The purpose of this study was to review potential, physiological, hormonal and neuronal mechanisms that may mediate the sleep changes. This paper investigates the literatures regarding the activity of the hypothalamic-pituitary-adrenal (HPA) axis, one of the main neuroendocrine stress systems during sleep in order to identify relations between stress and sleep disorder and the treatment of stress-induced insomnia. Sleep and wakefulness are regulated by the aminergic, cholinergic brainstem and hypothalamic systems. Activation of the HPA and/or the sympathetic nervous systems results in wakefulness and these hormones including corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), cortisol or corticosterone, noradrenaline, and adrenaline, are associated with attention and arousal. Stress-related insomnia leads to a vicious circle by activating the HPA system. An awareness of the close interaction between sleep and stress systems is emerging and the hypothalamus is now recognized as a key center for sleep regulation, with hypothalamic neurontransmitter systems providing the framework for therapeutic advances. An updated understanding of these systems may allow researchers to elucidate neural mechanisms of sleep disorder and to develop effective intervention for sleep disorder.

OBJECTIVE

β-Adrenoceptors are expressed in human and experimental animal breast cancer cells. However, the effect of the agonists and antagonists reported on cell proliferation and tumour growth was paradoxical, precluding their utilization as possible adjuvant therapy, mainly in the cases of refractory tumours.

METHODS

β-Adrenoceptor expression was analysed by immunofluorescence and RT-PCR. Cell proliferation was assessed by [(3) H]-thymidine incorporation, tumour growth by measuring with a calliper and ERK 1/2 phosphorylation by Western blotting.

RESULTS

β(2) -Adrenoceptor expression was confirmed in the mouse and human cells tested. Cell proliferation was increased by adrenaline (by α(2) -adrenoceptor action) and decreased in every tested cell line by the β-adrenoceptor agonist isoprenaline and the β(2) -adrenoceptor agonist salbutamol. Isoprenaline and salbutamol reduced tumour growth in every tumour tested (mouse C4-HD and CC4-3-HI and human IBH-4, IBH-6 and MDA-MB-231 cell lines growing as xenografts in nude mice). These effects were reversed by the β-adrenoceptor antagonist propranolol. The α(2) -adrenoceptor antagonist rauwolscine and the β(2) -adrenoceptor agonist salbutamol were equally effective in diminishing tumour growth. ERK 1/2 activation analysed in IBH-4 tumours correlated with tumour growth, with the β-adrenoceptor agonists decreasing its activation. Inhibition of ERK 1/2 phosphorylation in vitro was mainly mediated by the PKA pathway.

CONCLUSIONS

In our experimental models, the β-adrenoceptor agonists inhibited breast cancer cell proliferation and tumour growth, probably mediated by inhibition of ERK 1/2 phosphorylation. The β-adrenoceptor agonists were as effective as the α(2) -adrenoceptor antagonist rauwolscine, providing possible novel adjuvant treatments for breast cancer.

1. Congestive heart failure was induced in dogs by rapid pacemaker stimulation of the heart (240-280/min) for 14 days. This represents a model of low output heart failure which permits the study of the development and reversal of congestive heart failure in an anatomically intact circulation in the unanaesthetized animal. 2. Cardiac output was reduced by 54%. Pulmonary artery pressure gradually increased by a factor of 2.4 and pulmonary capillary pressure rose to 4.6 times basal values. The animals retained a mean of 1.1 litres of fluid. 3. At the same time there was a gradual increase of plasma levels of renin, angiotension II, aldosterone, noradrenaline and adrenaline. After the pacemaker stimulation was discontinued all hormone levels returned to normal, the retained fluid was excreted, and intracardiac pressures and cardiac output returned to baseline values. 4. When heart failure was established at the end of the pacemaker stimulation period an inappropriately high secretion of antidiuretic hormone in relation to plasma osmolality was observed in five of six dogs. 5. It is concluded that beside the well-known non-hormonal renal factors, these hormone systems may be involved in the formation of oedema in congestive heart failure. The inappropriately high levels of antidiuretic hormone may cause hyponatraemia by water retention, representing a state of 'dilutional hypo-osmolality'.

