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PubMed1999

Effect of adenosine and verapamil in catecholamine-induced accelerated atrioventricular junctional rhythm: insights into the underlying mechanism.

Accelerated AV junctional rhythm is postulated to be due to enhanced automaticity of a high AV junctional focus. The adenosine response of this rhythm was tested in 17 patients (7 males, 12-83 years). The indications of electrophysiology study were nonspecific palpitation (n = 5), unexplained syncope (n = 6), postablation of accessory pathways (n = 4), and postmodification of AV nodal reentry tachycardia (n = 2). The sinus node and AV nodal functions were normal. Pacing and programmed electrical stimulation failed to induce any arrhythmia at baseline. The accelerated junctional rhythm (cycle length = 553 +/- 134 ms) was initiated spontaneously in all patients after isoproterenol infusion (1-2 micrograms/min). It was not suppressible by overdrive pacing. Cessation of isoproterenol infusion terminated the rhythm in all patients. Adenosine (6 mg) reproducibly terminated the accelerated junctional rhythm in all patients. In six patients, adenosine suppressed the junctional rhythm without producing AV nodal block. In the other 11 patients, the junctional rhythm was terminated prior to the occurrence of AV nodal block. Verapamil was tested in ten patients and 5 mg of intravenous verapamil terminated the junctional rhythm in all patients. In conclusion, the mechanism of catecholamine-induced accelerated AV junctional rhythm is most likely enhanced automaticity, and catecholamine-induced accelerated AV junctional automaticity is sensitive to adenosine and verapamil. Adenosine appears to have differential effects on catecholamine-enhanced AV junctional automaticity and AV nodal conduction. This suggests that, under catecholamine stimulation, adenosine may have different mechanisms of action on AV nodal conduction and automaticity.

Adenosine↗
PubMed1999

Catecholamine facilitated reentrant ventricular tachycardia: uncoupling of adenosine's antiadrenergic effects.

INTRODUCTION: Adenosine has no direct electrophysiologic function in ventricular tissue, but in the presence of cyclic adenosine monophosphate (cAMP), stimulation exerts a potent antiadrenergic effect. This effect has been exploited in the recognition and treatment of ventricular tachycardia (VT) due to cAMP-mediated triggered activity and automaticity, which are respectively terminated and suppressed by adenosine. However, the effects of adenosine on catecholamine-facilitated reentrant VT are unknown. A pivotal issue is whether termination of VT with adenosine is mechanism specific, or whether it represents a nonspecific antiadrenergic effect. The purpose of this study, therefore, was to define the effects of adenosine in a well-characterized group of patients with catecholamine-facilitated reentrant VT. METHODS AND RESULTS: Fourteen patients with catecholamine-facilitated reentry were studied. In the 12 patients with structural heart disease (including two with arrhythmogenic right ventricular dysplasia), adenosine (260 to 550 microg/kg) failed to slow or terminate VT. Two patients without structural heart disease had intrafascicular tachycardia confined to the left posterior fascicle, a calcium-dependent, verapamil-sensitive arrhythmia. In the absence of isoproterenol, verapamil terminated VT but adenosine did not. However, when isoproterenol was subsequently required for facilitation of tachycardia, adenosine terminated VT in both patients. CONCLUSION: Adenosine has no antiadrenergic (antiarrhythmic) effect in patients with catecholamine-facilitated VT due to structural heart disease. Patients with verapamil-sensitive, left posterior intrafascicular reentry have an unusual dual response to adenosine. In the unstimulated state, adenosine has no effect on basal inward calcium current and, therefore, no effect on VT. However, when induction of VT requires amplification of the inward calcium current through stimulation of cAMP, adenosine sensitivity of VT becomes manifest. These results indicate that with few exceptions, termination of VT with adenosine is strongly suggestive of a cAMP-mediated triggered mechanism rather than reentry.

