membrane proteins, atrial natriuretic peptides, AMP-activated protein kinase and mitogen-activated protein kinase. Lipolysis needs to be reanalysed from the broader perspective of its specific physiological or pathological context since basal or stimulated lipolytic rates occur under diverse conditions and by different mechanisms.

We tested the hypothesis that long-term caffeine intake prevents the development of insulin resistance and hypertension in two pathological animal models: the high-fat (HF) and the high-sucrose (HSu) diet rat. We used six groups of animals: control; caffeine-treated (Caff; 1 g/l in drinking water during 15 d); HF; caffeine-treated HF (HFCaff); HSu; caffeine-treated HSu (HSuCaff). Insulin sensitivity was assessed using the insulin tolerance test. Blood pressure, weight gain, visceral fat, hepatic glutathione, plasma caffeine, insulin and NO, and serum NEFA and catecholamines were measured. Caffeine reversed insulin resistance and hypertension induced by both the HF and HSu diets. In the HF-fed animals caffeine treatment restored fasting insulin levels to control values and reversed increased weight gain and visceral fat mass. In the HSu group, caffeine reversed fasting hyperglycaemia and restored NEFA to control values. There were no changes either in plasma NO or in hepatic glutathione levels. In contrast, caffeine totally prevented the increase in serum catecholamines induced by HF and HSu diets. To test the hypothesis that inhibition of the sympathetic nervous system prevents the development of diet-induced insulin resistance we administered carvedilol, an antagonist of β1, β2 and also α1 adrenoceptors, to HF and HSu rats. Carvedilol treatment fully prevented diet-induced insulin resistance and hypertension, mimicking the effect of caffeine. We concluded that long-term caffeine intake prevented the development of insulin resistance and hypertension in HF and HSu models and that this effect was related to a decrease in circulating catecholamines.

Aim: The aim was to investigate whether high catecholamine (CA) excreters would respond less well to a group cognitive behaviour therapy (CBT) treatment for depression than others. Method: A sample of 70 adults with depression symptoms participated in a 12-week course of group CBT. Participants’ 24 hour urinary catecholamine levels at pre-therapy and post-therapy were used to classify them as High (N = 10); Low (N = 33) or Mixed (N = 27) according to a cut-off one standard deviation above a published mean for healthy adults. Beck Depression Inventory (BDI) and cognitions questionnaire (Automatic Thoughts Questionnaire; Beck Hopelessness Scale and Dysfunctional Attitudes Scale) were used. Results: Repeated measures ANOVA analyses showed an equal rate of mood improvement in all three groups over the course of CBT, despite the fact that the High excreters were on average more depressed throughout the study. Changes in depression symptoms were mirrored by improvements in cognitive measures in the three catecholamine groups. Conclusion: This study indicates that adults showing a biological marker of depression (elevated catecholamine levels) are equally able to benefit from CBT treatment as adults without this marker.

A comparative method of studying the biological bases of personality compares human trait dimensions with likely animal models in terms of genetic determination and common biological correlates. The approach is applied to the trait of sensation seeking, which is defined on the human level by a questionnaire, reports of experience, and observations of behavior, and on the animal level by general activity, behavior in novel situations, and certain types of naturalistic behavior in animal colonies. Moderately high genetic determination has been found for human sensation seeking, and marked strain differences in rodents have been found in open-field behavior that may be related to basic differences in brain neurochemistry. Agonistic and sociable behaviors in both animals and humans and the trait measure of sensation seeking in humans have been related to certain common biological correlates such as gonadal hormones, monoamine oxidase (MAO), and augmenting of the cortical evoked potential.

