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PubMed1984

Catecholamine-secreting malignant schwannoma in a patient with multiple intracranial aneurysms. Case report.

A case is reported of malignant schwannomatosis (malignant transformation of von Recklinghausen's disease) with catecholamine production in a patient with multiple intracranial aneurysms. The patient had a history of episodic hypertension and elevated levels of catecholamines in the serum and 24-hour urinary excretion. Postmortem examination revealed diffuse central nervous system (CNS) dissemination of the tumor from the thoracolumbar spinal malignant schwannoma. A high concentration of catecholamines was demonstrated in the tumor tissue, and histochemical and electron microscopy studies suggested the presence of catecholamines in the cytoplasm of some of the tumor cells. This patient's clinical and radiological features, including severe headache, vomiting, stiff neck, ptosis of the eye ipsilateral to the internal carotid-posterior communicating artery aneurysms, and local arterial narrowing, mimicked those of subarachnoid hemorrhage from a ruptured aneurysm. However, the clinical picture was caused by diffuse CNS dissemination of the tumor, another primary malignant schwannoma of the oculomotor nerve, and intimal fibrous thickening of the arterial wall.

Cranial Nerve Neoplasms↗
PubMed2001

[Catecholamine deposition and erythrocyte structural transformation in functional disorders of the sympathetic adrenaline system].

By means of ultra and cytochemical study the catecholamine inserts in erythrocytes look like dark lumps and beads the size and quantity of which being directly proportional to the sympathetic adrenaline system functional state. Under the conditions of catecholamine shortage the inserts reducing to fragments occurs and under catecholamine growth the increase in inserts size takes place. In both cases the erythrocyte structure disorder has been observed. Cytochemical method of catecholamine detection in erythrocytes also allows simultaneously to determine the erythrocyte morphological state.

Adrenal Gland Diseases↗
PubMed2002

Do catecholamines influence the level of plasma leptin in patients with phaeochromocytoma?

The relationship between plasma leptin and catecholamine concentrations during chronic and acute catecholamine excess is studied. Patients with phaeochromocytoma, divided according to gender, were examined under basal conditions (n = 18) and at selected time-points during surgical removal of the tumour (n = 12). Appropriate controls were used (n = 23) for the basal study. Plasma leptin was determined by radioimmunoassay (RIA) and plasma noradrenaline (NA) and adrenaline (A) by high-performance liquid chromatography (HPLC). Statistical evaluation employed Student's t-test, Wicoxon test and Spearman's correlation coefficient. Gender-related differences in plasma leptin in normal subjects was confirmed, and these were maintained in the patients. Phaeochromocytoma patients had normal plasma leptin levels in the basal state and decreased levels following the massive catecholamine surge provoked by surgery. Plasma leptin concentration did not correlate with plasma NA or A in either group studied. In the patients with phaeochromocytoma, acute but not chronic catecholamine excess affected plasma leptin, suggesting a role for sympathetic activity in modulating leptin release.

Adrenal Gland Neoplasms↗
PubMed1992

[Pathological status of catecholamines in the corpus striatum in hepatocerebral dystrophy (Wilson-Konovalov disease)].

The content of catecholamines in the striatum was measured in 2 patients suffering from hepatocerebral dystrophy (Wilson-Konovalov disease). It is noted that in different clinical manifestations of the disease, the changes in the content of noradrenaline in the striatum varied. A male patient with marked tremor spreading manifested a considerable rise of the content of catecholamines, primarily in the n. caudatus. At the same time in a female patient with a grave akinetic -rigid syndrome and the signs of liver failure, the content of catecholamines, particularly dopamine, in the putamen was low. In view of this fact it is assumed that disorders of cerebral metabolism of catecholamines, dopamine in particular, evidently related to deposition of excess copper, leading to the changes of their content in basal ganglia underline the clinical pleomorphism of the disease and play the key role in the development of extrapyramidal motor disturbances characteristic of hepatocerebral dystrophy.

Adult↗
PubMed1992

[Adrenal catecholamine releases during hypotension with continuous administration of calcium entry blockers and nitroglycerin].

We investigated the effect of nicardipine and diltiazem on adrenal catecholamine releases, and compared it with the effect of nitroglycerin in dogs. A 35% reduction in mean arterial pressure was achieved and maintained for 45 minutes. The dogs were observed until 60 minutes after the discontinuation of drug infusions. Adrenal catecholamine releases increased during hypotension with continuous administration of nicardipine, diltiazem and nitroglycerin, but they showed no significant differences between each drug. There was no more increase in adrenal catecholamine releases in spite of additional nicardipine administration. These results suggest that Ca2+ antagonist such as nicardipine directly inhibits the catecholamine releases from the adrenal glands.