Adenosine↗
PubMed1979

Plasma catecholamines, cyclic AMP and metabolic substrates in hemorrhagic shock of the rat. The effect of adrenal demedullation and 6-OH-dopamine treatment.

Plasma catecholamines, cyclic AMP and metabolic substrates in hemorrhagic shock of rats was studied in 4 groups of animals: 1) Control rats, 2) rats with adrenal demedullation, 3) rats with 6-OH-dopamine induced chemical sympathectomy, and 4) rats with combined demedullation and sympathectomy. The rats were bled to a systemic blood pressure of 35 mmHg. The basal plasma level of noradrenaline (NA), adrenaline (A) and dopamine (DA) in control animals was each about 1 nmol/1. After hemorrhage for 1 h the A levels had reached 50 nmol/l and there was little further rise after 4 h. The rise was eliminated by demedullation but unaffected by sympathectomy. NA levels rose continuously in the control and in the sympathectomized rats. At 1 h the level was about 4 nmol/l and at 4 h about 20 nmol/l. The demedullated rats showed a 3-fold increase in circulating NA, while little or no change was seen in the combined demedullated and sympathectomized rats. DA levels did not change in any of the groups during the first hour, but were markedly elevated after 4 h of hypotension. Cyclic AMP and glucose levels in plasma showed a rapid increase 1 h after hemorrhage and thereafter returned to or below basal values. Demedullation largely prevented the increase, while sympathectomy had no effect. The increase in lactate and pyruvate levels were diminished but not eliminated by either sympathectomy or demedullation. Glycerol levels were unchanged and FFA decreased in all groups of rats. The results show that the adrenal medulla is the dominating source of plasma catecholamines in hemorrhagic shock in rats. The initial increase in plasma glucose and cyclic AMP appear to be largely mediated by adrenal A. The subsequent fall in these parameters and derangement of circulatory homeostasis are not, in the present shock model, primarily due to a failure of catecholamine secretion, but rather to a decreased responsiveness of peripheral tissues to catecholamine stimulation.

Adrenal Medulla↗
PubMed1997

Insulin and catecholamines act at different stages of rat liver regeneration.

Insulin and catecholamines are known to exert effects on hepatocyte growth and metabolism. The binding of insulin, the plasma levels of insulin (INS), and the plasma catecholamine levels of epinephrine (EPI) and norepinephrine (NE) were measured during liver regeneration after partial hepatectomy (PH). A significant decrease (p < 0.05) of INS receptor binding capacity was found at 1, 2, and 3 days after operation. A single insulin injection (2.5 IU/kg body weight) at 24 h after sham operation or partial hepatectomy did not affect these changes of INS binding to hepatocytes. The plasma insulin and glucose levels were similar in both hepatectomized and sham-operated rats. Within 20 min after liver resection or sham operation, plasma NE and EPI concentrations increased rapidly. Then, a significant decrease was observed in plasma catecholamine levels at 1 h after laparotomy and PH. In both groups, laparotomized and partially hepatectomized plasma levels of NE at 4 h reached control values and remained unchanged at the 4- and 24-h periods. After PH, the levels of EPI remained elevated at 4 h in comparison with laparotomy. Adrenal tyrosine hydroxylase mRNA levels were significantly elevated at 4 h in both PH and sham-operated groups. These results suggest that signals that are initiated by catecholamines and transduced through second messengers presumably participate in the trigger mechanism of liver regeneration, while insulin (considered as a secondary mitogen) enhances a stimulus for liver regeneration.

Animals↗
PubMed1990

Inhibitory effects of catecholamines on cholinergically and non-cholinergically mediated contractions of guinea-pig isolated bronchial muscle.

