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PubMedDate not supplied

Effects of exogenous catecholamines on glucose and fat metabolism and on triglycerides in the rat liver during total parenteral nutrition.

An experiment was undertaken to investigate the effects of a continuous infusion of catecholamines on glucose and fat metabolism as well as on nitrogen balance and the amount of triglycerides in the rat liver. The animals were nourished by total parenteral nutrition for 5 days and divided into six groups (n = 5 in each group) on the basis of nonprotein calories given with or without an infusion of catecholamines: group G received 100% of nonprotein calories with glucose, group F received 50% of nonprotein calories with glucose, and the remaining 50% with lipid emulsion, groups Epi-G and Epi-F received epinephrine (1 microgram/kg body weight/min) in addition to the same total parenteral nutrition solution as group G or F, and groups Nor-G and Nor-F received norepinephrine (1 microgram/kg/min) in a similar manner. Each group was administered the same number of total calories (252 cal/kg/day) and the same amount of nitrogen (1.49 g/kg/day). Nitrogen balance was better in group G than in group F. Under catecholamine infusion, there were no significant differences in nitrogen balance between groups Epi-G, Nor-G, Epi-F, and Nor-F, but this parameter improved significantly in group Nor-F in comparison to group F. Liver triglycerides was higher in groups Epi-G and Nor-G than in groups Epi-F and Nor-F. Liver triglycerides was directly related to the blood sugar level. These results indicate that nitrogen conservation is improved with lipid emulsion and that glucose rather than lipid plays a significant role in the genesis of fatty liver, when they are administered under catecholamine-induced stress.

Animals↗
PubMed1987

Neonatal adaptation: naloxone increases the catecholamine surge at birth.

A marked increase in plasma catecholamines at birth has been described in animals and man. Because the factors that regulate catecholamine secretion are incompletely understood and because it has recently been suggested that endogenous opiates are important in the regulation of catecholamine secretion, we designed studies to determine the influence of opiate receptor blockade prior to delivery on the increase in plasma catecholamines at birth. Term fetal sheep were delivered by cesarean section and randomly assigned to receive naloxone or vehicle. Naloxone was given just prior to umbilical cord cutting as a 2 mg/kg bolus followed by 2 mg/kg/h. Naloxone administration resulted in significantly greater peak levels of plasma norepinephrine (peak levels of 1.5 +/- 0.4 versus 0.9 +/- 0.1 ng/ml) and epinephrine (peak levels of 1.4 +/- 0.7 versus 0.9 +/- 0.3 ng/ml) and higher norepinephrine values throughout the study period. Naloxone administration was associated with significantly elevated heart rate (peak 184 +/- 12 versus 207 +/- 13 beats per min) and blood pressure (peak 95 +/- 6 versus 88 +/- 2 mm Hg). These studies demonstrate that opiate receptor blockade from birth markedly augments the neonatal sympathoadrenal response in the term newborn lamb.

Animals↗
PubMed1980

Somatostatin analog: plasma catecholamine suppression mediated by the central nervous system.

The somatostatin analog, des-AA1,2,4,5,12,13-[D-Trp8]somatostatin (ODT8-SS), acts within the central nervous system to suppress the rise in plasma catecholamines associated with a variety of neural stimuli. Insulin-induced hypoglycemia or stress caused significant elevations in plasma catecholamines that were abolished by intracerebroventricular (icv) administration of ODT8-SS. Bombesin, carbachol, or 2-deoxyglucose, injected icv, evoked marked elevations in plasma epinephrine and norepineprine. These effects were also prevented by ODT8-SS given icv. In all experiments, ODT8-SS appeared to be more effective in lowering plasma epinephrine than in lowering plasma norepinephrine. Systemic administration of ODT8-SS was ineffective in lowering plasma catecholamine levels. Native somatostatin given icv produced inconsistent effects on plasma catecholamine levels. These data suggest that the somatostatin analog, ODT8-SS, acts within the central nervous system to modulate sympathetic nervous system activity. It is suggested, but not established, that this analog acts through the same receptor as native somatostatin.