Adrenal Glands↗
PubMed1977

Regulation of catecholamine biosynthesis in a transplantable rat pheochromocytoma.

Cells prepared from a transplantable rat pheochromocytoma synthesize norepinephrine from 14C-tyrosine, at a rate of 9.4 +/- 0.5 pml/min/mg of protein, in vitro. Incubation of the cells in a medium containing 56 mM K+ results in a 2- to 6-fold increase in norepinephrine synthesis. This increase in norepinephrine synthesis is dependent upon the presence of Ca++ in the incubation medium. Stimulation of the cells by 56 mM K+ increases the conversion of tyrosine to dopa in the presence of brocresine (an inhibitor of aromatic L-amino acid decarboxylase), and has no effect on the conversion of 3H-dopa to norepinephrine. Cells can be depleted of up to 70% of their catecholamine stores by prior incubation in 56 mM K+. Norepinephrine synthesis in catecholamine-depleted cells incubated under control conditions in only slightly (20-40%) greater than it is in nondepleted cells. However, 56 mM K+ PRODUCES A SIMILAR INCREASE IN NOREPINEPHRINE SYNTHESIS IN DEPLETED CELLS AS IT DOES IN NONDEPLETED CELLS. Inhibition of amine oxidase (flavin containing) by preincubaiton with pargyline does not greatly affect catecholamine synthesis. Incubation of the cells in 56 mMK+ results in an increase in tyrosine 3-monooxygenase activity. These results indicate that the depletion of catecholamine stores plays only a minor role in the increase in norepinephrine synthesis caused by the stimulation of chromaffin cells and suggest that the activation of tyrosine 3-monooxygenase plays a more important role in this phenomenon.

Animals↗
PubMed1992

Plasma and urinary catecholamines in primary fibromyalgia: a controlled study.

Plasma and urinary catecholamines were measured in a blinded manner among 30 patients with primary fibromyalgia (PF) and 30 healthy controls without significant pain to determine possible elevations of catecholamines in PF, as well as their correlations with psychological and clinical variables in this syndrome. Results showed no significant differences between fibromyalgia and control groups in any of the catecholamines measured, nor was there a correlation between catecholamine levels and any of the clinical features or psychologic measures.

Adult↗
PubMed1991

[Arterial hypertension. Density of alpha 1 and alpha 2 adrenergic receptors in blood platelets, beta adrenergic receptors in the lymphocytes and serum catecholamine levels].

The influence of the sympathetic nervous system on blood pressure is mediated predominantly by catecholamines norepinephrine and epinephrine acting on alpha- and beta-adrenoceptors. The study of human alpha-adrenergic and beta-adrenergic receptors in hypertension is hampered by the lack of easily accessible cardiovascular tissues. Therefore numerous investigators have used platelets as a model system to study alpha-adrenergic receptors and lymphocytes to study beta-adrenergic receptors in humans. During the last decade some studies with small patient numbers have been published, that generally did not detect significant differences in platelet alpha 2-adrenergic receptor density between normotensive and hypertensive subjects, however, most investigators have described higher density of beta-receptors in lymphocytes from hypertensive patients than in cells from normotensive control subjects. This study was carried out to analyse density of alpha 1- and alpha 2-adrenoceptors in platelet membrane preparations and beta-adrenoreceptors in lymphocytes before and after physiological increase in plasma catecholamines. It was found that density of alpha 1- and alpha 2-adrenoreceptors in platelet membranes of patients with stable blood hypertension was similar to that in the healthy individuals while beta-adrenergic receptors density in lymphocytes was higher. In normotensives posture induced rise in plasma catecholamines correlated with reduced alpha 1- and alpha 2-adrenoreceptors density as well as beta-adrenoreceptor density. Hypertensive subjects had similar rise in plasma catecholamines with upright posture, but no changes in receptor density was observed. These suggest that in hypertension alpha-adrenergic and beta-adrenergic regulation by agonist may be disturbed.

Adult↗
PubMed1991

[The changes in total and free catecholamine level in plasma in a patient with status asthmaticus].