The efflux of radioactivity after loading with trace amounts of tritiated 5-hydroxytryptamine ([3H]5-HT) or 5-hydroxytryptophan ([3H]5-HTP) was studied in perifused beta-cell-rich pancreatic islets from ob/ob mice. Analysis of the effluent revealed that more than 90% of the radioactivity was released as [3H]5-HT after loading with [3H]5-HTP. Increasing the concentration of glucose in the perifusion medium from 3 to 20 mmol/l enhanced the efflux when islets from fed mice were used and this effect was potentiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). Whereas 20 mM-glucose alone did not stimulate the efflux of 5-HT from islets isolated from mice starved for 3 days, a stimulatory effect was observed in the presence of IBMX. Stimulation of the efflux of radioactivity by glucose was inhibited if calcium was omitted from or adrenaline added to the medium. The results are consistent with the concept of exocytotic release of 5-HT occurring in response to stimulation of insulin secretion, although basal non-exocytotic transport must also be occurring across the beta-cell membrane.

Adrenaline inhibits insulin secretion via pertussis toxin-sensitive mechanisms. Since voltage-dependent Ca2+ currents play a key role in insulin secretion, we examined whether adrenaline modulates voltage-dependent Ca2+ currents of the rat insulinoma cell line, RINm5F. In the whole-cell configuration of the patch-clamp technique, dihydropyridine- but not omega-conotoxin-sensitive Ca2+ currents were identified. Adrenaline via alpha 2-adrenoceptors inhibited the Ca2+ currents by about 50%. Somatostatin which also inhibits insulin secretion was less efficient (inhibition by 20%). The hormonal inhibition of Ca2+ currents was not affected by intracellularly applied cAMP but blocked by the intracellularly applied GDP analog guanosine 5'-O-(2-thiodiphosphate) and by pretreatment of cells with pertussis toxin. In contrast to adrenaline and somatostatin, galanin, another inhibitor of insulin secretion, reduced Ca2+ currents by about 40% in a pertussis toxin-insensitive manner. Immunoblot experiments performed with antibodies generated against synthetic peptides revealed that membranes of RINm5F cells possess four pertussis toxin-sensitive G-proteins including Gi1, Gi2, Go2, and another Go subtype, most likely representing Go1. In membranes of control but not of pertussis toxin-treated cells, adrenaline via alpha 2-adrenoceptors stimulated incorporation of the photo-reactive GTP analog [alpha-32P]GTP azidoanilide into pertussis toxin substrates comigrating with the alpha-subunits of Gi2, Go2, and the not further identified Go subtype. The present findings indicate that activated alpha 2-adrenoceptors of RINm5F cells interact with multiple G-proteins, i.e. two forms of Go and with Gi2. These G-proteins are likely to be involved in the adrenaline-induced inhibition of dihydropyridine-sensitive Ca2+ currents and in other signal transduction pathways contributing to the adrenaline-induced inhibition of insulin secretion.

Patients, when admitted to an intensive care unit (ICU), have one thing in common: their illness is life-threatening. Patients may remain on ICU in a critical condition, needing support with their breathing, circulation, and/or kidneys for varying lengths of time, from days to weeks. During that time the patients will receive sedative and analgesic drugs to ensure compliance with artificial ventilation. Patients recovering from critical illness frequently have little or no recall of their period in ICU, or remember nightmare, hallucinations, or paranoid delusions. The nature, extent and reason for these difficulties, have been under-reported and consequently our purpose was to conduct a review of memory problems experienced by ICU patients. A systematic literature review of computer databases (Medline, PsycLit, and CINAHL) identified 25 relevant papers. In addition, other relevant articles were obtained, citation lists and associated articles retrieved. Due to lack of research on processes underlying memory problems in ICU patients all articles that introduced an insight into possible mechanisms were included in the review. There seem to be two possible processes contributing to memory problems in ICU patients. First the illness and treatment may have a general dampening effect on memory. Delirium and sleep disturbance are both common in ICU patients. Delirium can result in a profound amnesia for the period of confusion. Sleep deprivation exacerbates the confusional state. Slow wave sleep is important for the consolidation of episodic memories. Treatment administered to patients in ICU can have effects on memory. Opiates, benzodiazepines, sedative drugs such as propofol, adrenaline, and corticosteroids can all influence memory. In addition, the withdrawal of drugs, such as benzodiazepines, can cause profound withdrawal reactions, which may contribute to delirium. Second, we hypothesise that there is a process that affects memory negatively for external events but enhances memory for internal events. The physical constraints and social isolation experienced by ICU patients and the life-threatening nature of the illness may increase the experience of hypnagogic hallucinations. Attentional shift during hypnagogic images from external stimuli to internally generated images would explain why ICU patients have such poor recall of external ICU events, but can clearly remember hallucinations and nightmares. Patients describe these memories as being very vivid and this is explored in terms of flashbulb memory formation. The absence of memories for real events on ICU can result in ICU patients remembering paranoid delusions of staff trying to kill them, with little information to reject these vivid memories as unreal. This has implications for patients' future psychological health.

