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PubMed1989

[Changes in catecholamines of the striatum during 5% oxygen administration and the alleviating effects of flunarizine in rats].

Five percent oxygen was administered to rats under controlled respiration. The concentrations of catecholamines and their metabolites (dopamine, HVA, DOPAC, norepinephrine) were measured during 5% oxygen administration and subsequent recovery period. Flunarizine, a calcium channel blocker, was administered and its effects on catecholamine fluctuations were studied. Results were as follows. Dopamine increased with 5% oxygen administration. DOPAC and norepinephrine decreased and no changes were seen in HVA. After 20 min of hypoxia, catecholamine contents returned to the control levels in another 2 hours of air breathing. When flunarizine was administered in advance, changes in catecholamine content appeared to be lower during 5% oxygen administration and subsequent recovery period.

Animals↗
PubMed1989

Catecholamines in CSF, plasma, and tissue after autologous transplantation of adrenal medulla to the brain in patients with Parkinson's disease.

Catecholamine concentrations were measured in tissue samples of caudate and adrenal medulla in eight patients with Parkinson's disease who were taking L-dopa and were undergoing autologous transplantation of adrenal medulla to caudate nucleus. High-performance liquid chromatography with electrochemical detection was used for the measurement of analytes. Dopamine concentrations were quite similar in the caudate and the adrenal medulla; epinephrine and norepinephrine concentrations were some 600 times and 90 times higher, respectively, than that of dopamine in adrenal medulla but were barely detectable in caudate nucleus. Catecholamines and metabolites were also measured, before and after transplantation, in lumbar cerebrospinal fluid (CSF) and plasma 1 hour after the patients' first morning dose of L-dopa. The major fractions of the catecholamines in CSF were sulfoconjugated. The concentrations of sulfoconjugated but not free dopamine were modestly increased in CSF after the transplantation, although plasma concentrations were unchanged. CSF concentrations of free and conjugated norepinephrine and epinephrine, 3-methoxy-4-hydroxyphenylglycol, and homovanillic acid were unchanged after the transplantation. The data suggest that the grafted tissue does not retain its noradrenergic or adrenergic properties after transplantation, and that dopamine formation in the brain may be modestly increased. Plasma catecholamines were unaffected after the removal of one adrenal gland for the transplant.

Adrenal Medulla↗
PubMed1989

Effects of vasopressin and catecholamines on the maintenance of circulatory stability in brain-dead patients.

The effectiveness and reliability of long-term control of circulatory stability in brain-dead patients by combined administration of vasopressin and catecholamine was examined in detail. Twenty-five patients were divided into three groups according to the dose of vasopressin. The first group (n = 10) received no vasopressin, the second group (n = 2) an antidiuretic dose (0.1-0.4 U/hr), and the third group (n = 13) a pressor dose (1-2 U/hr), respectively. Patients given no vasopressin or an antidiuretic dose demonstrated circulatory deterioration and cardiac arrest within a short time after brain death, despite administration of a large dose of epinephrine. All patients with a pressor dose of vasopressin, however, demonstrated stable circulation as long as vasopressin and epinephrine were administered. Five patients in whom stable circulation was maintained by this technique were randomly chosen from the third group and studied under the following four conditions: (1) neither vasopressin nor epinephrine; (2) vasopressin only; (3) epinephrine only; and (4) both vasopressin and epinephrine. Compared with the controls (neither vasopressin nor epinephrine), vasopressin only increased the total peripheral resistance index, whereas epinephrine alone increased the cardiac index. Combined administration, however, raised the mean arterial blood pressure significantly by markedly increasing the total peripheral resistance index and cardiac index. Finally, in four brain-dead patients also randomly chosen from the third group, epinephrine, norepinephrine, and dopamine were compared in their circulatory effects with a pressor dose of vasopressin. Epinephrine increased both the total peripheral resistance index and cardiac index, whereas norepinephrine increased the total peripheral resistance index, compared with the baseline (no catecholamine). The required dose of norepinephrine, however, was four times that of epinephrine. The major effect of dopamine was to increase the cardiac index. We conclude that a pressor dose of vasopressin plays a central role in circulatory stabilization of brain-dead patients, and that long-term maintenance of stable circulation for a desired length of time is possible by the combined use of vasopressin and a catecholamine. Individually, catecholamines exhibit characteristic differences. Epinephrine has significant effects on both peripheral vessels and the heart, whereas norepinephrine keeps the circulation stable by increasing the total peripheral resistance index, with a much larger dose than epinephrine. Dopamine acts primarily on the heart.