Halothane was administered in oxygen to a young man in status asthmaticus whose bronchospasm did not respond to usual treatments. Plasma catecholamine concentrations were measured during and after bronchospasm. Fifteen minute inhalation of halothane produced marked bronchodilatation as reflected in decreased peak airway pressure, decreased wheezing and fall in PaCO2 from 110 mmHg to 45 mmHg. Treatment with halothane was discontinued after 120 min inhalation. Arterial blood samples were obtained to determine free and total catecholamine (CA) on the following four occasions: 1. during status asthmaticus, 2. fifteen minutes after inhalation of halothane, 3. one day after bronchospasm and 4. two days after bronchospasm. During attack, free norepinephrine and epinephrine concentrations were markedly elevated. These values decreased remarkably after administration of halothane. Total norepinephrine and epinephrine were also elevated during bronchoconstriction, and these high concentrations persisted after bronchodilatation. The changes in CA levels suggest that sympathoadrenal hyperactivity elicited by acute asthma can be suppressed by halothane as evidenced by the decreased concentration in free catecholamines, which are physiologically active. The levels in total catecholamine did not correlate with the patient's condition. Therefore, judgement based only on the levels in total CA might lead to misinterpretation in estimating sympathoadrenal activity.

Administration, Inhalation↗
PubMed1975

Catecholamine antagonism of acetylcholine and dibutyrl guanosine 3',-5'-monophosphate in the mammalian ventricular myocardium.

After chemical sympathectomy we could demonstrate a negative inotropic effect of acetylcholine (ACh) on the cat ventricular myocardium as a direct catecholamine antagonism. Dose-response relationships for isoproterenol (IP) reveal a noncompetitive inhibition of the inotropic action of the catecholamine by ACh. A concentration of 10(-6) M ACh reduced the maximal IP-induced increase in tension by 58 +/- 13 percent (6-hydroxydopamine pretreatment) and by 65 +/- 10 percent (reserpine pretreatment); inhibition by endogenous ACh (released by field stimulation) was 36 +/- 10 percent and 38 +/- 8 percent, respectively. A concentration of 10(-3) M bibutyryl guanosine 3',5'-monophosphate (cAMP) produced a 17 +/- 7 percent reduction of the catecholamine-induced increase in tension (reserpine pretreatment). A cholinergic influence on the myocardial mechanics and metabolism of the heart may be relevant under stress situations. Vagal inhibition of the ventricular function is accentuated by an elevated sympathetic tone (Levy, 1971). If catecholamine-induced myocardial necrosis in addition to secondary effects of altered vessels are produced also by direct damage of the myocardial cell, then an influence of acetylcholine as a "natural" antagonist may be important.

Acetylcholine↗
PubMed1991

Catecholamine concentrations in the hepatic portal system: effect of surgical stress upon portal levels.

The biological effects of a hormone are dependent on the concentration delivered to the target tissue. This is generally best reflected in the arterial concentration. However, the liver is unique in that it receives substantial additional blood flow from the portal venous system. This may be important in the case of the catecholamines, where extraction or spillover from the splanchnic circulation may occur. In this study we examined portal venous catecholamine concentrations in anesthetized, laparotomized rabbits. We compared the values with simultaneously sampled arterial levels to evaluate the effects of the splanchnic tissues upon a wide range of catecholamine concentrations delivered to the liver during a state of stress. Spillover of norepinephrine and extraction of epinephrine were observed in all rabbits. Mean (+/- SEM) arterial norepinephrine concentrations were elevated, 716 +/- 167 pg/ml (n = 11); mean portal concentrations were 178 +/- 37% higher (p less than 0.01), at 1,425 +/- 301 pg/ml, representing net spillover from splanchnic tissues. In addition, significant extraction of epinephrine was observed; arterial concentrations were 2,144 +/- 580 pg/ml (n = 11). Portal levels were 1,205 +/- 382 pg/ml, 38 +/- 7.45% lower than corresponding arterial concentrations (p less than 0.02). Furthermore, there was a concentration-dependent effect upon norepinephrine spillover; the highest arterial norepinephrine concentrations were associated with the lowest splanchnic spillover. This resulted in a negative correlation between the arterial norepinephrine levels and the percent increase from spillover into the portal vein (r = -0.81, p less than 0.003). We conclude that portal venous catecholamine concentrations are significantly different from arterial levels in anesthetized, laparotomized rabbits over a wide range of concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Effect of ACTH and its fragment on brain catecholamines in intact and adrenalectomized rats.