Total respiratory resistance was measured before and after nebulised phenylephrine in 5 babies (age range 7 to 17 months) with wheezy bronchitis, and in 2 babies (aged 2 and 6 months) with bronchiolitis. None showed a change in resistance after treatment. Total respiratory resistance was measured before and after nebulised adrenaline in another 14 babies (age range 4 to 13 months) with bronchiolitis. No fall in resistance was noted in any baby after treatment whether or not it was given by a conventional or an ultrasonic nebuliser. We conclude that alpha- and beta-adrenergic stimulants are ineffective in bronchiolitis and wheezy bronchitis in children under 18 months of age.

1. Intracellular recordings were obtained from the arterial smooth muscle cells of rat basilar artery during perivascular nerve stimulation and during the application of adrenoceptor agonists and antagonists. 2. Perivascular nerve stimulation evoked excitatory junction potentials. Increased stimulation resulted in action potentials which were associated with arterial constriction. 3. Bath-applied noradrenaline did not cause constriction but at high concentrations caused membrane depolarization. The depolarization caused by a given dose of noradrenaline was larger in the presence of cocaine. 4. Neither the depolarizations obtained by nerve stimulation nor those obtained by bath-applied noradrenaline were blocked by adrenoceptor blocking agents. 5. Unlike alpha-receptors, the receptors on the rat basilar artery were activated equally well by dopamine, adrenaline, and both optical isomers of noradrenaline. 6. Excitatory junction potentials could be obtained in the presence of high bath concentrations of noradrenaline.

1. Experiments measuring the rate of oxygen consumption of unanaesthetized new-born rabbits and the blood flow in brown adipose tissue of anaesthetized new-born rabbits are described.2. The increase in rate of oxygen consumption caused by I.V. infusion of noradrenaline, adrenaline and isoprenaline (2 mug/kg.min for 10 min) was blocked by propranalol (I.V. 1 mg/kg) but the increase caused by cold exposure was not. A larger dose of propranalol (5 mg) blocked the calorigenic response to cold exposure as well.3. Infusion of glucagon (I.V. 4 mug/kg.min for 10 min) caused a large increase in the rate of the rabbit's oxygen consumption and in blood flow through its brown adipose tissue. These responses, which reached a maximum within 10 min from the start of the infusion, were not blocked by propranalol (1 or 5 mg/kg).4. Infusion of corticotrophin (I.V. 1 i.u./kg.min for 10 min) also caused a large increase in the rate of oxygen consumption of new-born rabbits. The response reached a maximum about 20 min from the start of the infusion and it was not blocked by propranalol (5 mg/kg).5. These results support the conclusion that noradrenaline is released at sympathetic endings in brown adipose tissue and that the increase in blood flow caused by noradrenaline is secondary to its metabolic action on the tissue. They also suggest the possibility that glucagon and corticotrophin may act directly on brown adipose tissue and stimulate heat production during cold exposure.

Single bovine ventricular myocytes were superfused with Tyrode solution containing 1.8 mM CaCl2. The cells did not bear external load and contracted isotonically. Contraction and relaxation were characterized by the shortening and relengthening of the sarcomeres which resembled in their time course the isometric twitches of bovine papillary muscles. Resemblance was also found in regard to positive inotropic interventions as increase in the stimulation frequency, exposure to elevated [Ca]0 or to adrenaline. A two-microelectrode voltage-clamp technique was applied to the single myocyte. The transmembrane Ca inward current ICa was defined as difference current sensitive to 5 mM Ni or to 2 microM D600. During a voltage step from -45 to +5 mV, ICa peaked within 3 ms to -6 nA, afterwards it decayed to 15% of peak amplitude (incomplete inactivation with a 2 exponential time course). Experiments in Na-free media suggested that Na entry does not significantly contaminate ICa. Therefore, Ca entry could be calculated from ICa. The increment in total intracellular Ca concentration (delta[Ca]Ti) was estimated by referring Ca entry to the cell volume (50 pl). Within 100 ms delta[Ca]Ti came to 25 microM at control conditions, to 55 microM at [Ca]0 = 3.6 mM and to 88 microM when 0.1 microM adrenaline were present. The delta[Ca]Ti values were sufficient to activate contraction without the necessity of Ca-release from SR. Despite the new data, the relationship between Ca entry and activation of contraction was complex: during the "positive Herztreppe" ICa slightly attenuated but contractility doubled. Therefore, the old EC-model (M. Morad and Y. Goldman, Progr. Biophys. Mol. Biol. 27, 257 (1973)) was adapted. The Ca-entry's capability to load and to overload the intracellular Ca store (SR) is discussed.