Acoustic Stimulation↗
PubMed1989

In the rat, interleukin-1 alpha and -beta stimulate adrenocorticotropin and catecholamine release.

Recombinant interleukin-1 alpha and -beta (Il-1 alpha and -beta) have been evaluated for their abilities to stimulate ACTH and catecholamine secretion in the intact adult male rat. Additionally, the role of adrenergic-dependent pathways in mediating Il-1-induced ACTH release has been assessed. The iv or intracerebroventricular injection of either Il-1 alpha or Il-1 beta caused dose-related increases in plasma ACTH, epinephrine, and norepinephrine levels. While at low iv doses (less than or equal to 10 ng), Il-1 beta was more effective than Il-1 alpha at releasing ACTH, no measurable differences were noted at higher doses. In contrast, Il-1 beta was significantly more active at all doses in elevating plasma ACTH levels after intracerebroventricular injection. Similarly, Il-1 alpha was more effective than Il-1 beta at stimulating epinephrine, but not norepinephrine, secretion after icv injection. Because of the ability of catecholamines to alter ACTH secretion, we then examined the role of adrenergic-dependent pathways as possible mediators of Il-1-induced ACTH secretion. Blockade of adrenergic receptors by the concomitant administration of prazosin and propanolol prevented the simultaneous actions of phenylephrine and isoproterenol on the corticotrophs, but did not significantly alter the effect of peripherally administered Il-1 alpha on ACTH release. These results suggest that both Il-1 alpha and Il-1 beta stimulate ACTH and catecholamine secretion in the rat. Despite the ability of the lymphokine to elevate plasma epinephrine and norepinephrine values, circulating catecholamines do not appear to represent essential modulators of ACTH release induced by acutely injected Il-1.

Adrenergic alpha-Antagonists↗
PubMed1975

Effect of lithium on catecholamine-induced antidiuresis and cyclic AMP in dog kidneys.

Patients treated with lithium salt have an inability to concentrate urine, possible due to the inhibition of the antidiuretic effect of vasopressin. Since beta adrenergic stimulation also induces antidiuresis, a possible effect of lithium on the catecholamine-induced antidiuresis was investigated in dog kidneys. The urinary concentrating ability induced by the iv injection of isoproterenol 0.1 mug/kg was markedly inhibited in the lithium-treated animals (plasma lithium 1.13 plus or minus 0.10 mM). The increase of cyclic AMP concentration by 1 muM isoproterenol was also significantly less in the renal medullary slices obtained from the lithium-treated animals than in those obtained from the control animals. These findings suggest that the inability to concentrate urine in the patients treated with lithium salt is probably due to the inhibition of the antidiuretic effect of catecholamine as well as that of vasopressin; and the inhibitory mechanism of lithium on the catecholamine-induced antidiuresis is possibly through the inhibition of the catecholamine-dependent cycle AMP system in renal medulla.

Aminohippuric Acids↗
PubMed1982

Circulating catecholamine and glucagon responses to insulin-induced blood glucose decrement in a patient with pheochromocytoma.

In a gastrectomized woman with an adrenal pheochromocytoma we observed hypertensive crisis in association with postprandial hypoglycemic episodes. To assess whether hypoglycemia could be responsible for the hypertensive crises, we measured circulating catecholamines and glucagon during an insulin-induced blood glucose decrement carried out by an artificial endocrine pancreas. When the blood glucose level reached 36 mg/dl, a severe hypertensive crisis occurred. At this time, circulating catecholamines increased 2-fold (norepinephrine, from 2200 to 3568 pg/ml; epinephrine, from 950 to 1750 pg/ml), while no changes in glucagon were observed. Our observation suggests that in patients with pheochromocytoma, hypoglycemia may trigger a marked release of catecholamines independent of glucagon secretion. This response probably is mediated by activation of the sympathetic nervous system. Our results also suggest that the pancreatic A-cell response to blood glucose decrement is totally suppressed in patients with pheochromocytoma by the chronically high levels of circulating catecholamines. Thus, hypoglycemia may be added to the list of other well known factors which may provoke hypertensive emergencies in patients with pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1983

Role of catecholamines in the ketonemic response to somatostatin in normal man.

