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PubMed1998

[Determination of natural antibodies to catecholamines in health and disease].

AIM: Enzyme immunoassay (EIA) determination of the level of natural antibodies (n-Ab) to catecholamines in patients with metabolic disturbances and cardiovascular diseases, correlation between content of n-Ab to these bioregulators and clinical diagnosis, biochemical indices. MATERIALS AND METHODS: EIA with specially synthetized artificial antigens was used to determine n-Ab to catecholamines (adrenaline, noradrenaline, dopamin) in 41 patients with cardiovascular diseases and metabolic disturbances (ischemic heart disease, essential hypertension, hyperlipoproteinemia) and in 10 healthy subjects (donors, controls). RESULTS: Changes in the levels of antibodies to catecholamines correspond to the clinical diagnosis. Interrelations exist between n-Ab to catecholamines and biochemical parameters in the disease. CONCLUSION: The trends in the amount of n-Ab to catecholamines are a unique marker of metabolic disturbances of these endogenic substances and can be used in diagnosis.

Antibodies, Anti-Idiotypic↗
PubMed1982

The role of catecholamines in metabolic acidosis.

Catecholamines (noradrenaline and adrenaline) are catabolic hormones secreted during stress. They initiate many metabolic processes including increased production of both ketoacids and lactic acid. Support for a direct participation of these hormones in the development and/or maintenance of ketoacidosis includes: (1) the high incidence of stress (approx. 70%) as a precipitating factor for ketoacidosis; (2) the elevated plasma levels of noradrenaline (norepinephrine) in patients with ketoacidosis; (3) the rise in plasma concentrations of ketone bodies during catecholamine infusion; and (4) the reduction in the incidence of ketoacidosis with beta-adrenergic pharmacological blockade. Support for a direct participation of catecholamines in the development and/or maintenance of lactic acidosis includes: (1) the common association of stress and lactic acidosis; (2) the rise in plasma lactate concentration during adrenaline (epinephrine) infusion; (3) the precipitation of lactic acidosis by adrenaline intoxication and phaeochromocytoma; and (4) the vasoconstrictor effects of catecholamines leading to tissue anoxia and lactic acid production. Thus, in susceptible patients, catecholamines may be principal determinants of whether ketoacidosis and/or lactic acidosis develops.

Acidosis↗
PubMed2004

Elevated catecholamine metabolites in patients with Costello syndrome.

Costello syndrome is a rare congenital anomaly syndrome with a predisposition to specific tumors, including neuroblastoma, rhabdomyosarcoma, and transitional cell carcinoma of the bladder. The increased risk for solid tumors led to the proposal of a tumor screening protocol. A screening test for neuroblastoma consists of measuring catecholamine metabolites in urine, an assay that may also be used for diagnostic confirmation of a suspected catecholamine secreting tumor. We report eight patients with Costello syndrome with elevated catecholamine metabolites, vanillylmandelic acid (VMA) and/or homovanillic acid (HVA), in urine. Each patient had additional laboratory and/or imaging studies. None of the patients was found to have a neuroblastoma or another catecholamine secreting tumor. In two cases, the assays were performed because the patients were symptomatic with diaphoresis and hypertension, respectively, and in the other six cases the assays were performed in order to screen for neuroblastoma. The pathophysiology for the catecholamine metabolite abnormality in these patients with Costello syndrome remains unclear. However, it appears that in this patient group an elevation above the normal limit, defined as 2 standard deviations (SD) above the mean for age, is more likely to be a variant, rather than a sign of a neuroblastoma. Thus, it may be prudent not to use this assay as a screening test, and to take the frequently elevated results into consideration when interpreting diagnostic assays.

Abnormalities, Multiple↗
PubMed2001

Immunotoxic destruction of distinct catecholamine subgroups produces selective impairment of glucoregulatory responses and neuronal activation.