The actions of catecholamines on the responses evoked by electrical field stimulation or by acetylcholine and substance P in guinea-pig bronchial strip chain have been examined. Electrical field stimulation evoked a biphasic contraction, consisting of a cholinergically-mediated fast contraction followed by a non-cholinergically-mediated slow contraction. All catecholamines tested caused a concentration-dependent reduction in the height of the biphasic contraction, where non-cholinergic contractions were more potently inhibited. The inhibitory effect of isoprenaline was largely prevented by propranolol (2 microM) alone, whereas those of noradrenaline and adrenaline were prevented by treatment with both propranolol (2 microM) and yohimbine (2 microM). The inhibitory effect of dopamine was unaffected either by propranolol (2 microM), yohimbine (2 microM) or haloperidol (10 microM). Submaximal contractions of bronchial muscle evoked by exogenous acetylcholine (2 microM) or substance P (0.2 microM) were also inhibited by catecholamines, except dopamine, but the effects were antagonized by propranolol (2 microM) alone. The results suggest that in guinea-pig isolated bronchial muscle, catecholamines can inhibit both cholinergic and non-cholinergic excitatory neurotransmissions not only by postjunctional beta-adrenoceptors but also by prejunctional alpha 2-adrenoceptors.

Animals↗
PubMed1966

On the relation between ATP splitting and secretion in the adrenal chromaffin cell: extrusion of ATP (unhydrolysed) during release of catecholamines.

1. Cats' adrenal glands were acutely denervated and perfused, in situ, with Locke's solution.2. When the medullary secretogogue Ba (2-10 mM) was added to the perfusion medium, large amounts of AMP and traces of ATP were found in the venous effluent from the adrenal gland along with the catecholamines. In this respect Ba mimicked the physiological secretogogue, acetylcholine.3. Control perfusions with known concentrations of ATP showed that under such conditions ATP was rapidly broken down within the adrenal vasculature.4. When such intravascular hydrolysis of ATP was suppressed by perfusing with a Ca-free, Mg-free Locke's solution containing 1-2 mM EDTA, catecholamine secretion induced by Ba was accompanied by the discharge of large amounts of ATP but relatively little AMP.5. The ATP that accompanied catecholamine secretion in such circumstances is assumed to derive from the ;heavy' nucleotide-rich chromaffin granules and it is concluded that the mechanism for catecholamine secretion does not depend on hydrolysis of the ATP within these granules.6. The release of ATP (unhydrolysed) supports the hypothesis that the chromaffin granules discharge their contents at the cell surface by the process of ;reverse pinocytosis'.

Adenine Nucleotides↗
PubMed1984

Co-release of enkephalins and precursors with catecholamines from the perfused cat adrenal gland in situ.

We have compared the nature of the enkephalin-like material derived from proenkephalin present in the intact cat adrenal gland with the material co-released with catecholamines from the perfused adrenal in response to splanchnic nerve stimulation and to perfusions with solutions containing acetylcholine (ACh) or high potassium chloride (KCl). In cat adrenals most of the enkephalin-like material was in the form of large enkephalin-containing peptides. Free (met)enkephalin immunoreactivity represented only 25% of the total (met)enkephalin immunoreactivity as determined by enzymatic digestion of large enkephalin-containing fragments. Electrical stimulation (15 Hz) of the splanchnic nerve or perfusion of the gland with ACh (0.1 mM) or KCl (50 mM), applied for 10 min, induced an immediate release of free (met)enkephalin immunoreactivity, (met)enkephalyl-arg-phe immunoreactivity, and of large (met)enkephalin-containing peptides. The release by all three modes of stimulation followed a pattern that paralleled the output of catecholamines. A rapid fatigue of all secretory processes developed during the stimulation periods, similar to that observed for catecholamines. During splanchnic nerve stimulation, each nanomole of catecholamine output was accompanied by the output of 0.4 pmol free (met)enkephalin immunoreactivity, of 1.1 pmol total (met)enkephalin immunoreactivity and of 0.1 pmol (met)enkephalyl-arg-phe immunoreactivity. Analysis of the perfusate by high-pressure liquid chromatography revealed that (met)enkephalin, (met)enkephalyl-arg-phe and (met)enkephalyl-arg-gly-leu were released in molar ratios of 4 to 1 to 1 which is similar to the ratio found in the precursor, proenkephalin. The ratio of total (met)enkephalin immunoreactivity to free (met)enkephalin immunoreactivity in the perfusate was the same (approximately 2.7) during two successive periods of splanchnic nerve stimulation separated by 10 min. When release was evoked by increasing the K+ concentration to 50 mM-KCl, this ratio was increased more than twofold compared with that obtained by electrical stimulation of the splanchnic nerve. Analysis of the perfusate by gel filtration showed that, during splanchnic nerve stimulation, 47% of the total (met)enkephalin immunoreactivity eluted in fractions containing fragments of low molecular weight. When KCl was used as stimulus only 12% of total (met)enkephalin immunoreactivity eluted in these fractions. The results indicate that the nature of the released peptides depends on the type of stimulus used to evoke release.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1984