In order to determine if a rise of circulating catecholamines occurs during somatostatin (SRIF) infusion in normal man, and if this increase plays a significant metabolic role, we infused four normal subjects with SRIF (500 micrograms/h) alone or associated with either alpha-(phentolamine) or beta-(propranolol) adrenergic blocking agents. During SRIF infusion, the initial small decrease in blood glucose was followed by a rise of epinephrine from 25-46 ng/liter (range) to 117-143 ng/liter (range) (P less than 0.05) at 80 min and norepinephrine from 204 +/- 16 to 418 +/- 60 ng/liter at 90 min (P less than 0.05). Thereafter, plasma nonesterified fatty acids, blood glycerol, and ketone bodies increased significantly. Phentolamine adjunction modified neither the catecholamines rise, nor the metabolic changes. Propranolol adjunction did not modify the glucose fall and the catecholamine rise, but resulted in blunted increments of fatty acids and glycerol and in an almost complete suppression of the increase of ketone bodies. These results suggest that the enhanced lipolysis and ketogenesis observed during SRIF infusion are not only due to the SRIF-induced insulin deficiency but also in part to a beta-receptor mediated effect of catecholamines.

Adult↗
PubMed1995

The contribution of the sympathoadrenomedullary system to the etiology of essential hypertension: a study using plasma and platelet catecholamine concentrations.

Platelets take up and store noradrenaline and adrenaline in proportion to plasma concentrations and may, therefore, provide an integrated index of sympathoadrenomedullary arousal. Plasma and platelet catecholamine concentrations were measured in 290 European and 155 Asian subjects, and were related to blood pressure, insulin levels, and social class. Plasma noradrenaline concentrations correlated with systolic and diastolic blood pressure in both ethnic groups (r = 0.20-0.30), and these levels were significantly elevated in hypertensive subjects (P < 0.003). In Europeans, but not in Asians, these relationships remained significant after adjusting for age and gender, and were independent of the relationship between insulin and blood pressure. There were much weaker relationships between platelet catecholamine concentrations and blood pressure, which were dependent on age and gender as covariates. In neither ethnic group was there any relationship of either plasma or platelet catecholamine concentrations with insulin concentrations, body mass index, or glucose intolerance. European subjects in manual occupations had significantly higher concentrations of plasma noradrenaline than those with nonmanual occupations. The findings suggest a significant role for the sympathetic nervous system in the determination of blood pressure, but do not provide evidence for a connection between hyperinsulinemia and sympathetic nervous system activity. The role of platelet catecholamines as an epidemiological marker of stress has not been supported.

Adolescent↗
PubMed1986

Plasma catecholamines in the lesser spotted dogfish and rainbow trout at rest and during different levels of exercise.

The hypothesis that there is an increase in plasma catecholamines during exercise in fish and that they play an important role in the cardiovascular adjustments during exercise was investigated in the lesser spotted dogfish and rainbow trout. In resting fish plasma catecholamines were at a concentration of 10(-9)-10(-8) mol l-1. During spontaneous swimming in the dogfish, adrenaline increased by 3.3 times to 1.9 X 10(-8) mol l-1 and noradrenaline increased by 2.3 times to 3.2 X 10(-8) mol l-1. In rainbow trout swimming at a steady 1 body length s-1 (Ls-1) in a water channel, the levels of both amines decreased to approximately 25% of the resting values. When swimming to apparent exhaustion at approximately 2 Ls-1, adrenaline was 10 times the resting value at 1.4 X 10(-8) mol l-1, whereas noradrenaline was 2.2 times the resting value at 2.3 X 10(-8) mol l-1. Only after repeated burst swimming for 2-3 min did the levels of plasma catecholamines increase substantially above the resting values. In the dogfish, both amines were at 10(-7) mol l-1, whereas in the rainbow trout, noradrenaline was at 8.5 X 10(-8) mol l-1 and adrenaline was at 2 X 10(-7) mol l-1. These levels were compared with the concentrations of catecholamines used by other workers to elicit changes in the branchial vasculature, gas exchange at the gills or gas transport to the tissues. In lesser spotted dogfish, the levels of adrenaline and noradrenaline present in the plasma during spontaneous swimming have 80% and 50% of maximum effect on gill blood vessels, respectively, whereas in rainbow trout the levels present when swimming to apparent exhaustion have approximately 20% of maximum effect on the branchial vasculature. The levels present in the trout after repeated burst swimming have 40% of maximum effect on blood vessels in the gills. The difference between the dogfish and the trout may be related to the lack of innervation of the gill blood vessels in the former. Enhancement of gas exchange across the gills of rainbow trout can be demonstrated by using adrenaline at the concentration found after repeated burst swimming. It is possible, however, that the concentration of adrenaline found in the plasma of trout after swimming to apparent exhaustion may cause an increase in the concentration of oxygen in arterial blood, thus enhancing oxygen delivery to the tissues.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