Brain catecholamine metabolism was monitored by distribution of labelled noradrenaline (3H-NA) after intraventricular injection to intact and adrenalectomized rats. The adrenalectomy produced an increased disappearance rate of the labelled pool in the hypothalamus, hippocampus and neocortex. These changes could be prevented by hydrocortisone pretreatment. Painful stimuli resulted in an increased disappearance of the labelled pool in both intact and adrenalectomized rats. The implantation of hydrocortisone into the tuberoinfundibular region prevented the stress-induced changes of the catecholamine metabolism. Intraventricular administration of ACTH1-24 and ACTH4-10 produced a significant increase of the disappearance rate in different brain regions of adrenalectomized rats. The blocking of catecholamine synthesis by intraventricular injection of alpha-methyl-m-tyrosine resulted in a marked decrease of the labelled pool but did not prevent the ACTH-induced decrease of the tracer pool. On the other hand, the blocking of monoamine-oxydase activity by Pargyline led to a marked increase of the labelled pool but intraventricular administration of ACTH led to an increase of the disappearance rate. The mechanism of ACTH action on brain catecholamine metabolism is still obscure, however, an increased release of the NA to ACTH peptides is very likely in the light of the present observations.

Adrenal Glands↗
PubMed1991

[Organ preservation with the combination of vasopressin and catecholamine in brain dead donors].

Brain dead donor can not be maintained the systemic circulation more than 48 hours despite rather large dosage of catecholamine. The combined administration of arginine vasopressin (ADH) and catecholamine (epinephrine or dopamine) succeeded in long-term circulatory maintenance after brain death. We examined the renal and hepatic function by the method of circulatory maintenance. Twenty brain dead patients were randomly separated into two groups. Ten patients were maintained the systemic blood pressure with ADH and epinephrine (Group E). And the other ten were maintained with ADH and dopamine (Group D). Circulation was maintained with a small dosage of catecholamine at least six days in all donors. Urine output was well controlled, and serum BUN and creatinine were normal for 14 days. Daily creatinine clearance was always normal in both groups. Serum GPT, cholinesterase and alkaliphosphatase were the same in both groups, but total bilirubin was lower in group D than in group E on the seventh day. The combination of ADH and catecholamine preserved the kidney and liver after brain death for more than a week. This method will be of great value in organ transplantation from brain dead organ donors.

Brain Death↗
PubMed1990

D2 dopamine receptors modulate calcium channel currents and catecholamine secretion in bovine adrenal chromaffin cells.

Although dopamine is known to be present in sympathetic ganglia, its role and mode of action as a peripheral neurotransmitter are still poorly understood. Dopaminergic agonists have been shown to inhibit adrenal catecholamine release and calcium uptake. However, the specific dopamine receptor subtype mediating these effects and the receptor transduction mechanism remain unknown. We now provide evidence demonstrating 1) that slowly inactivating, voltage-gated calcium channels serve as a target site for dopaminergic modulation of chromaffin cell function and 2) that it is the D2 receptor subtype which mediates dopaminergic inhibitory effects on catecholamine secretion, 45Ca uptake and voltage-gated calcium currents. Whole cell patch clamp electrophysiological techniques were used to monitor directly voltage-gated Ca++ channels. The D2 agonist apomorphine but not the D1 agonist SKF 38393 reduced reversibly a slowly inactivating, voltage-gated calcium current in cultured chromaffin cells and this effect was blocked by the D2 receptor antagonist haloperidol. The presence of D2 but not D1 dopamine receptors on chromaffin cell membranes was demonstrated by radioligand binding methods, using the specific D1 and D2 receptor radioligands, [3H]SCH23390 and [3H]N-methylspiperone, respectively. Nicotine- and KCl (60 mM)-evoked catecholamine secretion and 45Ca uptake were inhibited by the D2 agonist, apomorphine, but not by the D1 agonist, SKF 38393. These inhibitory effects were prevented by the D2 antagonist, sulpiride, but not by the D1 antagonist, SCH 23390. D2 dopamine receptors appear to function as inhibitory modulators of adrenal catecholamine secretion with a mode of action involving inhibition of calcium channel currents.

Adrenal Glands↗
PubMed1989

Facial swelling secondary to inhaled bronchodilator abuse: catecholamine-induced sialadenosis.