Long-term facilitation of peptidergic transmission by catecholamines in guinea-pig inferior mesenteric ganglia.

Intracellular recordings were obtained from neurones of isolated guinea-pig inferior mesenteric ganglia. Repetitive stimulation (10-20 Hz for 1-2 s) of the hypogastric nerves evoked, in addition to the fast excitatory post-synaptic potential (e.p.s.p.), a non-cholinergic e.p.s.p. the mediator of which has previously been suggested to be substance P or a related peptide. When applied to the ganglia in the concentrations of 1-100 microM for 3-5 min, adrenaline, isoprenaline and noradrenaline produced an initial, short-lasting depression which was followed by a marked augmentation of the non-cholinergic e.p.s.p. lasting from minutes to over hours. Employed in comparable concentrations dopamine caused a slight depression that was not followed by a detectable increase of the non-cholinergic e.p.s.p. The catecholamine-induced depression and subsequent enhancement of the non-cholinergic e.p.s.p. was prevented by alpha-adrenergic antagonists (dihydroergotamine and phenoxybenzamine, 1-10 microM) and beta-adrenergic antagonists (propranolol and dichlorisoprenaline, 5-10 microM), respectively. The membrane depolarization induced by the putative transmitter substance P (1 microM) was augmented by isoprenaline; the enhancement which could be blocked by beta-antagonists was not preceded by a depression. Application of dibutyryl cyclic AMP (10 microM-1 mM) by either superfusion or intracellular ionophoresis mimicked the enhancing effect of catecholamines. It is concluded that catecholamines, with the noticeable exception of dopamine, exerted a biphasic effect on the non-cholinergic e.p.s.p. of the inferior mesenteric ganglion cells: an initial depression that was mediated by alpha-adrenergic receptors and probably reflected a presynaptic inhibitory effect of catecholamines and, on the other hand, an enduring facilitation mediated by beta-adrenergic receptors which appeared to be linked to activation of post-ganglionic cyclic AMP.

Action Potentials↗
PubMed1995

Contribution of SK and BK channels in the control of catecholamine release by electrical stimulation of the cat adrenal gland.