Blood Circulation↗
PubMed1986

Alpha 2-adrenoceptors do not regulate catecholamine secretion by bovine adrenal medullary cells: a study with clonidine.

Experiments have been performed with perfused bovine adrenal glands, with freshly isolated chromaffin cells, and with chromaffin cells maintained in tissue culture to investigate the suggestion that there are alpha-adrenoceptors present which regulate catecholamine secretion. Only one set of observations has lent support to this suggestion: the rather specific alpha 2-adrenoceptor agonist clonidine inhibits catecholamine secretion evoked by the physiological secretagogue, acetylcholine, and by the related nicotinic agonists, carbachol and nicotine. All other observations detract from the suggestion. Other alpha-adrenoceptor agonists (noradrenaline, adrenaline, tramazoline, phenylephrine, and alpha-methyl-noradrenaline) are virtually ineffective at inhibiting secretion evoked by carbachol. In addition, the alpha-adrenoceptor antagonists phentolamine, phenoxybenzamine, and yohimbine not only fail to enhance the secretion of catecholamines evoked by carbachol but also fail to offset the inhibitory action of clonidine. The data suggest that functional alpha 2-adrenoceptors of the classical type are not present upon bovine chromaffin cells and that, in this tissue, clonidine must act in some other way. In the bovine adrenal medullary chromaffin cell clonidine probably acts at the nicotinic receptor because it does not reduce catecholamine secretion evoked by depolarizing concentrations of potassium or veratridine but does reduce the carbachol-evoked influx of 22Na that can be measured in the presence of tetrodotoxin and ouabain and which probably reflects entry through the nicotinic channel. Furthermore, clonidine can abolish, in reversible fashion, the acetylcholine-activated inward current determined with patch-clamp.

Adrenal Medulla↗
PubMed1986

Effects of propranolol on catecholamine synthesis and uptake in the central nervous system of the rat.

These studies were undertaken to determine the effects of propranolol on catecholamine synthesis and uptake in the rat central nervous system. The effects of propranolol on catecholamine synthesis were studied in vitro in striatal and hypothalamic synaptosomes, and also in vivo. In addition, the effects of propranolol on catecholamine uptake in striatal and hypothalamic synaptosomes were evaluated. Propranolol inhibited synaptosomal catecholamine synthesis and uptake in both tissues. Norepinephrine uptake in the hypothalamus was most sensitive to propranolol inhibition (IC50 = 5 microM). Dopamine synthesis in striatal synaptosomes was also inhibited markedly, with an IC50 = 8 microM. After in vivo administration, propranolol decreased the accumulation of dopa in the striatum, confirming propranolol's synthesis inhibiting effect in dopaminergic terminals. Studies of soluble striatal tyrosine hydroxylase revealed that propranolol has a direct inhibitory effect on the enzyme. These results indicate that propranolol administration may cause a potentiation of norepinephrine activity specifically at alpha receptors, due to concurrent beta receptor blockade and inhibition of norepinephrine reuptake and a decrease in dopamine activity at dopaminergic receptor sites due to an inhibition of dopamine formation.

Animals↗
PubMed1988

Prostaglandin E receptor enhancement of catecholamine release may be mediated by phosphoinositide metabolism in bovine adrenal chromaffin cells.

In the presence of ouabain, prostaglandin (PG) E2 stimulated a gradual secretion of catecholamines from cultured bovine adrenal chromaffin cells. PGE2 or ouabain alone evoked a marginal secretory response. The synergism of ouabain was also observed with muscarine. PGE2, like muscarine, induced a concentration-dependent formation of inositol phosphates: rapid rises in inositol trisphosphate and inositol bisphosphate followed by a slower accumulation of inositol monophosphate. This effect on phosphoinositide metabolism was accompanied by an increase in cytosolic free Ca2+. The potency of PGs (PGE2 greater than PGF2 alpha greater than PGD2) to stimulate catecholamine release was well correlated with that to affect phosphoinositide metabolism and that to increase the level of intracellular Ca2+. PGE2 did not stimulate cAMP generation significantly in bovine chromaffin cells. The effect of PGE2 on catecholamine release was mimicked by 12-O-tetradecanoylphorbol 13-acetate and A23187, but not by the cAMP analogue dibutyryl cAMP nor by forskolin. These results indicate that PGE2 may enhance catecholamine release from chromaffin cells by activating protein kinase C in concert with the increment of intracellular Ca2+.