The toxin-antibody complex anti-d(beta)h-saporin (DSAP) selectively destroys d(beta)h-containing catecholamine neurons. To test the role of specific catecholamine neurons in glucoregulatory feeding and adrenal medullary secretion, we injected DSAP, unconjugated saporin (SAP), or saline bilaterally into the paraventricular nucleus of the hypothalamus (PVH) or spinal cord (T2-T4) and subsequently tested rats for 2-deoxy-D-glucose (2DG)-induced feeding and blood glucose responses. Injections of DSAP into the PVH abolished 2DG-induced feeding, but not hyperglycemia. 2DG-induced Fos expression was profoundly reduced or abolished in the PVH, but not in the adrenal medulla. The PVH DSAP injections caused a nearly complete loss of tyrosine hydroxylase immunoreactive (TH-ir) neurons in the area of A1/C1 overlap and severe reduction of A2, C2, C3 (primarily the periventricular portion), and A6 cell groups. Spinal cord DSAP blocked 2DG-induced hyperglycemia but not feeding. 2DG-induced Fos-ir was abolished in the adrenal medulla but not in the PVH. Spinal cord DSAP caused a nearly complete loss of TH-ir in cell groups A5, A7, subcoeruleus, and retrofacial C1 and a partial destruction of C3 (primarily the ventral portion) and A6. Saline and SAP control injections did not cause deficits in 2DG-induced feeding, hyperglycemia, or Fos expression and did not damage catecholamine neurons. DSAP eliminated d(beta)h immunoreactivity but did not cause significant nonspecific damage at injection sites. The results demonstrate that hindbrain catecholamine neurons are essential components of the circuitry for glucoprivic control of feeding and adrenal medullary secretion and indicate that these responses are mediated by different subpopulations of catecholamine neurons.

Adrenal Medulla↗
PubMed1996

Growth hormone treatment of hypophysectomized rats increases catecholamine-induced lipolysis and the number of beta-adrenergic receptors in adipocytes: no differences in the effects of growth hormone on different fat depots.

Growth hormone (GH) has a lipolytic effect in adipose tissue but this effect may differ in adipose tissue from various fat depots. This latter possibility was investigated in the present study, in which the effects of GH in vivo on catecholamine-induced lipolysis and the number of beta-adrenergic receptors in isolated adipocytes from different fat depots of hypophysectomized rats were investigated. Female and male Sprague-Dawley rats were hypophysectomized or sham-operated at 45 days of age. One week after the operation, hormonal replacement therapy with L-thyroxine and hydrocortisone acetate was given. In addition, groups of rats were treated with GH (1.33 mg/kg per day, given as two daily subcutaneous injections). After 1 week of hormonal treatment, adipocytes were isolated from the parametrial, epididymal and inguinal fat pads, and glycerol release after catecholamine-stimulation and 125I-cyanopindolol binding were measured. Hypophysectomy resulted in a marked decrease in the lipolytic response to catecholamines. GH treatment significantly increased catecholamine-induced lipolysis with similar effects in adipocytes from parametrial or epididymal and inguinal fat depots in both female and male rats. There were no differences between norepinephrine compared with isoproterenol-induced responses. 125I-cyanopindolol binding was reduced after hypophysectomy and normalized by GH treatment, without differences between parametrial and inguinal adipose tissue regions. We conclude that the lipolytic effects of GH in the rat may partly be mediated by a stimulatory effect on beta-adrenergic receptors in adipocytes. In addition, GH exerted similar effect on catecholamine induced lipolysis and beta-adrenergic receptors in adipocytes from parametrial, epididymal and inguinal fat depots.

Adipocytes↗
PubMed2002

Catecholamines are present in larval Xenopus laevis: a potential source for cardiac control.

Changes in noradrenaline (NA), adrenaline (A), and dopamine (DA) levels in the heart, kidneys, and whole body (without heart and kidneys) during embryonic development were investigated in the frog, Xenopus laevis using high-performance liquid chromatography (HPLC). In addition, the presence of cells immunoreactive to tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH) and/or phenylethanolamine-N-methyltransferase (PNMT) in the heart of Xenopus larvae was investigated using immunohistochemical techniques. The presence of nerve fibers was visualized using antibodies against acetylated tubulin (AcT). NA and DA concentrations in the heart were low and steady in NF 40-56, showed an increased value at NF 57, and decreased again in froglets. A trend toward higher concentrations of A was observed at NF 43-49 and NF 57. Cells immunoreactive to TH, DBH, and PNMT were found in the heart from NF 40, and the TH immunoreactive cells became more abundant in the whole heart at later stages. The presence of catecholamines in the non-innervated larval heart together with the finding of TH/DBH/PNMT immunoreactive cells suggests that catecholamines are synthesized and stored in the heart and could therefore have a paracrine role in cardiac control in Xenopus larvae. Detectable concentrations of catecholamines were also found in kidneys and whole bodies (except heart and kidneys). Therefore, catecholamine-producing cells outside the heart can be an important source of circulating catecholamines involved in adrenergic cardiac control in Xenopus larvae.