1. Transmural electrical stimulation (10 Hz, 1 ms, 40 V for 10 s) of cat adrenal glands perfused at room temperature with Krebs-Hepes solution produced catecholamine secretory responses which were reproducible when stimulations were applied at 5 min intervals. Such responses were inhibited about 20% by atropine (1 microM) and 80% by hexamethonium (30 microM). Apamin (100 nM) increased the secretory response 2.5-fold in the presence of atropine and 8-fold in the presence of hexamethonium. 2. Potentiation by apamin of secretory responses evoked by 100-pulse trains was similar at 5, 10 and 20 Hz (about 2-fold). When glands were continuously stimulated at 3 Hz, apamin increased 4-fold the initial secretion plateau. Continuous stimulation at a higher frequency (20 Hz) produced a sharp secretory peak followed by a small, sustained plateau; apamin did not alter this plateau. Apamin also enhanced the secretory responses obtained with sustained stimulation with acetylcholine (10 or 200 microM). 3. Secretion peaks induced by brief acetylcholine pulses (10 microM for 10 s) applied to isolated and superfused cat adrenal chromaffin cells were enhanced more than 3-fold by 100 nM apamin. Charybdotoxin (10 nM) did not enhance these secretory peaks. 4. In perfused cat adrenal glands, charybdotoxin (10 nM) affected neither the secretion evoked by trains of electrical stimulation applied at different frequencies nor the secretion evoked by acetylcholine pulses. 5. In 0.5 mM [Ca2+]o, apamin enhanced 3-fold the secretion evoked by electrical stimulation trains of 100 pulses (10 Hz, 10 s) and almost 6-fold the acetylcholine (10 microM for 10 s)-induced secretion. In 5 mM Ca2+, apamin enhanced the secretory responses to electrical stimulation and acetylcholine 2- and 10-fold, respectively. Charybdotoxin enhanced 2.5-fold the secretory response to electrical stimulation in 0.5 mM Ca2+, although this effect was not statistically significant. A synergistic interaction between the two toxins on catecholamine release induced by electrical stimulation was observed at low but not at high [Ca2+]o. 6. Simultaneous release of acetylcholine and catecholamines upon electrical stimulation was achieved in glands in which the endogenous acetylcholine stores in the splanchnic nerve terminals had been prelabelled by perfusion with [3H]choline. While apamin enhanced more than 2-fold the postsynaptic release of catecholamines, the presynaptic release of acetylcholine remained unaffected. 7. The results are compatible with the hypothesis that, under physiological conditions, Ca(2+)-activated SK channels present in chromaffin cells control the firing patterns of action potentials induced by the acetylcholine released from splanchnic nerves during stress.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed2004

Etomidate elevates intracellular calcium levels and promotes catecholamine secretion in bovine chromaffin cells.

Etomidate, an intravenous imidazole general anaesthetic, is thought to produce anaesthesia by modulating or activating ionotropic Cl(-)-permeable GABA(A) receptors. Chromaffin cells are known to express functional GABA(A) receptors with properties similar to their neuronal counterparts. We have shown that activation of the GABA(A) receptors, with specific GABA(A) agonists, leads to cellular excitation. Our goal was to determine whether etomidate mimicked this response and to explore the functional consequences of this activation. Imaging experiments with the Ca(2+)-indicator dye fura-2 were used to assay [Ca(2+)](i). Bovine adrenal chromaffin cells were superfused with a variety of GABA(A)-selective drugs to determine their effects on [Ca(2+)](i). Amperometric measurements were used to assay catecholamine release in real-time. We show that bovine adrenal chromaffin cells were excited by etomidate at clinically relevant concentrations. Etomidate directly activated GABA(A) receptors found in chromaffin cells thereby elevating [Ca(2+)](i). The effects of etomidate were mimicked by the specific GABA(A) agonist muscimol and blocked by the specific antagonist bicuculline. Our data show that low concentrations of etomidate modulated GABA(A) receptor activation by muscimol. Blockade of voltage-dependent Ca(2+) channels prevented the elevation of [Ca(2+)](i) by GABA. Application of etomidate directly to the chromaffin cells elicited robust catecholamine secretion from these cells. The data indicate that clinically relevant concentrations of etomidate can directly activate GABA(A) receptors, which, due to the positive anion equilibrium potential, depolarizes chromaffin cells. This depolarization activates voltage-dependent Ca(2+) channels thereby stimulating catecholamine release. Our data suggest that circulating catecholamine levels may be elevated after etomidate application.

Animals↗
PubMed2002

Angiotensin I-converting enzyme inhibition increases cardiac catecholamine content and reduces monoamine oxidase activity via an angiotensin type 1 receptor-mediated mechanism.