CATECHOLAMINE-ACTIVATED SODIUM/PROTON EXCHANGE IN THE RED BLOOD CELLS OF THE MARINE TELEOST GADUS MORHUA

The effects of catecholamines on the pH and the cellular ion and water content were investigated in red blood cells from the Atlantic cod (Gadus morhua). Noradrenaline induced a rapid decrease in the extracellular pH (pHe) of red blood cells suspended in a CO2/bicarbonate or in a CO2/bicarbonate-free buffer system. The noradrenaline-induced changes in pHe were a saturable function of the external sodium ion concentration and were inhibited by amiloride but not by DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid, final concentration of both 10(-4) mol l-1). The catecholamine-induced extracellular acidification was accompanied by an intracellular alkalization and protons were moved from their electrochemical equilibrium. Proton extrusion was associated with an increase in the red blood cell sodium and chloride concentrations. In the presence of DIDS, the chloride movements were blocked and the net proton efflux under these conditions matched the net sodium influx. The results strongly suggested the activation of a sodium/proton exchanger by catecholamines in the red blood cells of the Atlantic cod. The red blood cell receptor affinity for adrenaline was three times higher than that for noradrenaline. Comparison with data in the literature for in vivo catecholamine concentrations indicated that adrenaline was more effective than noradrenaline in activating the red blood cell sodium/proton exchanger in the Atlantic cod in vivo.

Journal Article↗
PubMed1990

Platelet and plasma catecholamines in relation to plasma minerals and parathyroid hormone following acute myocardial infarction.

Epinephrine has been shown to lower the plasma concentrations of several minerals and elevate those of parathyroid hormone (PTH). In order to evaluate the possible clinical importance of such experimental observations, 34 patients with acute myocardial infarction (AMI) were studied with daily determinations of plasma catecholamines, minerals, and PTH during the first week after AMI and at follow-up one month later. In addition, platelet catecholamines were determined as they fluctuate more slowly than plasma catecholamines. After infarction initial platelet epinephrine and norepinephrine levels were higher (p less than 0.05 for both) in nonsurvivors than survivors during a one year follow-up. Results suggested that activation of the sympathoadrenal system influences calcium homeostasis following AMI, but that the impact of sympathoadrenal activation on mineral metabolism is of minor clinical significance in the average AMI patient. High platelet catecholamine levels may predict a poor outcome after AMI.

Adrenal Medulla↗
PubMed1981

Thyroid hormone regulation of the catecholamine effects in human adipose tissue.

The possibility of a relationship between the thyroid hormone level and the peripheral action of catecholamines was examined in 4 normal-weight and 19 obese euthyroid subjects as well as in 27 hyperthyroid subjects by comparing the serum thyroid hormone level and the in vitro effect of catecholamines on lipolysis and cyclic AMP accumulation in adipose tissue incubated with and without isopropyl noradrenaline (ISNA) or noradrenaline (NA). ISNA- and NA-induced rates of lipolysis and cyclic AMP production were significantly correlated with free thyroxine index (r = 0.63-0.74) and with the serum triiodothyronine level (r = 0.83-0.87). The thyroid hormone level was neither correlated with basal rate of lipolysis nor with basal cyclic AMP production (r < 0.2). These results suggest that the magnitude of catecholamine-induced cyclic AMP production by peripheral cells may be regulated by the level of circulating thyroid hormones. The effect of thyroid hormones on lipolysis appears to be specifically linked to the action of catecholamines.