Adrenal Medulla↗
PubMed1988

Catecholamine toxicity in cerebral cortex in dissociated cell culture.

Identification of endogenous toxins and characterization of the mechanisms by which toxins produce cell injury and death may help understand both normal modeling of cell populations and connections in the CNS as well as abnormal cell loss. The toxicity of catecholamines intrinsic to the CNS was investigated using the model system of rat cerebral cortex in dissociated cell culture. All catecholamines tested, including norepinephrine (NE), dopamine, and epinephrine, were toxic to neurons as well as glia at a concentration of 25 microM when added to cultures 24 hr after plating. Toxicity was evident after 48 hr exposure to NE, as monitored by loss of cells from the cultures. Toxicity did not seem to be mediated by adrenergic receptors because, although the beta-adrenergic agonist isoproterenol (but not the alpha-adrenergic agonist phenylephrine) was similar in its toxic effect to NE, the beta-adrenergic antagonist atenolol did not block the toxic effect of NE. Toxicity could be mimicked by hydrogen peroxide, a product of the oxidative degradation of catecholamines. Toxicity of NE was blocked by catalase. The neurotoxin 6-hydroxydopamine (6-OHDA), supposedly selective for catecholaminergic neurons, was found to be toxic over the same concentration range as NE. These results suggest that endogenous catecholamines may play a role in normal and abnormal cell death, and suggest that caution be used in relying on the specificity of 6-OHDA and other supposedly selective neurotoxins.

Adrenergic beta-Antagonists↗
PubMed1985

Lack of beta-adrenergic role for catecholamines in the development of hyperglycemia and ketonaemia following acute insulin withdrawal in type I diabetic patients.

In order to evaluate the role of beta-receptor mediated effects of catecholamines in the metabolic deterioration following insulin withdrawal in insulin-dependent diabetic patients we have measured in 5 patients metabolic substrate and hormone concentrations during a 6 hours arrest of insulin infusion, without or with a simultaneous infusion of propranolol. During insulin deprivation plasma epinephrine and norepinephrine increased slightly (from 107 +/- 10 ng/L to 173 +/- 6 ng/L and from 307 +/- 37 ng/L to 518 +/- 77/ng/L respectively (p less than 0.05), cortisol decreased physiologically, but growth hormone and glucagon were not significantly modified. Free insulin decreased progressively from 12.2 +/- 2.5 mU/L to 5.4 +/- 1.1 mU/L (p less than 0.01). Blood glucose and ketone bodies rose sharply before any significant change in catecholamine levels. Plasma free fatty acids and blood glycerol increased progressively and their rise appeared somewhat temporally related to the variations of catecholamine levels. The addition of propranolol to insulin deprivation did not modify the changes in hormone concentrations in spite of a slightly greater rise of epinephrine (from 78 +/- 4 ng/L to 179 +/- 7 ng/L, p less than 0.05) and norepinephrine (from 395 +/- 80 ng/L to 679 +/- 153 ng/L, p less than 0.05). The rises of glucose and ketone bodies were unaffected whereas the increases of free fatty acids and glycerol were slightly blunted. In conclusion, we have no evidence for a beta-adrenergic mediated role for catecholamines in the development of hyperglycaemia and ketonaemia in non-stressed insulin deprived diabetic patients, and only small evidence for a permissive effect on lipolysis.

Adult↗
PubMed1986

Effects of naloxone and thyrotropin-releasing hormone on plasma catecholamines, corticosterone, and arterial pressure in normal and endotoxemic rats.