Antihypertensive and cardioprotective effects of angiotensin I-converting enzyme (ACE) inhibitors are well established and have usually been attributed to the inhibition of angiotensin II (ANG)-mediated effects at vascular or ventricular (angiotensin type 1) AT(1) receptors. One other important mechanism involves ANG-induced interactions with the sympathetic nervous system, which might include alterations of cardiac catecholamine concentrations during ACE inhibition due to a modulation of monoamine oxidase (MAO) activity. Tissue catecholamines were studied in spontaneously hypertensive rats that were long-term treated with captopril (50 or 0.5 mg/kg/day), enalapril (10 or 0.1 mg/kg/day), an AT(1) receptor antagonist (candesartan-cilexetil, 3 mg/kg/day), or a calcium antagonist (mibefradil, 18 mg/kg/day). The kinetic parameters of MAO were then determined in vitro in the presence of ANG, captopril, enalaprilat, or candesartan. Noradrenaline and adrenaline contents were doubled in the left ventricle by captopril, enalapril, or candesartan independently of hypotensive potency but not in liver or cortex. In parallel, cardiac MAO activity was reduced by all doses of captopril (49/29%), enalapril (52/24%), or candesartan (38%). Mibefradil, which does not interact with the renin-angiotensin system, did not alter cardiac catecholamines or MAO activity when an equipotent antihypertensive dose was applied. In vitro MAO activity was not influenced by ANG, enalaprilat, or captopril at concentrations of up to 1 mM. It is concluded that diminished AT(1) receptor stimulation decreases cardiac MAO activity, probably by regulating MAO expression, since ANG, ACE inhibitors, and AT(1) antagonists had no effect on MAO activity in vitro. This action contributes to an increase in cardiac catecholamine content that may improve cardiac sympathetic control during therapy.

Angiotensin II↗
PubMed2002

Chromaffin cell catecholamine secretion: bisindolylmaleimide compounds exhibit novel and potent antagonist effects at the nicotinic cholinergic receptor in pheochromocytoma cells.

Activation of protein kinase C (PKC) stimulates nicotine-induced catecholamine secretion. PKC down-regulation by prolonged pretreatment with phorbol 12-myristate 13-acetate diminished nicotine-induced catecholamine secretion only slightly (approximately 16%), suggesting substantial PKC independence of nicotinic receptor activation. However, we found that bisindolylmaleimide compounds (which are also putative PKC chemical inhibitors) dramatically inhibited nicotine-induced catecholamine secretion (IC(50) values of approximately 24-37 nM). This inhibition was specific for the nicotinic cholinergic receptor. Catecholamine secretion induced by other nicotinic agonists (such as epibatidine, anatoxin, or cytisine) was also powerfully antagonized by bisindolylmaleimide II (IC(50) values of approximately 60-90 nM). Even high-dose nicotinic agonists failed to overcome the inhibition by bisindolylmaleimide II, suggesting noncompetitive nicotinic antagonism by this class of compounds. Nicotinic inhibition by bisindolylmaleimide seemed not to be readily reversible. Structure-activity studies of bisindolylmaleimide compounds revealed that bisindolylmaleimides I through III are the most potent nicotinic antagonists at the nicotinic cholinergic receptor in PC-12 cells (IC(50) < or =37 nM), whereas bisindolylmaleimide IV and V have far less nicotinic antagonist activity (IC(50) >1 microM); the active compounds I through III have cationic tails at an indole nitrogen, whereas the least potent compounds IV and V do not. By contrast, a free NH within the maleimide ring is crucial for PKC inhibition by this class of compounds. We conclude that bisindolylmaleimides I through III are some of the most potent noncompetitive neuronal nicotinic antagonists, indeed the most potent such antagonists we have observed in PC-12 cells. Nicotinic antagonism of these compounds seems to be independent of PKC inhibition.

Animals↗
PubMed1997

Utilization of iron-catecholamine complexes involving ferric reductase activity in Listeria monocytogenes.