Adipose Tissue↗
PubMed1982

Catecholamine stimulation of cyclic AMP and progesterone production in rat corpora lutea of different ages.

In vitro effects of catecholamines (adrenaline and noradrenaline) and adrenergic antagonists on adenosine 3',5'-cyclic monophosphate (cAMP) and progesterone production by rat corpora lutea (CL) of different ages (1-8 days old) were studied. To obtain defined ages of CL a pregnant mare's serum gonadotrophin (PMSG) model was used. The effect of catecholamines on cAMP decreased with luteal age while the effect on progesterone production was maximal on 5 day old CL. The beta-blocker propranolol inhibited the effects of catecholamines in concentrations around 10-(5) M. The effects of LH could only be inhibited with higher doses of propranolol known to exert unspecific effects. These results support the theory that LH and catecholamine effects on rat corpora lutea are mediated through different receptors.

Age Factors↗
PubMed1988

Regional differences in the catecholamine content of the rat brain: effects of neonatal castration and androgenization.

The long-term organizational influence of perinatal androgen manipulations upon the central noradrenergic and dopaminergic systems was investigated in the rat. Males were castrated or sham-operated upon within 24 h of birth. Newborn females received either five daily sc injections of 100 micrograms of testosterone in oil, or vehicle only. Groups of animals were then decapitated at ages ranging from 12 to 180 days. Levels of noradrenaline and dopamine were measured in six brain regions using high-performance liquid chromatography with electrochemical detection. The results confirm that the noradrenaline and dopamine content of the brain are affected by perinatal androgen exposure and show that brain catecholamine levels alter during the first six months of life, in some areas merely increasing, but in others rising and later falling. Sex differences in catecholamine levels may be apparent at particular ages, but the direction of the difference is frequently reversed as the animals grow older. In the hypothalamus and amygdala broadly similar patterns of time-related changes in catecholamine levels were observed. However, although in other regions (cerebral cortex, cerebellum, corpus striatum and corpora quadrigemina) sex differences in the noradrenaline and dopamine content were frequently detected, on most occasions they were not affected in any recognizable fashion by steroid manipulation in the newborn. Once adult patterns of gonadotropin secretion and behaviour became established in early adulthood, a functional relationship between brain catecholamine levels and the early effects of testosterone is no longer so apparent. Nevertheless, it would seem that testosterone, acting during the neonatal period, tends to accelerate the fall in brain amine levels that occurs as the animals grow older.

Age Factors↗
PubMed1996

Circulating catecholamines and metabolic effects of captopril in NIDDM patients.

OBJECTIVE: To evaluate the effects of captopril on circulating catecholamine levels in NIDDM patients and the possible relationship between captopril-related changes in circulating catecholamine levels and insulin sensitivity. RESEARCH DESIGN AND METHODS: Fourteen nonobese normotensive NIDDM men (aged 44.5 +/- 5.1 years) underwent a 2-h euglycemic-hyperinsulinemic clamp (40 mU.m-2.min-1). Baseline evaluation of insulin sensitivity was followed by the random assignment of each patient to either captopril or placebo treatment, according to a crossover double-blind design. Euglycemic-hyperinsulinemic clamp studies were then repeated for all patients after both placebo and captopril treatments. Plasma norepinephrine (NE) and epinephrine (E) levels were assessed before, during, and after each clamp. RESULTS: Resulting data showed that plasma catecholamine levels increased during baseline euglycemic-hyperinsulinemic clamp (NE: +23.6% time 0 vs. time 120 min, P < 0.05; E: +24.8% time 0 vs. time 120 min, P < 0.05). Captopril treatment significantly increased total glucose uptake (from 19.0 +/- 9.0 to 26.8 +/- 10.1 mmol.kg-1.min-1, P < 0.05) and reduced baseline plasma NE (P < 0.001) and E (P < 0.05) levels. However, the magnitude of the NE (+25.7% time 0 vs. time 120 min, P < 0.001) and E (+27.2% time 0 vs. time 120 min, P < 0.05) increments during euglycemic hyperinsulinemia were not affected by the drug. Percentage changes in the ratio of total body glucose uptake to circulating insulin levels and corresponding decrements of baseline plasma E levels after captopril therapy were negatively correlated (r = -0.57, P < 0.05). CONCLUSIONS: The reduction of circulating catecholamines could contribute, at least in part, to the captopril-related amelioration of insulin sensitivity.