Animals↗
PubMed1996

Catecholamine-induced leukocytosis: early observations, current research, and future directions.

Recent studies demonstrate that acute psychological stress in man affects lymphocyte circulation. It has been suggested that catecholamines are responsible for these changes. The present review summarizes findings regarding catecholamine-induced lympho- and leukocytosis, starting with observations dating back to the beginning of this century. Particular attention is given to the mechanisms of this phenomenon and the potential site of origin of newly appearing leukocytes. Characteristically, two phases are recognized after catecholamine administration: a quick (<30 min) mobilization of lymphocytes, followed by an increase in granulocyte numbers with decreasing lymphocyte numbers. Many studies have shown that catecholamines predominantly affect natural killer (NK) cell and granulocyte circulation, whereas T- and B-cell numbers remain relatively unaffected. The changes in lymphocyte circulation seem to be mainly mediated via activation of beta2-adrenoceptors, whereas granulocyte increases involve alpha-adrenoceptor stimulation. Results further indicate that the marginal pool and the spleen are the major sources for freshly recruited lymphocytes, whereas granulocytes are predominantly released from the marginal pool and the lung. Results from acute psychological stress or physical exercise models corroborate the results obtained with catecholamine administration. Together, the data demonstrate that components of the innate immune system participate in the classical fight/flight response.

Acute Disease↗
PubMedDate not supplied

No effect of the calcium antagonist, isradipine, on plasma catecholamines in irreversible chronic obstructive pulmonary disease (COPD). A randomized, double-blind, placebo-controlled study.

Calcium antagonists have been claimed to decrease the pulmonary artery pressure and increase oxygen uptake and cardiac output in patients with chronic obstructive pulmonary disease (COPD). This should tend to decrease the plasma levels of catecholamines. The purpose of the present study was to assess the effects of the vasodilating calcium antagonist, isradipine, on resting and exercise levels of catecholamines in patients with COPD. Eighteen patients with severe respiratory insufficiency (FEV1<1.01) were investigated. During maximum exercise, the baseline levels of plasma noradrenaline rose from 2.27 nmol/l (0.41-7.66: mean, range) to 3.86 nmol/l (1.3-12.2) (P = 0.0002) and plasma adrenaline rose from 0.39 nmol/l (0.07-1.02) to 0.64 nmol/l (0.07-1.77) (P = 0.0001). The patients were randomly allocated to receive either capsules of placebo or capsules of 5 mg of isradipine and were reinvestigated after 2 h and 3 months. There was no significant difference between the two groups concerning the change in plasma catecholamines, neither at rest nor at exhaustion. Furthermore, the increase in catecholamines during exercise in the two groups did not differ from each other, neither before administration of isradipine nor after. In conclusion, a vasodilating calcium antagonist did not alter the resting level or exercise induced increase in plasma catecholamines.

Adrenergic alpha-Agonists↗
PubMed1994

In vivo release of catecholamines in the locus coeruleus.

To investigate the release of endogenous dopamine, noradrenaline and adrenaline in the locus coeruleus, this brain area was superfused with artificial cerebrospinal fluid (CSF) through push-pull cannulae and the release of catecholamines was determined in the superfusate radioenzymatically. Collection of superfusates in time periods of 10 min revealed that release rates of the three catecholamines fluctuated, thus pointing to the existence of ultradian rhythms with following mean periods (minutes per cycle): noradrenaline 52 +/- 4, dopamine 37 +/- 2, adrenaline 36 +/- 2. The rhythm frequency of noradrenaline was significantly lower than the frequencies of dopamine and adrenaline. When the locus coeruleus was superfused with neuroactive drugs, superfusates were collected in time periods of 3 min. Superfusion with tetrodotoxin (1 mumol l-1) for 12 min elicited a prompt and sustained decrease (-70%) in the release rates of dopamine and adrenaline. The release rate of noradrenaline was also reduced, although to a lesser extent (-40%). Superfusion with veratridine (50 mumol l-1) led to an immediate and very pronounced enhancement in the release rates of dopamine, noradrenaline and adrenaline. The veratridine-induced increase in catecholamine outflow was decreased strongly by simultaneous superfusion with tetrodotoxin. The findings suggest that the release of endogenous catecholamines in the locus coeruleus fluctuates according to ultradian rhythms. Changes in the release on superfusion with veratridine and tetrodotoxin demonstrate the neuronal origin of the three catecholamines. The observed differences in the release characteristics between noradrenaline on the one hand and dopamine and adrenaline on the other might indicate that noradrenaline is partly released from somatodendritic sites of the noradrenergic cell bodies in the locus coeruleus.