Listeria monocytogenes is a ubiquitous potentially pathogenic organism requiring iron for growth and virulence. Although it does not produce siderophores, L. monocytogenes is able to obtain iron by using either exogenous siderophores produced by various microorganisms or natural catechol compounds widespread in the environment. In the presence of tropolone, an iron-chelating agent, growth of L. monocytogenes is completely inhibited. However, the growth inhibition can be relieved by the addition of dopamine or norepinephrine under their different isomeric forms, while the catecholamine derivatives 4-hydroxy-3-methoxyphenylglycol and normetanephrine did not relieve the inhibitory effect of tropolone. Preincubation of L. monocytogenes with chlorpromazine and yohimbine did not antagonize the growth-promoting effect of catecholamines in iron-complexed medium. In addition, norepinephrine stimulated the growth-promoting effect induced by human transferrin in iron-limited medium. Furthermore, dopamine and norepinephrine allowed 55Fe uptake by iron-deprived bacterial cells. The uptake of iron was energy dependent, as indicated by inhibition of 55Fe uptake at 0 degrees C as well as by preincubating the bacteria with KCN. Inhibition of 55Fe uptake by L. monocytogenes was also observed in the presence of Pt(II). Moreover, when assessed by a whole-cell ferric reductase assay, reductase activity of L. monocytogenes was inhibited by Pt(II). These data demonstrate that dopamine and norepinephrine can function as siderophore-like compounds in L. monocytogenes owing to their ortho-diphenol function and that catecholamine-mediated iron acquisition does not involve specific catecholamine receptors but acts through a cell-bound ferrireductase activity.

Catecholamines↗
PubMed1983

Catecholamine surge and lung function after delivery.

Lung function was measured at 30 minutes and again at 2 hours after birth in 12 infants delivered vaginally, in 15 infants delivered by elective caesarean section under general anaesthesia (GA), and in 15 delivered under epidural anesthesia (EDA). Umbilical arterial blood was analysed for pH and for concentrations of catecholamines and cortisol. No important differences in gestational age, birthweight, Apgar scores, or haematocrit were found among the three groups. Tidal volume and minute ventilation measured 30 minutes after birth were lower in infants delivered by caesarean section than in those delivered vaginally and at 2 hours the tidal volume was still lower in the babies delivered by caesarean section than in those delivered vaginally. Dynamic compliance was lower at 30 minutes in the group that had a caesarean section than in the vaginal group, and this difference was significant at two hours. Tidal volume, minute ventilation, and dynamic compliance in the GA and EDA groups did not differ. The catecholamine and cortisol concentrations at birth were higher in the vaginal group than in the group delivered by caesarean section. Two hours after birth there was a significant correlation (r = 0.84) between the catecholamine concentrations of the infants born vaginally and lung compliance. The lower dynamic lung compliance in infants delivered by elective caesarean section might be explained by delayed absorption of liquid in the lung due to lack of catecholamine surge.

Anesthesia, Epidural↗
PubMed1993

Heart rate variability and circulating catecholamine concentrations during steady state exercise in healthy volunteers.

OBJECTIVES: To assess whether exercise induced suppression of heart rate variability in the low frequency domain (0.06-0.15 Hz) is related to the increase in circulating catecholamine concentrations. DESIGN: Randomised crossover trial of three exercise tests characterised by different workloads. Pharmacological simulation of exercise-induced changes in vagal and sympathetic activity. PARTICIPANTS: Six healthy men with a mean age of 31.2 (SD 3.0) years. INTERVENTIONS: Three different workloads of steady state cycling ergometry: control state without cycling, cycling at a target heart rate of 100 beats/min, and cycling at a target heart rate of 150 beats/min. Intravenous infusion of atropine (target heart rate 100 beats/min) followed by the additional infusion of adrenaline and noradrenaline. MAIN OUTCOME MEASURES: Fast Fourier analysis of heart rate variability; blood pressure; and venous plasma concentrations of lactate, adrenaline, and noradrenaline. RESULTS: During the control exercise period there were no changes in the assessed variables compared with the preceding resting period. During exercise at a heart rate of 100 beats/min systolic blood pressure increased and heart rate variability decreased. During exercise at a heart rate of 150 beats/min systolic blood pressure and lactate, adrenaline, and noradrenaline concentrations increased. In addition, low frequency (LF) was lower than during exercise at 100 beats/min, high frequency (HF 0.15-0.80 Hz) resembled that during exercise at 100 beats/min, and diastolic blood pressure was reduced. Infusion of atropine caused no changes in blood pressure or plasma concentrations of lactate, adrenaline, and noradrenaline and decreased heart rate variability. The additional infusion of adrenaline and noradrenaline completely suppressed heart rate variability and increased blood pressure. CONCLUSIONS: The reduction in LF and HF during exercise at a heart rate of 100 beats/min, which is not characterised by increased plasma catecholamine concentrations, and during atropine infusion suggests that heart rate variability in the supine state is largely influenced by vagal activity. The additional reduction in LF during exercise at 150 beats/min and during catecholamine infusion may reflect a negative feedback of circulating catecholamines on the sympathetic control of heart rate.