A patient with asthma presented with a history of recurrent episodes of facial swelling. The swelling occurred in the preauricular area and extended to the angle of the jaw. The patient attributed these episodes to a "food allergy" as they occurred during or immediately following meals. The only medication the patient was using was inhaled epinephrine (Primatene MistR), two puffs, ten to twenty times a day. Subsequent evaluation revealed that the patient had sarcoidosis. Differential diagnosis of the facial swelling included food-related angioedema, sarcoid parotitis, or catecholamine-induced sialadenosis, which is a rare complication associated with excessive catecholamine administration. A gallium-67 citrate scan demonstrated abnormal pulmonary and hilar uptake of the radiotracer, but not lacrimal or parotid gland uptake, strongly arguing against sarcoidosis as the cause of the facial swelling. Episodes of swelling completely abated when the patient stopped using the epinephrine inhalers. At 5 months of follow-up she has had two recurrent episodes of facial swelling, each time associated with the use of inhaled epinephrine. Thus this patient's facial swelling most likely represents catecholamine-induced sialadenosis. This adverse drug reaction, associated with excessive use of inhaled catecholamines must be kept in mind in patients who abuse inhaled beta-adrenergic agonists and report parotid swelling.

Administration, Inhalation↗
PubMed1989

[Relationship between social factors and urinary catecholamine concentrations in pregnant women].

Catecholamine concentrations were measured in urine obtained from pregnant women to estimate the stress resulting from their lifestyles. Adrenaline and noradrenaline were analysed by high performance liquor chromatography (HPLC), creatinine was measured by Jaffe's method, and the catecholamine-creatinine ratio in urine was calculated. Adrenaline concentrations in 24-hour urine were higher in working women (n = 35) than non-working women (n = 20) (p less than 0.001) and the admission group (n = 20) (p less than 0.05), but noradrenaline concentrations showed no significant difference among three groups. Catecholamine concentrations were measured in 89 pregnant women three times in 24 hours. Marked circadian variations were observed with adrenaline and noradrenaline. Both concentrations were lowest in early morning, and increased after work (or evening) (p less than 2.0 X 10(-8)). Adrenaline concentrations were decreased on retiring to bed (p not equal to 1.0 X 10(-5)), while noradrenaline concentrations remained high until retiring to bed. There seems to be a relationship between catecholamine output and working or the familial factor. In working women (n = 53), noradrenaline concentrations were higher than in non-working women (n = 36) in early morning (p less than 0.05) and on retiring to bed (p less than 0.05). On the other hand, in women living with parents (n = 56), adrenaline concentrations were higher than those in women living without parents (n = 33) in early morning (p less than 0.05) and on retiring to bed (p less than 0.05). From these results, it may be concluded that working women or women living with parents are under much stress in their lives.

Chromatography, High Pressure Liquid↗
PubMed1988

Plasma catecholamine changes during excision of pheochromocytoma.

Sequential changes in plasma norepinephrine (NE) and epinephrine (EPI) concentration were correlated with changes in blood pressure and cardiac rate in 14 patients undergoing surgery because of pheochromocytoma. All patients had elevated preoperative plasma catecholamine levels that increased during induction of anesthesia, intubation, and skin incision, but mean values did not become significantly higher than preoperative values until tumor manipulation. Episodes of hypertension were associated with increased plasma catecholamine levels, and plasma catecholamine levels and blood pressure decreased dramatically after tumor resection. NE and EPI were usually secreted simultaneously, but release of either NE or EPI alone occurred on some occasions. There were marked variations in the concentration ratio of NE to EPI in plasma at different periods of observation, which suggests that pheochromocytomas release varying amounts of catecholamines in a random fashion. Studies of the effect of the duration of preoperative preparation on intraoperative blood pressure, pulse rate, and cardiac arrhythmias failed to demonstrate that treatment for 14 days or longer was more effective than treatment for 4 to 7 days. Neither the brief nor the prolonged period of therapy prevented development of severe hypertension during tumor manipulation.

Adolescent↗
PubMed1985

[Effect of hypokinesia and muscle training on catecholamine levels of the myocardium of rats in postnatal ontogeny].

Following muscular training and hypokinesia in postnatal ontogenesis (10 weeks) rats were examined by fluorometry for the content of catecholamines at rest and after extreme exertion (swimming). Regular muscular training led to an increase in catecholamine concentration in the myocardium. Hypokinesia decelerated catecholamine accumulation by the myocardium. A single extreme swimming exercise brought about a decrease in catecholamine concentration in the myocardium. The minimal adrenaline concentration was the same, being equal to 0.04 microgram/g crude tissue whatever the age and locomotion pattern.

Animals↗

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