Animals↗
PubMed1979

Quantitative radioautographic light and electron microscopic analysis of the localization of monoamines in the median eminence of the rat. I. Catecholamines.

By means of light and electron microscopic radioautography a quantitative study of the regional distribution of catecholamines in the median eminence of the rat was carried out. One hour after intraventricular injection of 3H-dopamine the highest radioautographic reaction was recorded in the external zone, especially in the lateral palisade zone where many neurosecretory terminals are separated from the basal lamina of the portal pericapillary space by a glial "cuff". This area showed the highest percentage (52%) of labelled catecholamine containing neurosecretory terminals as well as the maximal silver grain density per one terminal. In the medial palisade zone where direct neurovascular contacts with the capillary loops prevail, only 27 per cent of neurosecretory terminals were found to harbour tritiated dopamine. On the average 35 per cent of neurosecretory terminals in the median eminence of the rat contain catecholamines (both dopamine and noradrenaline). Pretreatment of animals with recretory terminals as well as grain density over terminals were decreased in both the medial and lateral palisade zones, although to a lesser degree in the latter. The site of origin of catecholamine fibers as well as the mode of catecholamine action at the level of the median eminence are discussed.

Animals↗
PubMed1992

Catecholamine alterations in experimental hydrocephalus.

Experimental hydrocephalus was induced in rats by intracisternal injection of kaolin suspension. The amounts of norepinephrine and dopamine were determined in the whole brain and specific brain regions at 1 week (acute phase) and 4 weeks (chronic phase). The turnover of catecholamine, an index of the activity of catecholamine-containing neurons, was determined by measuring the decrease in catecholamine contents 2 h after intraperitoneal injection of alpha-methyl-p-tyrosine (250 mg/kg), an inhibitor of tyrosine hydroxylase. We observed that the catecholamine contents in kaolin-induced hydrocephalus were not significantly different from control values. Following injection of alpha-methyl-p-tyrosine, there was decrease in levels of catecholamines in both control and hydrocephalic rats. This decrease was, however, significantly less in induced hydrocephalus than in control animals. This result suggested that in hydrocephalus, the activities of norepinephrinergic and dopaminergic neurons are reduced.

Animals↗
PubMed1986

The effect of insulin and catecholamines on the activities of 3-hydroxy-3-methyl glutaryl coenzyme A reductase and acyl-coenzyme A: cholesterol-o-acyltransferase in isolated rat hepatocytes.

This study was concerned with the effect of insulin and catecholamines on the rate limiting enzymes of cholesterol metabolism in rat hepatocytes. Insulin was found to increase the activity of 3-hydroxy-3-methyl glutaryl coenzyme A reductase and to have no effect on the activity of acyl-coenzyme A: cholesterol-o-acyltransferase. Noradrenaline and isoprenaline increased the activities of both 3-hydroxy-3-methyl glutaryl coenzyme A reductase and acyl-coenzyme A: cholesterol-o-acyltransferase. The effect of noradrenaline or isoprenaline in the presence of insulin was that of a lower stimulatory response on 3-hydroxy-3-methyl glutaryl coenzyme A reductase but comparable to that found with either catecholamine alone. The combination of either catecholamine with insulin had no effect on the activity of acyl-coenzyme A: cholesterol-o-acyltransferase. These observations suggest that the activities of 3-hydroxy-3-methyl glutaryl coenzyme A reductase and acyl-coenzyme A: cholesterol-o-acyl-transferase are regulated independently by insulin in the presence or absence of catecholamines. By contrast, catecholamines appear to regulate both enzyme activities in a similar fashion.