Adult↗
PubMed1966

Diagnostic value of detailed metabolic pathway investigations in two cases of phaeochromocytoma with minimal increase in total catecholamine output.

Two patients with phaeochromocytoma having atypical biochemical features are described. Total catecholamine excretion was normal in one and only slightly raised in the other; both had a diagnostic rise in output of metadrenaline and 4-hydroxy-3-methoxymandelic acid whilst 4-hydroxy-3-methoxyphenylglycol excretion was increased in one of them. During hypertensive attacks adrenaline excretion became greater than that of noradrenaline. The diagnostic usefulness of separate adrenaline and noradrenaline estimations in addition to catecholamine metabolite assay is discussed. A lack of relationship between tumour catecholamine content and urinary catecholamine output is emphasized.

Catecholamines↗
PubMed2004

Urinary catecholamines and metabolites in the immediate postoperative period following major surgery.

BACKGROUND: Induction of anaesthesia can precipitate catecholamine release from an undiscovered pheochromocytoma and induce a hypertensive crisis. However, it is assumed that catecholamine and metabolite values resulting from the effects of surgery per se in the early postoperative period would overlap with the values generated by a tumour, and it is not known how soon after biochemical investigations can be carried out. AIM: To study patterns of urinary catecholamine excretion and the feasibility of biochemical screening for phaeochromocytomas in the immediate postoperative period in otherwise healthy subjects undergoing a single type of major surgical procedure. METHODS: Catecholamines and metabolites were measured for each mole of creatinine in single voided urine on one preoperative and four postoperative days in five subjects who underwent elective coronary artery bypass graft surgery with an uncomplicated postoperative course. Reference ranges were established from 33 healthy normotensive volunteers. RESULTS: Excretion of adrenaline, noradrenaline, dopamine, vanillylmandelic acid, and metadrenaline was within normal limits. Normetadrenaline excretion was mildly raised in four patients, but did not exceed 1.5 times the upper reference limit, and returned to normality by the fourth postoperative day. CONCLUSION: It is feasible to perform simple urinary screening for possible phaeochromocytoma in the immediate postoperative period.

Adrenal Gland Neoplasms↗
PubMed1975

Catecholamine-ouabain interaction on the isolated perfused rat heart.

The effect of catecholamine-depleting pretreatments, reserpine, and 6-hydroxydopamine (6-OH-DA) on left ventricular pressure (LVP) and the inotropic response to graded doses of ouabain (up to 300 mug/0.05 ml) was studied in isolated perfused rat and guinea-pig hearts. In rats, reserpine and 6-OH-DA depleted the cardiac content of catecholamine, but did not increase initial LVP and did not reduce the inotropic response to the highest dose of ouabain. It is concluded that in isolated rat hearts, these catecholamine-depleting pretreatments nearly abolish the inotropic response to ouabain, and this effect appears to be mediated mainly through an increase in initial LVP. The reason why catecholamine depletion failed to increase initial LVP in guinea pigs remains unexplained.

Animals↗