The monoamine systems in the rodent brain are involved in general activity, exploratory behavior, emotionality, socialization, dominance, sexual and consummately behaviors, and intracranial self-stimulation. Preliminary studies have related norepinephrine and enzymes involved in its production and degradation to human sensation seeking. A model is suggested that relates mood, behavioral activity, sociability, and clinical states to activity of the central catecholamine neurotransmitters and to neuroregulators and other transmitters that act in opposite ways on behavior or stabilize activity in the arousal systems. Stimulation and behavioral activity act on the catecholamine systems in a brain–behavior feedback loop. At optimal levels of catecholamine systems activity (CSA) mood is positive and activity and sociability are adaptive. At very low or very high levels of CSA mood is dysphoric, activity is restricted or stereotyped, and the organism is unsocial or aggressively antisocial. Novelty, in the absence of threat, may be rewarding through activation of noradrenergic neurons.

Problems with current hypotheses of catecholamine involvement in antidepressant action are reviewed. The theories examined include those that attribute a key role to increased brain norepinephrine (NE) availability or to the desensitization of brain beta adrenergic receptors. Although these hypotheses are consistent with a great deal of relevant laboratory and clinical data there arc an increasing number of findings that cannot be explained by them. These contradictions include findings on the lag time between pharmacological and therapeutic effects of antidepressants, the actions of propranolol and thyroid hormones on depression, the relationship between cortisol secretion and depression, the net effect of chronic antidepressants on noradrenergic neurotransmission, and the functions of cyclic AMP in the CNS. To reconcile the discordant data in these areas of research, a new formulation, the output hypothesis, which is derived from the foregoing theories, is proposed. The new hypothesis assumes that depression or adverse behavioral effects of stress results when the output of brain cells bearing noradrenergic receptors is too low to meet increased demand resulting from stress or other biologically disruptive events. According to this view antidepressants act by a mechanism akin to adaptation to chronic stress in which there is a prolonged increase in postsynaptic noradrenergic receptor activation in the brain. The prolonged increase is necessary for NE to induce, via the beta adrenoceptor–cAMP system, trophic or long-term metabolic effects that increase the output of catecholamine effector cells to a level commensurate with demand.

An experimental design aiming at analysing the consequences of genetic selection from 1977 to 1998–2000 on the evolution of stress-responsive systems in the French Large White (LW) and Landrace (LR) pig populations was conducted by INRA and IFIP-Institut du Porc. Large White sows were inseminated with semen from LW boars born in 1977 (frozen semen) or in 1998 and their second-generation offspring were station-tested. Landrace sows were inseminated with semen from LR boars born in 1977 (frozen semen) or in 1999 to 2000, and their progeny was station-tested. Urinary concentration of stress hormones (cortisol and catecholamines) and traits related to carcass composition (estimated carcass lean content (ECLC) and global adiposity) and meat quality (pH 24 h) were measured. For the two populations, selection carried out since 1977 led to an increase in ECLC and a decrease in carcass adiposity. Between 1977 and 1998 to 2000, urinary concentrations of stress hormones were unchanged in the LR breed, but were decreased in the LW breed. Moreover, for the animals generated from LW boars born in 1977 and in 1998, urinary cortisol levels were negatively correlated with ECLC. Therefore, in the LW breed, selection carried out for higher ECLC resulted in a decrease in cortisol production, as well as a reduction of catecholamine production that may be responsible for the lower ultimate pH of meat. Therefore, selection carried out for increased carcass lean content led, in this breed, to large modifications in the functioning of the stress-responsive systems, thereby influencing a large range of physiological regulations and technical properties such as carcass composition and meat pH, which remained however in the normal range for acceptable meat quality.

Various catecholamines and catecholamine antagonists have been examined for their effects on the third larval moult of the parasitic nematode, Dirofilaria immitis, cultured in vitro. The non-selective α and β agonist, noradrenaline, and the β agonist, isoprenaline, had no effect on the timing of the third stage moult when used at a concentration of 10−5M. The α-adrenergic antagonist. phentolamine, resulted in worm mortality at 10−5M. At 10−7M, both phentolamine and the β-antagonist, propranolol caused a significant reduction in the numbers of larvae capable of completing the third stage moult. Idazoxan, an a2-antagonist, at 10−5M did not affect worm mortality but did completely prevent ecdysis. The potential of these compounds as possible filaricides is discussed.