Animals↗
PubMed1975

Urinary catecholamine excretion and thyroid hormone blood level in the course of severe acute brain damage.

Urinary catecholamine excretion and thyroid hormone blood level were studied in 16 patients following severe cerebral trauma. Increased excretion rates of epinephrine and norepinephrine were found. There was no significant difference in the catecholamine excretion when compared with generally traumatized patients. The relationships between catecholamine excretion, increased metabolic rates, and negative nitrogen balance indicate that in patients with a midbrain syndrome there exists an additional diencephalic metabolic factor, which leads to a rise in fat oxidation and perpetuation of catabolism. Early high caloric parenteral nutrition seems to inhibit the initial increase of catecholamine excretion and thus protects the body from an unnecessary breakdown of its own reserves. If the course is classified according to neurological stages, it can be shown that patients with a traumatic apallic syndrome in poor condition have a high increase of catecholamine excretion. Secretion of thyroid hormones is not influenced significantly by cerebral trauma.

Adolescent↗
PubMed1997

Systemic and cardiac catecholamines during elective PTCA and during immediate PTCA for acute myocardial infarction.

This study investigated arterial and coronary venous catecholamine concentrations in patients undergoing either elective coronary angioplasty (PTCA) or direct PTCA for acute myocardial infarction. We included 17 patients with stenoses of the left anterior descending coronary artery (LAD) and 10 patients with acute anterior myocardial infarction (AMI) undergoing PTCA. During the initial balloon dilatation arterial and coronary venous plasma concentrations of norepinephrine and epinephrine were determined. In elective PTCA, coronary occlusion (2 min) resulted in a transient increase of arterial concentrations of norepinephrine (2.04 +/- 0.30 vs. 1.26 +/- 0.13 nmol/L before dilatation) and epinephrine (0.52 +/- 0.08 vs. 0.34 +/- 0.04 nmol/L) in the first minute of reperfusion, whereas coronary venous concentrations of catecholamines were not changed after dilatation. Among the 10 patients with AMI, immediate reperfusion of the LAD (TIMI grade 3) was achieved in 6 patients. In these patients, baseline arterial concentrations for norepinephrine (3.91 +/- 1.16 nmol/L) and epinephrine (4.68 +/- 2.07 nmol/L) were elevated and no transcardiac gradient for catecholamines was found. In the first minute after successful reopening of the LAD we detected a distinct rise of the transcardiac norepinephrine gradient from -0.10 +/- 0.53 to 85.02 +/- 24.64 nmol/L, which declined in the fifth minute of reperfusion of 4.36 +/- 2.30 nmol/L. Conversely, venous epinephrine and arterial concentrations for both catecholamines remained unchanged within the observation period. In the four patients with incomplete (TIMI 0-2) reopening of the LAD, we found no cardiac washout of norepinephrine. In summary, a transient rise of systemic catecholamines, but no cardiac release of norepinephrine was observed in patients after brief coronary occlusion. Conversely, a massive washout of norepinephrine from the infarcted myocardium occurred during AMI.

Acute Disease↗
PubMed1979

d-Amphetamine-induced increase in catecholamine synthesis in the corpus striatum of the rat: persistence of the effect after tolerance.

The effect of d-amphetamine on in vivo catecholamine synthesis in four regions of rat brain was determined by measuring the accumulation of dopa after inhibiton of dopa decarboxylase. In doses up to 2.5 mg/kg, d-amphetamine caused dose-dependent increases in striatal dopa accumulation to a maximum of 280% of control; further increases in dose resulted in smaller effects until 10 mg/kg d-amphetamine was not significantly different from control. d-Amphetamine did not alter dopa accumulation in telencephalon, in diencephalon-mesencephalon, or in pons-medulla oblongata. d-Amphetamine did not affect either dopamine levels in striatum or NE levels in pons-medulla oblongata; at high doses, d-amphetamine did reduce norepinephrine levels in telencephalon and in diencephalon-mesencephalon. Daily administration of pre-session but not of post-session d-amphetamine produced tolerance to the effects of d-amphetamine on milk consumption in rats. The ability of d-amphetamine to increase striatal catecholamine synthesis was not altered by the development of tolerance to d-amphetamine. These results suggest that tolerance to d-amphetamine is not related to its effect on catecholamine synthesis but instead occurs via changes in aspects of catecholamine metabolism other than synthesis via change in catecholamine release, reuptake, or receptor sensitivity, or via changes in non-catecholaminergic mechanisms.

Animals↗
PubMed1978

Effect of amiloride on catecholamine-induced changes in ion transport in short-circuited frog skin.

The effect of amiloride (10(-6) M), added either before or after the catecholamine, on the adrenaline- or isoprenaline-induced changes in short-circuit current and Na and Cl fluxes of isolated skin of Rana temporaria was investigated. At the catecholamine concentration used the increment in short-circuit was the same in the absence or presence of amiloride (ca. 7.1 neq.cm-2.min-1) and the amiloride inhibition was the same in the absence or presence of catecholamine (ca. 9.4 neq.cm-2.min-1). Amiloride inhibited the Na and Cl influxes of the control period (by --8.63 +/- 1.28 and --2.08 +/- 0.75 neq.cm-2.min-1, respectively) but did not prevent the increase of these fluxes on the addition of adrenaline. There was no evidence of amiloride inhibition of the Na and Cl effluxes. There was an association between the increase of Na efflux and net Cl efflux following adrenaline, which if secreted together by a neutral NaCl pump would not contribute to the increased short-circuit current. The increased short-circuit current was correlated with the increased Na influx throughout the experiment if allowance is made for the periods where there is a lag between the current and isotopic measurement (i.e., the period immediately after the addition of a drug). It is tentatively suggested that the catecholamine-induced increase in Na influx is not altered by the amiloride concentration used in this study. In addition the magnitude of the changes induced by catecholamine in the influx and efflux of both Na and Cl seem to be unaffected.

Amiloride↗
PubMed1980

Effect of priming volume on serum catecholamines during cardiopulmonary bypass.

Several theories have been proposed to explain the transient hypotension which occurs upon the initiation of cardiopulmonary bypass. The present study investigated the possibility that addition of the lactated Ringer's solution pump priming volume to the circulation causes dilution of circulating catecholamines leading to the hypotension. Circulating epinephrine and norepinephrine levels were measured during cardiopulmonary bypass in patients anaesthetized with halothane. The results demonstrate dilution of circulating catecholamines at the start of bypass in conjunction with the observed hypotension. During the bypass period, mean blood pressure graudally recovered to normotensive levels even though circulating catecholamine levels remained significantly lowered, indicating a mechanism for the recovery of blood press which is not sympathoadrenal. The results obtained from this study demonstrate a temporal relationship between catecholamine dilution by the pump priming volume and the observed hypotension. Whether catecholamine dilution is the sole factor causing the hypotension remains to be determined.

Adult↗
PubMed1988

Measurement of catecholamines, met-enkephalin, somatostatin and substance P-like immunoreactivities in 12 human pheochromocytomas.

The present study was designed to evaluate the simultaneous presence of epinephrine (E), norepinephrine (NE), met-enkephalin (ME)-, somatostatin (SRIF)- and substance P (SP)- like immunoreactivities (LI) in extracts of 12 pheochromocytomas obtained at the time of surgery from 10 patients. Moreover, catecholamines and ME-LI levels were measured in peripheral plasma of each patient. Each pheochromocytoma was characterized by a high variability of ME-LI, SRIF-LI, SP-LI, E and NE levels. The highest E concentrations were found in tumors from patients with Multiple Endocrine Adenomatosis (MEA) IIa syndrome, whereas in sporadic pheochromocytomas NE was the main catecholamine. Among the neuropeptides ME-LI showed the highest intratumoral concentration, and SP-LI the lowest. No correlations were found between intratumoral levels of catecholamines and any of the neuropeptides or between any of the different neuropeptides measured. Plasma catecholamine levels were not correlated with intratumoral catecholamine levels. Plasma ME-LI was higher than normal in only one patient. No correlation was observed between tumoral CA or peptide content and the clinical picture. Our study confirms that human pheochromocytoma cells can synthetize different neuropeptides. The variability of the clinical picture very likely depends on the biochemical and biological heterogeneity of this chromaffin tumor.

Adrenal Gland Neoplasms↗