To investigate the possible involvement of the adrenal cortex and medulla in the cardiovascular effects of naloxone and thyrotropin-releasing hormone (TRH) in endotoxic shock, plasma epinephrine, norepinephrine, dopamine, and corticosterone were measured along with hemodynamic variables during naloxone and TRH treatment of normal and endotoxemic rats. In the absence of endotoxemia, naloxone (3 mg/kg, iv) did not significantly alter mean arterial pressure or plasma catecholamine or corticosterone levels. In contrast, following TRH administration (4 mg/kg, iv), an increase in mean arterial pressure was associated with significant increases in plasma epinephrine, norepinephrine, and corticosterone. TRH also produced a transient increase in plasma glucose levels. Endotoxic shock was associated with marked increases in plasma catecholamine levels, with epinephrine levels showing the greatest change, and significant though less pronounced increases in corticosterone. Both naloxone and TRH significantly elevated mean arterial pressures of endotoxemic rats, although neither of these compounds significantly altered the plasma catecholamine and corticosterone responses to endotoxin. Naloxone and TRH also failed to alter endotoxin-induced changes in plasma glucose levels. These results indicate that the cardiovascular effects of naloxone and TRH in endotoxic shock do not simply arise from an enhancement of adrenal catecholamine or corticosterone secretion.

Animals↗
PubMed1986

[Plasma catecholamines, free and conjugated, in the hemodialyzed chronic renal failure patient].

Free, sulfo and glucuro-conjugated catecholamines (dopamine, noradrenaline and adrenaline) were measured to study their metabolism in 35 non-selected patients with chronic renal failure, and under hemodialysis for various periods of time. Our data demonstrate a statistically significant increase of free dopamine, and free noradrenaline concentration in these patients, while that of free adrenaline was not different from controls. However a careful scrutiny of 35 individual data suggests that sub-groups of patients with either high normal or low plasma free noradrenaline concentration could exist; this likely heterogeneity could be a good explanation for conflicting conclusions provided by previous reports. Suspecting that conjugated catecholamines might be altered in these patients, plasma sulfo and glucuro-conjugated amines were measured. We have found a predictable and highly significant increase of sulfo-conjugated catecholamines; glucuroconjugated dopamine and noradrenaline were unchanged, while glucuroconjugated adrenaline was significantly increased. The physiological meaning, if any, of these new observations on conjugated catecholamines cannot be assessed at the moment.

Adult↗
PubMed1988

Adrenomedullary catecholamine release in the fetus and newborn: secretory mechanisms and their role in stress and survival.

Catecholamines released by the adrenal medulla during birth play a key role in the adaptation of the newborn to extrauterine life. Respiratory, metabolic and cardiovascular adaptations to the hypoxia and other stresses associated with delivery are dependent upon a profound surge of adrenomedullary activity which occurs despite the immaturity of connections between the central nervous system and the adrenal. The "non-neurogenic" response seen in the fetus and neonate is thus essential to survival, and any interference either with catecholamine release or with catecholamine actions at adrenergic targets results in loss of the ability to survive hypoxia or other stressors. The immature secretory mechanism disappears as a result of development of neural connections, and factors which accelerate ontogeny of neural competence thus lead to premature loss of non-neurogenic secretory capabilities and a consequent increase in vulnerability. The fetus and neonate also have unusual proportions of adrenergic receptor subtypes in many tissues; these confer reactivity to specific stimuli associated with birth and with periods in which tissue differentiation may be under adrenergic control. Again, the ontogenetic switchover of receptor-mediated mechanisms appears to be a function of the development of neuronal competence, but in this case an important role may be played by a secondary surge in sympathetic tone occurring during the postnatal period. Through specialized mechanisms mediating catecholamine secretion and adrenergic responses, the adrenal medulla thus appears to provide both physiological and trophic signals to the fetus and neonate.

Adaptation, Physiological↗
PubMed1987

Evidence against the adenosine-catecholamine antagonism in the canine heart in situ.

Adenosine has been reported to attenuate the positive inotropic effects of catecholamines in isolated heart preparations of rodents. These results were not confirmed in anesthetized dogs during intracoronary infusion of isoprenaline. However, these experiments did not establish the effects of adenosine on the inotropic effects of endogenously released catecholamines. Therefore cardiac sympathetic nerve stimulation was performed in 5 anesthetized, vagotomized dogs. The left circumflex coronary artery was perfused at a constant pressure of 130 +/- 4 mmHg. The contractile function of the circumflex-perfused myocardium was analyzed by sonomicrometry. Cardiac sympathetic nerve stimulation at 1, 2, 5, 10 and 20 Hz increased systolic segment shortening in a frequency-dependent manner from 10.9 +/- 2.6 at control to 15.3 +/- 3.4% at 20 Hz. During intracoronary infusion of adenosine (50 micrograms/kg/min) cardiac sympathetic nerve stimulation still increased systolic segment shortening from 9.9 +/- 3.5 at control to 16.3 +/- 4.5% at 20 Hz. The lack of an adenosine-catecholamine antagonism in the present experiments was not due to the sequence of procedures, nor to the marked flow increase induced by adenosine, since systolic segment shortening at rest was reduced during adenosine infusion, and since during intracoronary infusion of papaverine and sodium nitroprusside similar results were obtained. The observation of an adenosine-catecholamine antagonism in rodents should be restricted to this species at present.

Adenosine↗
PubMed1986

The catecholamine concentration in central veins of hypertensive patients--an aid not without problems in locating phaeochromocytoma.

The concentrations of adrenaline, noradrenaline and cortisol in blood sampled at routine attempts at catheterization of the adrenal and renal veins, the inferior vena cava and the azygos and hepatic veins were measured in six patients with a phaeochromocytoma and six patients with hypertension due to other causes. In the non-tumour patients the adrenaline and noradrenaline concentrations, compared with normal values for peripheral venous blood, were abnormally high in five out of seven samples from the site of the left adrenal vein but in only one out of seven from the right side. In all the adrenal vein samples with an abnormally high catecholamine concentration the cortisol level was also elevated, and it was at least 100 per cent higher than in samples from the inferior vena cava. This suggests that a high catecholamine concentration linked with an elevated cortisol level is merely an indication of correct adrenal vein sampling and is not necessarily evidence of a tumour. In successful attempts of sampling adrenal venous blood (cortisol levels increased), concentrations of adrenaline and noradrenaline of up to 100 and 20 nmol/l, respectively, can be regarded as normal. From a retrospective analysis of catecholamine levels in the six tumour patients it is clear that owing to the variability of venous drainage from the right adrenal gland, the technique of adrenal venous blood sampling may be unreliable and even misleading in attempts to locate a phaeochromocytoma. This is also true in patients with generally elevated catecholamine levels.

Adrenal Gland Neoplasms↗
PubMed1987

Ascorbic acid as an antioxidant in measurements of catecholamines in plasma.

Sodium metabisulfite, commonly used to prevent the oxidation of catecholamines during extraction from plasma onto alkaline alumina, does not prevent their subsequent degradation in acetic acid eluates. However, ascorbic acid, a potent antioxidant, is extracted with the catecholamines onto the alumina and prevents such destruction. However, ascorbic acid may interfere with the electrochemical measurement of catecholamines, unless sequential oxidation and reduction are used. Other methods of minimizing catecholamine oxidation in acetic acid eluates include refrigerating at 4 degrees C and capping the sample vials to exclude atmospheric oxygen.

Aluminum Oxide↗
PubMed1985

Naloxone potentiates the cardiovascular effects of catecholamines in canine hemorrhagic shock.

Endogenous opioids are released during stress and appear to contribute to the cardiovascular suppression seen in shock. When the opiate receptor antagonist naloxone is administered intravenously to anesthetized dogs subjected to hemorrhage, mean arterial pressure, maximal left ventricular dp/dt, and cardiac output increase. This study tests the hypothesis that naloxone acts by potentiating the effects of neurally and adrenally released catecholamines. If this hypothesis is correct, then blockade of endogenous catecholamine release should attenuate the response to naloxone, and administration of exogenous adrenergic agonists prior to naloxone treatment should restore the response. Catecholamine release was attenuated by a combination of surgical adrenal denervation and pharmacological ganglionic blockade. Adrenal denervation or chlorisondamine alone attenuated and, in combination, blocked the response to naloxone in hemorrhaged dogs. Infusion of alpha- and beta-adrenergic agonists at a constant rate prior to treatment restored the response to naloxone. Naloxone appears to improve cardiovascular function in hemorrhagic shock by potentiating the effect of released catecholamines and not by increasing sympathoadrenal discharge.

Adrenal Glands↗
PubMed1985

[Levels of catecholamines in the hypothalamus, hypophysis and in the adrenal in sheep after whole-body exposure to gamma rays].