An antiserum directed against tyrosine hydroxylase (TH), the rate-limiting enzyme in the synthesis of dopamine, was used to study the pigeon retina. Labeled cells were observed in both the inner nuclear layer (INL) and ganglion cell layer (GCL). Two populations of TH-immunoreactive neurons were observed in the INL. Some of these cells were 7−10 μ in diameter and gave rise to processes that arborized in three Layers of the inner plexiform layer (IPL). These cells appeared similar to the dopaminergic amacrine cells described previously (Marc, 1988). Other labeled cells in the INL were 12−20 μ in diameter and were recognizable as a previously described subpopulation of TH-immunoreactive displaced ganglion cells (Britto et al., 1988).

A population of labeled cells was observed in the GCL. Counts of these cells in two retinae revealed 5000 and 7000 cells, respectively. They ranged in size from 8−15 μ in diameter in the central retina and from 8−20 m in diameter in the peripheral retina. The density of labeled cells was highest in the central retina and red field and lowest in the retinal periphery. The difference in cell size and cell density as a function of eccentricity is characteristic of the total population of ganglion cells in the avian retina (Ehrlich, 1981; Hayes, 1982). Some of the TH-positive cells in the GCL could be classified as ganglion cells for two reasons: (1) The axons of many of the TH-positive cells in the GCL were TH-immunoreactive as well and could be followed to the optic nerve head. (2) The injection of rhodamine-labeled microspheres into the nucleus geniculatus lateralis, pars ventralis (GLv), resulted in the retrograde labeling of many of the TH-positive cells in the contralateral retina.

Immunohistochemical and retrograde tracing techniques were combined to study the retinal ganglion cells which project to the pars ventralis of the lateral geniculate nucleus (GLv) in the pigeon. Using two different fluorescent tracers, two histochemically-distinct populations of ganglion cells were found to project to both the GLv and the optic tectum. The first population of ganglion cells exhibited tyrosine hydroxylase-like immunoreactivity and represented about 20% of all ganglion cells which were retrogradely labeled from the GLv. The second population of ganglion cells showed substance P-like immunoreactivity and represented about 13% of all ganglion cells projecting to the GLv. These results confirm earlier suggestions that the retinal axons projecting to the GLv also project elsewhere and demonstrate that heterogeneity of retinal ganglion cells transmitters is evident even within a single retino-recipient nucleus such as the GLv.

Data on the cerebrovascular effects of catecholamines after head injury are difficult both to interpret and to compare. Diverse parameters with regard to brain trauma animal models, methods of determining the effects on the cerebral blood flow and metabolism and choice of end-points have been used. Many studies investigate the cerebrovascular effects of catecholamines over a range of cerebral perfusion pressures above the range recommended by current guidelines. The relationship between patient outcome and the use of a specific substance to improve cerebral perfusion has not been investigated. Dopamine, norepinephrine and phenylephrine all seem to increase cerebral blood flow in various animal models and in patients. The data suggest that norepinephrine may be the most predictable. It is associated with an improved restoration of global and regional oxygenation when compared to dopamine. Dopamine has been associated with an increase in brain oedema. There is further evidence that dopamine has many disadvantages in critically ill patients due to its ability to suppress circulating concentrations of most anterior pituitary-dependent hormones. Both aspects would further discourage its use. Data on phenylephrine are scarce. It has been associated with increased intracranial pressure and a failure to improve cerebral oxygenation despite markedly improved cerebral perfusion pressure. For all other catecholamines and related substances there are insufficient data on the cerebrovascular effects after head injury. This suggests that norepinephrine may be the catecholamine that is the most suitable substance to maintain or restore adequate cerebral perfusion. The data, however, are insufficient to formulate a guideline.

Stress neuroendocrine systems (hypothalamic–pituitary–adrenal axis and sympathetic nervous system) were studied in 100 female pigs from each of the five main genetic lines used in Europe for pork production: Piétrain, Large White, Landrace, Duroc and Meishan. Levels of cortisol and catecholamines were measured in urine collected at the farm, after transportation to the slaughterhouse and the next morning before slaughter. With the exception of the Piétrain line that showed intermediate levels of cortisol despite its extreme leanness, a significant positive relationship was found between basal cortisol levels and fatness, both across and within (except in Piétrain and Duroc) lines. Basal cortisol levels were 2.46-fold higher in Meishan (20.46 ng/mg creatinine) than in Large White pigs (8.30 ng/mg creatinine), the two extreme breeds. Post-transportation levels were highest but proportional to basal levels, suggesting that the adrenal reactivity to adrenocorticotropic hormone is a major source of variability between lines. Levels of catecholamines were less variable between lines but correlated also with fatness, partlyviapartial correlations with cortisol levels. In serum collected at exsanguination, creatine kinase activity was correlated with muscularity across the five breeds. However, this was due to a much larger activity than expected in Piétrain pigs, although all animals were negative for the allele of the ryanodine receptor gene responsible for stress sensitivity. Serum glucose levels were inversely related to fatness. These data show that the differences between breeds or lines can be utilised by cross-breeding and that this can lead to changes in stress hormones and in turn to some degree of changes in carcass traits.

The sympathetic nervous system is involved in the control of energy metabolism and expenditure. Diet-induced thermogenesis is mediated partly by the ß-adrenergic component of this system. The aim of the present study was to investigate the role of genetic variation in the ß2-adrenoceptor in diet-induced thermogenesis. Data from twenty-four subjects (fourteen men and ten women; BMI 26·7(sem 0·8) kg/m2; age 45·2(sem1·4) years) with different polymorphisms of the ß2-adrenoceptor at codon 16 (Gly16Gly, Gly16Arg or Arg16Arg) were recruited for this study. Subjects were given a high-carbohydrate liquid meal, and the energy expenditure, respiratory exchange ratio, and plasma concentrations of NEFA, glycerol, glucose, insulin and catecholamines were measured before and over 4 h after the meal. The AUC of energy expenditure (diet-induced thermogenesis) was not significantly different between polymorphism groups, nor was the response of any of the other measured variables to the meal. In a multiple regression model, the only variable that explained a significant proportion (32 %) of the variation in diet-induced thermogenesis was the increase in plasma adrenaline in response to the meal (P<0·05). The ß2-adrenoceptor codon16 polymorphisms did not contribute significantly. In conclusion, an independent contribution of the codon 16 polymorphism of the ß2-adrenoceptor gene to the variation in thermogenic response to a high-carbohydrate meal could not be demonstrated. The interindividual variation in thermogenic response to the meal was correlated with variations in the plasma adrenaline response to the meal.

Slower weight gain and less visceral fat had been observed when rats fed a high-fat diet were supplemented with freeze-dried bitter melon (BM) juice; the metabolic consequences and possible mechanism(s) were further explored in the present study. In a 4-week experiment, rats were fed a low-fat (70 g/kg) or a high-fat (300 g/kg) diet with or without BM (7·5 g/kg or 0·75%). BM-supplemented rats had lower energy efficiency, visceral fat mass, plasma glucose and hepatic triacylglycerol, but higher serum free fatty acids and plasma catecholamines. In the second experiment, 7-week BM supplementation in high-fat diet rats led to a lowering of hepatic triacylglycerol (P<0·05) and steatosis score (P<0·05) similar to those in rats fed a low-fat diet. BM supplementation did not affect serum and hepatic cholesterol. However, plasma epinephrine and serum free fatty acid concentrations were increased (P<0·05). In the third experiment, BM(7·5 and 15 g/kg) and 1·5 % BM lowered triacylglycerol concentration in red gastrocnemius and tibialis anterior (P<0·05) muscle, but a dose–response effect was not observed. These data suggest that chronic BM feeding leads to a general decrease in tissue fat accumulation and that such an effect is mediated in part by enhanced sympathetic activity and lipolysis. BM or its bioactive ingredient(s) could be used as a dietary adjunct in the control of body weight and blood glucose.