Adult↗
PubMed1981

Importance of new catecholamine pathways in control of blood pressure.

The first comprehensive maps of central catecholamine pathways referred to both noradrenaline and dopamine neurons. They described the catecholamine neurons as having their cell bodies in the brainstem with spinal axons descending mainly from two medullary cell groups (A1 and A2) and with ascending axons arising mainly from more rostral groups (A3-A13). More recent work utilising immunohistochemistry has established the presence of adrenaline neurons in the brain, in two medullary cell groups (C1 and C2). While these were originally thought to lie within the rostral part of the A1 and A2 cell groups, work from this laboratory has now established that the adrenaline neurons are topographically distinct from the A1 and A2 cells, do not fluoresce with standard methods, and are collected into three groups, the third group (C3) lying in the midline of the rostral medulla. Work in this laboratory using a combination of histochemical fluorescence and retrograde transport of horseradish peroxidase has demonstrated that existence of a descending dopaminergic projection from the hypothalamus to the spinal cord, indicating that descending pathways can arise well above the medulla. Recent studies on the A1 neurons have established the presence of projections from the A1 cells to the median eminence of the hypothalamus and towards the nucleus tractus solitarius in the medulla. Other experiments have demonstrated that most of the descending catecholamine axons do not arise from the A1 and A2 cell groups in the caudal medulla, but higher up in the brainstem especially from the A5 and A7 cell groups. These new descriptions of central catecholamine neurons will necessarily modify the interpretation of many experiments on the central regulation of arterial pressure.

Animals↗
PubMed1988

Hepatic hemangioendothelioma of infancy associated with elevated alpha fetoprotein and catecholamine by-products.

Five cases of hepatic hemangioendothelioma (HH) were seen in infants ranging from 2 days to 5 months of age. The cases were studied by clinical chemistry, immunohistochemical staining, and electron microscopic techniques. Serum alpha-fetoprotein (AFP) levels were elevated in each of the four patients in whom levels were obtained. The highest elevation was noted in a 2-day-old infant with a diffuse, unresectable lesion involving the right lobe. Two patients who underwent complete resections of their solitary HH had normalization of their AFP levels. This study suggests that AFP levels in patients with HH are closely related to the patients' age, with the youngest patient having the highest levels of AFP. Catecholamine by-products (VMA and HVA) were elevated in one of four patients in whom levels were obtained, this infant was 3 months old at the time of presentation. She also had an elevated AFP level, a diffuse unresectable lesion involving the entire liver, multiple pulmonary nodules, and cutaneous hemangiomas. Immunohistochemical study failed to demonstrate the source of AFP or the catecholamine by-products in the tumor of this patient, suggesting that the source of catecholamine by-products could be stress-induced catecholamine secretion.

Antigens↗
PubMed1991

Plasma catecholamine levels in cyclic antidepressant overdose.

Cyclic antidepressant overdose is a major cause of morbidity and mortality in self-poisoned patients. The major cause of mortality with cyclic antidepressant overdose is cardiotoxicity. We determined plasma catecholamine levels in 41 symptomatic acute overdose patients to identify interactions between QRS duration (a marker for cardiotoxicity) and a presumed hyper-adrenergic state. Using a linear multivariable regression analysis, QRS duration correlated with the presence of cyclic antidepressant, plasma norepinephrine levels, the ratio of norepinephrine to epinephrine level, and pulse rate (p less than 0.001, r2 = 0.42). Commensurate physiologic changes were not found in the presence of elevated catecholamine levels in the cyclic antidepressant overdose group. One possible explanation for the blunted systemic response to the elevated catecholamine levels is adrenergic desensitization. Investigation of serial catecholamine levels during cyclic antidepressant overdose may lead to modification of our current theories of cardiotoxicity and therapy.

Adolescent↗