The changes were studied in the levels of catecholamines and L-DOPA in the control system of reproduction cycle (hypothalamus, hypophysis) and in adrenal glands of sheep after all-body irradiation with 60Co at the total dose of 6.7 Gy for seven days. The power input per hour of irradiation source was 0.039 Gy. The catecholamines (noradrenaline, dopamine and adrenaline) and L-DOPA were determined, after having been isolated from the tissues, by the method of spectral fluorimetry. After all-body exposition to gamma-radiation noradrenaline dropped in hypothalamus in comparison with the control group of sheep, most significantly in the rostral (by 74.2%) and caudal part (by 40%). A similar drop like in the case of noradrenaline was also observed in dopamine, the concentrations of which decreased in rostral hypothalamus by 72%, in medial hypothalamus by 94% and in caudal hypothalamus by 60%. Adrenaline shows a drop in hypothalamus, most significant in caudal region (by 62%). In relation with that the level of a precursor for the synthesis of catecholamines and L-DOPA has been changed which achieved, in the studied regions of hypothalamus in sheep, significantly lower levels than were determined in the control group of sheep. As regards the hypophysis, after irradiation no significant changes in the levels of noradrenaline and adrenaline were recorded, however, dopamine and L-DOPA dropped significantly (P less than 0.01). The exposition to gamma-radiation also causes a decrease in the concentrations of catecholamines and L-DOPA in the adrenal glands of sheep, most significant in noradrenaline (by 61%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Ethanol-induced adrenomedullary catecholamine secretion in LS/Ibg and SS/Ibg mice.

Ethanol, administered i.p., produced a dose-dependent increase in plasma norepinephrine and epinephrine concentrations in LS/Ibg (LS) but not in SS/Ibg (SS) lines of mice. Ethanol-induced elevations of plasma epinephrine in LS mice were approximately 10-fold greater than those observed in SS mice. Plasma epinephrine and norepinephrine attained peak concentrations at 20-min post-ethanol administration at doses ranging from 2.8 to 4.1 g/kg. Plasma catecholamines remained elevated for approximately 1 hr and returned to basal values 2 hr after ethanol administration. Significant correlations were obtained between blood ethanol (r = 0.99), plasma epinephrine (r = 0.92) and plasma glucose (r = 0.98) as a function of ethanol dose in LS mice. Chlorisondamine (3 mg/kg), a ganglionic blocker, abolished completely the ethanol-induced increase in plasma catecholamines. These results confirm previous suggestions that the response is centrally mediated through an increased sympathetic outflow rather than by a direct effect on the adrenal medulla. The increase in plasma epinephrine and associated hyperglycemia produced by ethanol was not observed with pentobarbital or halothane anesthesia. Ethanol-induced hypothermia was diminished markedly (47%) by an elevated ambient temperature (28 degrees C) without reducing the hyperglycemic response to ethanol. These results suggest that ethanol-induced hypothermia does not mediate ethanol-induced adrenomedullary catecholamine secretion and concomitant hyperglycemia. It is proposed that the differential ethanol-induced secretion of adrenomedullary catecholamines in LS and SS mice is due to differential central nervous system sensitivities to ethanol.

Adrenal Medulla↗
PubMed1985

Effects of low-dose morphine and fentanyl infusions on urinary and plasma catecholamine concentrations during scoliosis surgery.

Plasma and urinary catecholamines were measured in 20 patients during scoliosis surgery to determine whether low dose fentanyl (1.5-2.5 micrograms . kg-1 . min-1) and morphine (150-250 micrograms . kg-1 . min-1) affect the catecholamine stress response to surgery differently. In all patients epinephrine (1.6-11.4 micrograms/kg) was injected locally at the operative site for hemostasis. This was an advantage because exogenous and endogenous epinephrine undergo the same fate and the increase in epinephrine might enhance otherwise subtle effects. The data indicate that both narcotics have similar effects on catecholamine metabolism but that even low doses of fentanyl are more effective than morphine in obtunding the catecholamine response to painful stimuli. Also, postoperative differences in plasma epinephrine indicate that recovery of awareness, and thus the onset of postoperative pain, is more rapid in patients receiving fentanyl.

Adolescent↗