(1) The effects of changes in the intramitochondrial volume, benzyl alcohol treatment and calcium-induced mitochondrial aging on the behaviour of liver mitochondria from control and glucagon-treated rats are reported. (2) The stimulatory effects of glucagon on mitochondrial respiration, pyruvate metabolism and citrulline synthesis could be mimicked by hypo-osmotic treatment of control mitochondria and reversed by calcium-induced aging of mitochondria or by treatment with 20 mM benzyl alcohol. Hypo-osmotic treatment increased the matrix volume whilst aging but not benzyl alcohol decreased this parameter. (3) Liver mitochondria from glucagon and adrenaline-treated rats were shown to be less susceptible to damage by exposure to calcium than control mitochondria and frequently showed slightly (15%) elevated intramitochondrial volumes. (4) Aging, benzyl alcohol and hypo-osmotic media increased the susceptibility of mitochondria to damage caused by exposure to calcium. (5) Glucagon-treated mitochondria were less leaky to adenine nucleotides than control mitochondria. (6) These results suggest that glucagon may exert its action on a wide variety of mitochondrial parameters through a change in the disposition of the inner mitochondrial membrane, possibly by stabilisation against endogenous phospholipase A2 activity. This effect may be mimicked by an increase in the matrix volume or reversed by calcium-dependent mitochondrial aging.

1. In the unanaesthetized cat, an injection of 0.75 mg of morphine into a lateral cerebral ventricle produced strong hyperglycaemia; on intravenous injection, 10 to 30 times larger doses were required. Other effects produced with both injections were shivering, pupillary dilatation, opening of the eyes, miaowing, periods of excitation, and analgesia. Between the periods of excitation the cat did not react to objects moving in front of its eyes and it had a vacant stare.2. Noradrenaline, adrenaline, and 5-hydroxytryptamine (5-HT) injected intraventricularly (250 mug, twice) depressed the hyperglycaemia due to intraventricular morphine, and noradrenaline also depressed the hyperglycaemia due to intravenous morphine. Adrenaline produced the strongest and 5-HT the weakest depression. 5-HT did not depress the other effects of morphine, but the catecholamines depressed most of them; only analgesia and the vacant stare appeared to be unaffected.3. Reserpine injected intraventricularly (0.5 mg, twice) greatly accentuated the hyperglycaemia as well as the other effects produced by intraventricular morphine, but pupillary dilatation and opening of the eyes no longer occurred; the protrusion of the nictitating membranes produced by the reserpine persisted.4. Pentobarbitone sodium injected intraperitoneally in an anaesthetizing dose practically abolished the morphine hyperglycaemia, but injected intraventricularly in a dose of a few milligrammes, it had a two fold effect: depression followed by enhancement of the morphine hyperglycaemia. The enhancement may be due to sensitization of the effect of the adrenaline released by morphine, since adrenaline hyperglycaemia was enhanced as well.5. Morphine did not seem to act on structures in the walls of either the lateral or third ventricle when producing its hyperglycaemic effect on intraventricular injection. The action may therefore be on more caudally situated parts of the neuro-axis, on the central grey, on structures in the floor of the fourth ventricle or of the lateral recesses, or even on structures near the ventral surface of the brain stem.

1. Right adrenal and various cardiovascular responses to stimulation of the peripheral end of the right splanchnic nerve have been investigated in the presence and absence of exogenous adrenocorticotrophin, ACTH1-24, (5 ng min-1 kg-1). The adrenal-clamp technique was employed in conscious calves in which the pituitary stalk had been cauterized 3-4 days previously. 2. The I.V. infusion of ACTH1-24 increased mean plasma ACTH concentration by about 1200 pg/ml and mean right adrenal cortisol output by about 500 ng min-1 kg-1. Stimulation of the peripheral end of the right splanchnic nerve at 4 Hz for 10 min produced a further rise in cortisol output, amounting to about 400 ng min-1 kg-1 (P less than 0.01). These changes in output were reflected accurately by changes in peripheral plasma cortisol concentration. 3. