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PubMed1995

Circulating chromogranin A and catecholamines in human fetuses at uneventful birth.

Chromogranin A (CGA), a large acidic 48-kD protein, costored and coreleased by exocytosis with catecholamines, has been shown to be a precursor of peptides that exert feedback regulatory control on catecholamine secretion. In plasma, CGA levels increase in response to a large-amplitude physical stimulation in adult subjects and may be related to catecholamine levels. Any skin information is not yet available when the sympathoadrenal system is highly active during birth. This activation is strongly related to parturition circumstances such as the mode of delivery. The aim of our study was to determine CGA plasma levels in infants delivered vaginally or by elective cesarean section and to investigate the possible correlation between CGA and catecholamine concentrations. Plasma levels of catecholamines (norepinephrine and epinephrine) and CGA were assessed by HPLC with electrochemical detection and immunoenzymology, respectively. CGA and norepinephrine concentrations were significantly higher (p < 0.0002 and p < 0.02) in infants vaginally born than in the group delivered by elective cesarean section. A significant relationship (p < 0.04) was found between CGA and norepinephrine levels. However, for epinephrine, no significant difference was found between both groups. These results demonstrate the fetus' ability to corelease CGA and norepinephrine massively in response to stress of birth.

Adult↗
PubMed1979

Abnormal plasma catecholamine responses in acromegalics.

Plasma dopamine, norepinephrine, and epinephrine responses to bromocriptine (2.5 mg orally) or to LRH (100 microgram iv) were studied in seven acromegalic patients. In contrast to normal men, in whom plasma concentrations of catecholamines decrease markedly, acromegalic subjects fail to show decreases in plasma dopamine, norepinephrine, or epinephrine in response to bromocriptine (four of four studied) or LRH (three of four studied). Mean basal plasma catecholamine concentrations do not differ in acromegalic patients, normal men, and a group of nonacromegalic endocrine control patients. Since it appears that bromocriptine and LRH suppress plasma catecholamine concentrations through mechanisms at brain catecholamine neurons, these data are compatible with disordered catecholamine neurons in the brain of patients with acromegaly.

Acromegaly↗
PubMed1988

A kinetic study of chlorpromazine on the hyperglycemic response in rats. I. Effect of chlorpromazine on plasma catecholamines.

The effect of chlorpromazine (0.5 and 4 mg/kg) on plasma catecholamines (adrenaline and noradrenaline) concentrations was investigated in rats. After an i.v. bolus administration of chlorpromazine, plasma adrenaline and noradrenaline concentrations showed a dose dependent increase. In order to clarify the pharmacokinetics of catecholamines in plasma, i.v. infusion of adrenaline or noradrenaline was also carried out. Plasma catecholamines after i.v. infusion showed typical characteristics of a one compartment model with a zero order production rate of endogenous catecholamines. From the data observed, a mathematical model was constructed to elucidate the relationship between the pharmacokinetics (brain concentrations) and the pharmacologic effect (plasma catecholamines concentrations) of chlorpromazine in rats. The results indicated that the time courses of plasma adrenaline and noradrenaline concentrations after an i.v. administration of chlorpromazine were described reasonably well by a simple pharmacokinetic-pharmacodynamic model.

Animals↗
PubMed1989

Endogenous and exogenous catecholamines can accentuate myocardial ischemia only when coronary blood flow is below a critical level.

Seventy-eight dogs with graded constriction of the left main coronary artery were studied to determine the coronary blood flow at which the heart is vulnerable to catecholamine induced ischemia. The left main coronary artery was cannulated with a Griggs' type self-perfusing cannula. The coronary blood flow (CBF) was reduced by graded constriction of the extra-corporeal circuit connected with this cannula. Blood flow rates between 12 and 117 ml/min/100 g were studied. Cardiac activation was achieved by either intracoronary administration of a physiological dose of catecholamine (noradrenaline; 0.4 microgram/kg/min or adrenaline; 0.2 microgram/kg/min), or by electrical stimulation of the left stellate ganglion (4 Hz, 2 msec, 10 V for 5 min). When CBF was below 30 ml/min/100 g, accentuated myocardial ischemia was always indicated by lactate production, myocardial creatine phosphate depletion, ischemic ST segment changes, and elevated left ventricular end diastolic pressure (LVEDP) during these stimulations. When CBF was above 50 ml/min/100 g, catecholamine clearly accelerated the cardiac function and myocardial metabolism with no signs of ischemia. When CBF was between 30 and 50 ml/min/100 g signs of accentuated myocardial ischemia appeared during catecholamine activation in only 1/2 of the dogs. This study indicated that the critical level for CBF at which endogenous or exogenous catecholamine can produce ischemia is between 30 and 50 ml/min/100 g.

Adrenergic Fibers↗
PubMed1983

Studies of catecholamine effect on cyclic AMP in human cultured thyroid cells: their interaction with thyrotrophin receptor.

Even though adrenergic nerve terminals between and around thyroid follicles and catecholamine stimulation of thyroid adenylate cyclase have been reported, there is no uniform concept on catecholamine interaction with thyrotrophin (TSH) receptors. Therefore, the effect of catecholamines on TSH-stimulated cyclic AMP (cAMP) accumulation in human follicular thyroid cells has been investigated, to thus eliminating the extrathyroidal actions of catecholamines. Epinephrine, norepinephrine and isoproterenol appeared to be rapid and potent stimulators of intracellular cAMP accumulation, the half maximum increase doses being 4 X 10(-7)M, 1 X 10(-5)M and 5 X 10(-7)M, respectively. While propranolol (1 X 10(-5)M) prevented the stimulatory effect of catecholamines and failed to inhibit the effect of bovine TSH, phentolamine (1 X 10(-5)M) enhanced the potency of norepinephrine and bovine TSH, leaving that of epinephrine unchanged. The effects of epinephrine (2 X 10(-8)M) and isoproterenol (2 X 10(-8)M) were additive to that of bovine TSH (0.5 mU/ml), but the effect of simultaneous stimulation with norepinephrine (5 X 10(-7)M) and bovine TSH (0.5 mU/ml) was lower than expected. Prenalterol, a selective beta 1-agonist, did not stimulate cAMP accumulation, while terbutaline, a selective beta 2-agonist, exerted a potent stimulation. Metoprolol, a selective beta 1-adrenergic blocker, did not affect the response of thyroid follicular cells to isoproterenol. These results demonstrate the existence of beta-adrenergic receptors in human thyroid follicular cells, mainly of the type beta 2, apparently not correlated with TSH receptor. The existence of alpha-adrenergic receptors which counter-regulate TSH functional responses in human thyroid follicular cells is suggested.

Adrenergic beta-Agonists↗
PubMed1989

Effect of atrial natriuretic peptide on catecholamine release from human pheochromocytoma.

The effect of synthetic alpha human atrial natriuretic peptide on catecholamine release from human pheochromocytomas was studied both in vivo and in vitro. Iv infusion of atrial natriuretic peptide at a rate of 0.1 microgram.kg-1.min-1 for 60 min into two normotensive patients with pheochromocytoma caused a small decrease in the mean blood pressure, increase in the heart rate, and marked increase in the plasma level of norepinephrine (2.08 to 6.83 nmol/l, and 1.15 to 2.83 nmol/l, respectively) compared with 0.60 +/- 0.10 to 1.19 +/- 0.20 nmol/l in normal subjects. Treatment with atrial natriuretic peptide also increased the plasma epinephrine level from 0.34 to 1.27 nmol/l, and from 0.67 to 0.79 nmol/l in the patients with pheochromocytoma, but not in the normal subjects (0.05 +/- 0.01 to 0.05 +/- 0.01 nmol/l). After removal of the tumour, the responses of the plasma norepinephrine and epinephrine to atrial natriuretic peptide infusion were normalized. There was no significant effect of 10(-8) to 10(-5) mol/l atrial natriuretic peptide on the basal release of catecholamines from isolated superfused pheochromocytoma tissue. Atrial natriuretic peptide (10(-7) mol/l) did not affect the increase in catecholamine release induced by glucagon (10(-5) mol/l). These results suggest that the exaggerated responses of plasma catecholamines to atrial natriuretic peptide in patients with pheochromocytoma may be due to a washout effect resulting from change in blood flow in the vessels feeding the tumour rather than increased sympathetic nerve activity induced by hypotension and hypovolemia. The results also suggest that atrial natriuretic peptide dose not have any direct action on pheochromocytoma tissue causing catecholamine release.

Adrenal Gland Neoplasms↗
PubMed2000

Baseline and stimulated catecholamine secretion in normotensive patients with active acromegaly: acute effects of continuous octreotide infusion.

OBJECTIVE: Alterations in catecholamine plasma levels may contribute to the cardiovascular complications of acromegaly. Since few data are available on the catecholamine secretory dynamics in active acromegaly and no evidence exists on catecholamine variations during GH decrease, we studied acromegalic patients before and during octreotide administration. METHODS: We evaluated the catecholamine responses to upright posture and a cold pressure test (CPT) in 11 acromegalic (A) patients before and during continuous administration of octreotide (500 microgram/24h by s.c. pump) compared with 11 normal (N) subjects. RESULTS: All the acromegalic patients showed left ventricular cardiac hypertrophy. The cardiovascular responses to upright posture were similar between normal subjects and acromegalics both before and during octreotide treatment. The basal levels of norepinephrine (NE) were significantly higher in A patients compared with N subjects (423+/-45 vs 264+/-32pg/ml, P<0. 05) and decreased during therapy (291+/-32pg/ml; P<0.01). The increase in plasma NE during upright posture was significantly lower in A than in N subjects (P<0.01), but was restored to normal during octreotide treatment. CPT increased systolic and diastolic blood pressure, pulse rate and NE plasma levels in N (P<0.05) but not in A subjects both before and during octreotide treatment. CONCLUSIONS: Our data demonstrate the presence of increased basal NE levels in acromegalic patients with a defective sympathetic response to stimuli. Short-term octreotide infusion is able to induce a reduction in the basal levels of NE and a normalization of the catecholamine response to posture.

Acromegaly↗
PubMed1977

Catecholamine metabolism in the patients with rheumatoid arthritis.

The amount of urinary catecholamine of healthy subjects and patients with rheumatoid arthritis, particularly before and after synovectomy, was studied. (1) The urinary catecholamine of patients with rheumatoid arthritis showed a lower value than that of healthy subjects. The greater the amount of intraarticularly injected steroids was and the more severe the stage and class of rheumatoid arthritis were, the lower the level of adrenaline was and the more reduced the activity of phenylethanolamine-N-methyltransferase was. (2) The level of urinary noradrenaline in patients with rheumatoid arthritis was lower than that of healthy subjects, but there was no relationship between the level of noradrenaline and the amount of intraarticularly injected steroids. Considering that noradrenaline tended to approach to the normal level as the stage of class of rheumatoid arthritis was more severe, the level of urinary noradrenaline in patients with rheumatoid arthritis seems to reflect the existence of a certain compensatory system in the enzyme system of catecholamine metabolism rather than the influence of the adrenal cortex system. (3) The urinary catecholamine was decreased after synovectomy; especially, noradrenaline level was remarkably decreased. These results suggest that catecholamine plays an important role in the appearance of pain or other clinical signs in rheumatoid arthritis.

Adult↗
PubMed1989

Plasma catecholamines in some airline passengers.

Assuming that the act of flying may provoke mental stress and increments in plasma catecholamines, in-flight plasma catecholamines were compared in two groups of passengers: a group of ordinary passengers (Group 1, n = 15) and a group of passengers who had just completed a cognitive, behavioural treatment programme against flight phobia (Group 2, n = 13). No difference in catecholamines was observed between the groups. However, 10 of the subjects in Group 1 and 12 of the subjects in Group 2 had in-flight plasma adrenaline higher than the highest mean +2 SD (above 0.40 nmol/l) of resting plasma adrenaline observed in healthy subjects in a long series of studies previously or simultaneously done in our laboratory. Subjects in Group 2 (n = 12) showed an average decrease of 50% from in-flight to post-flight plasma adrenaline. Plasma noradrenaline values were not elevated compared to normal resting levels, but an average reduction of 24% was observed between in-flight and post-flight in Group 2. We could not detect any difference between passengers treated for flight phobia and ordinary passengers. However, in-flight plasma catecholamines, particularly adrenaline, seem to be elevated in some airline passengers of various backgrounds. The most plausible explanation seems to be the discomfort and fear some people feel when flying; however, we cannot exclude that the physiological act of flying per se increased plasma catecholamines. Relatively larger variations in plasma adrenaline compared to noradrenaline may favour the first of these two possible explanations.

Adult↗
PubMed1984

Myocardial catecholamines following cold cardioplegic arrest during open-heart surgery.

Preservation of both right and left ventricular subendocardial and subepicardial muscle was assessed using quantitative polarization microscopy (birefringence measurements) with preservation of myocardial catecholamines measured by fluorescence microscopy in biopsies from 20 consecutive patients who underwent open heart surgery with cold cardioplegic arrest (St. Thomas' Solution). Six of the 7 patients with clinical complications were predicted from the birefringence results. One developed left ventricular deterioration during bypass, two patients right ventricular deterioration, one patient both left and right ventricular deterioration and two patients had poor left ventricular function before bypass. Birefringence measurements were thus reliable in predicting post-operative cardiac outcome. There were no significant changes during the bypass period in the catecholamine scores, even in those patients who had clinical complications. Fluorescence microscopy showed that the "free" myocardial nerve net and the pericoronary nerve plexuses retained their catecholamine stores equally well. This indicated that St. Thomas' cardioplegia preserves myocardial catecholamine stores, depletion of which would remove a potentially important compensatory mechanism in cardiac pump failure. There may however be a temporary blockade in the release of endogenous cardiac catecholamine (noradrenaline) stores from the adrenergic nerve terminals following cold cardioplegic arrest despite myocardial pump failure.

Adult↗
PubMedDate not supplied

Changes in blood catecholamine levels in neonatal and growing lambs.

Changes in the palsma catecholamine (A and NA) and FFA concentrations were followed in 12 lambs from birth to 6 months of age. At birth plasma A, NA and FFA levels were higher than those at 6 months of age. Within first 3 days of life plasma A concentration markedly increased, and that of NA decreased, but on the 10th day of age both catecholamines returned to the levels found after first suckling. At this time significant decline in plasma FFA level occured. Later on up to 100 days blood A did not change, whereas NA stabilized on a relatively high level, which resulted in a marked increase of total catecholamine concentration and in a high NA/A ratio. The weaning stress caused a marked increase in blood total catecholamine and FFA levels. No relationship between plasma catecholamine and FFA levels was found during the whole period of growth considered.

Age Factors↗
PubMed2003

Catecholamine responses to environmental stressors in trained and untrained men after 3-day bed rest.

INTRODUCTION: The effect of decreased physical activity with reduced gravitational stress on activity, sensitivity, and reactivity of the sympathetic nervous system (SNS) is not fully recognized. We hypothesized that the effect is most pronounced in physically active subjects. Thus, basal plasma norepinephrine [NE] and epinephrine [E], and catecholamine responses to physiological stimuli were determined after 3 d of horizontal bed rest (BR) in subjects differing in level and kind of habitual activity. METHODS: Before and after BR, 11 untrained students, 8 endurance athletes, and 10 power/strength athletes were submitted to oral glucose tolerance test (OGTT) and orthostatic stand test (OST). Another 32 men (12 untrained, 10 endurance athletes, and 10 power/strength athletes) underwent cold pressor test (CPT) and graded exercise test (GET) performed until volitional exhaustion. RESULTS: After BR, basal [NE] was decreased only in athletes (p < 0.01). Increases in both catecholamines during OGTT were diminished (p < 0.05), particularly in endurance athletes. Plasma [NE] response to standing was not affected by BR in individual groups, but it was diminished in the whole group (p < 0.05). Bed rest did not affect the increases in catecholamines induced by CPT and GET. Heart rate response to OST, and BP responses to OST, CPT, and glucose ingestion were enhanced. CONCLUSIONS: Basal sympathetic activity is diminished after 3 d of BR in physically active men. Although catecholamine responses to glucose load and standing were reduced, the general reactivity and sensitivity of SNS were not attenuated since catecholamine responses to the most (exercise) and least (CPT) powerful stimuli were unchanged.

Adult↗
PubMed1975

Supersensitivity to catecholamines after impairment of extraneuronal uptake or catechol-O-methyl transferase.

In cat papillary muscle and nictitating membrane block of extraneuronal catechol-O-methyl transferase (COMT) by 3',4'-dihydroxy-alpha-methyl propiophenone (U-0521) or of extraneuronal uptake by hydrocortisone causes supersensitivity to catecholamines whenever the experimental conditions result in a high sensitivity of the organ to catecholamines. After block of monoamine oxidase the extraneuronal O-methylation of (-)-[3H]norepinephrine by the isolated nictiating membrane is due to two O-methylating systems (Km and Vmax: 7.5 muM and 0.73 nmoles - g-1 - min-1, and 131 muM and 8.5 nmoles - g-1 - min-1, respectively). Hydrocortisone (28 muM) blocked the activity of the high affinity system without affecting the low affinity system. Apparently, there exists an extraneuronal compartment of high affinity that has a hydrocortisone-sensitive uptake mechnism; this compartment influences the concentration of catecholamines below the Km of this compartment. Supersensitivity ensues when either uptake or enzyme is blocked. Since the sensitivity effects of U-0521 and hydrocortisone are not additive, the high affinity compartment must a) metabolize most of the catecholamine transported into the compartment, and b) have a limited storage capacity for catecholamines after block of COMT.

Animals↗
PubMed1991

[Plasma catecholamines in brain death].

The purpose of this study was to find out whether a severe fall in plasma catecholamines levels can be observed in brain dead patients, that might contribute to haemodynamic disturbances in these patients. Plasma catecholamines (epinephrine and norepinephrine) were measured by HPLC combined with electrochemical detection in 18 consecutive brain dead patients referred to the multiorgan donors unit at the Bordeaux University Hospital. Two samples were obtained: the first one at the time of donor referral (11.2 +/- 9 h after the clinical onset of brain death), and the second one just before organ procurement (19.8 +/- 1 h after the clinical onset of brain death). The results showed that plasma catecholamines levels were similar in both samples, with mean values within the normal range. There was no correlation between the plasma levels of each of the catecholamines and the mean arterial pressures at the time of sampling. Very high plasma catecholamines levels have been found by other authors after brain injuries. After the onset of brain death, they return to basal rest values and do not continue to fall as is the case in animal experiments. The haemodynamic disturbances observed in brain dead patients therefore cannot be due only to sympathoadrenal failure.

Adult↗
PubMed1991

[The use of ketamine and midazolam for analgesia and sedation in ventilated patients subject to obligatory treatment with catecholamines].

This study was undertaken to compare two regimens for analgesic sedation in intensive care patients with exogenous catecholamine therapy, giving special regard to catecholamine demand and hemodynamic parameters. A total of 20 ventilated patients in a surgical intensive care unit were investigated in a prospectively randomized design. Exogenous catecholamine therapy with epinephrine and/or norepinephrine was started at systolic pressure (SAP) less than 85 mmHg or mean arterial pressure (MAP) less than 65 mmHg to maintain cardiovascular function. For analgesic sedation, patients received bolus injections of about 0.2 mg/h fentanyl and 2.5 mg/h midazolam (fentanyl group, n = 10) or an infusion of about 50 mg/h ketamine and 2.5 mg/h midazolam by syringe pump (ketamine group, n = 10). Before the investigation, all patients received fentanyl and midazolam. The study period was 48 h. During the course of the study, mean catecholamine dosage increased significantly in the fentanyl group from 12.1 to 16.3 micrograms/min (+33%, P = 0.003). In the ketamine group, mean catecholamine dosage decreased from 43.9 to 38 micrograms/min (-13%, P = 0.19). No significant differences in group levels or time course were observed with regard to MAP, heart rate, cardiac index, pulmonary capillary wedge pressure, and shunt volume. Levels of pulmonary artery pressure (PAP) were comparable in both groups (ketamine group 29 mmHg, fentanyl group 26 mmHg). In time course, PAP increased by about 5 mmHg in the ketamine group but not in the fentanyl group (P = 0.009). The average central venous pressure (CVP) was 12 mmHg in both groups. At the end of the investigation, CVP decreased in the fentanyl group and increased in the ketamine group (P = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

[Effect of catecholamines on the smooth muscles of the esophageal groove of calves].

The effect of noradrenaline and adrenaline on isolated smooth muscle from the reticular groove of calves was studied. Both catecholamines caused a concentration-dependent (1.1.10(-6) mol/l) contraction of the transversal muscle strips from the floor of the reticular groove. This excitatory effect was antagonized by prazosin (10(-7)) mol/l), and by high concentrations of yohimbine (10(-6) mol/l) and atropine (10(-5)) mol/l). Tetrodotoxin (3.10(-6) mol/l), an inhibitor of nerve conduction, did not change the contraction induced by catecholamines (55.10(-6)) mol/l). Catecholamines did not produce a contraction of the longitudinal muscle from the lips of the reticular groove. The beta-adrenergic agonist isoprenaline (55.10(-6) mol/l) even elicited a reduction of acetylcholine (55.10(-6)) mol/l) induced contraction of both the transversal and the longitudinal muscle from the reticular groove. The relaxing effect of isoprenaline was antagonized by propranolol (55.10(-6)) mol/l). According to these results the excitatory effect of catecholamines on the smooth muscle cells occurs through alpha-adrenergic receptors, whereas the relaxing effect is mediated by beta-adrenergic receptors of the muscle cell. The excitatory effect of catecholamines on the transversal muscle appears to be predominant. Atropine appears to be an unspecific blocking agent of alpha-adrenergic receptors.

Animals↗
PubMed1990

Plasma catecholamines and their physiologic thresholds during the first ten days of life in sheep.

We studied serial plasma catecholamine levels in healthy newborn sheep over the first ten days of life. The results show that plasma norepinephrine values in newborn sheep are 3-4 fold higher, and plasma epinephrine values are two-fold higher than values in term fetal sheep. These elevations are sustained over the first 10 days of life. Cardiovascular (heart rate and blood pressure) and metabolic parameters (glucose and free fatty acids) are also significantly elevated above fetal levels. We performed graded catecholamine infusions in newborn animals and adult ewes to determine the minimum plasma catecholamine concentrations necessary for discernible physiologic effects. In response to step-wise increases in epinephrine or norepinephrine infusion rates, there were immediate increases in blood pressure and other physiologic responses. This pattern was seen in both newborn and adult animals, and differed from previous observations in fetal sheep where log-linear, dose response curves characteristic of a threshold response were seen. These results suggest that during the first two weeks of life plasma catecholamine levels are elevated above the threshold value for physiologic responses. These sustained elevations in circulating catecholamines are important in the maintenance of physiologic homeostasis.

Animals↗
PubMed1989

[Myocardial catecholamine content in heart failure--I: Regional distribution in explanted hearts. Comparison between dilated cardiomyopathy and coronary heart disease].

To quantify the myocardial catecholamine content in heart failure patients and to assess the regional distribution of catecholamines, we investigated norepinephrine and dopamine concentrations in explanted hearts from 34 patients in end-stage heart failure. 28 patients with cardiomyopathy were compared with six patients with coronary artery disease. In comparison with the right atria of a control group without heart failure, reduced myocardial norepinephrine contents (in pg/micrograms non-collagen protein (NCP] were found in all areas of the explanted hearts: controls: right atrium 17.6 +/- 6.6; cardiomyopathy: right atrium 7.1 +/- 7.9, right ventricle 4.4 +/- 2.7, septum 3.8 +/- 1.5, left ventricle 3.5 +/- 1.4. Coronary artery disease: right atrium 7.0 +/- 6.9, right ventricle 4.2 +/- 2.6, septum 3.6 +/- 1.4, left ventricle 3.4 +/- 1.4. Highest norepinephrine levels were measured in the right atrium. Right ventricle, septum, base and midventricular portion of the left ventricle had lower concentrations and were not different from each other. In contrast to reduced norepinephrine (NE) levels in all patients, dopamine (Dop) was inhomogenously elevated (only in a subgroup of 44%). Catecholamine contents in any two arbitrarily selected areas correlated significantly (NA: r = 0.53-0.77; Dop: r = 0.81-0.93, p less than 0.05 in all cases). The patients with heart failure due to dilated cardiomyopathy and to coronary artery disease did not differ in myocardial catecholamine levels or distribution. In end-stage heart failure a significant loss of myocardial norepinephrine independent from the underlying disease is found. It affects all areas of the hearts but does not equalize catecholamine content in ventricles and atria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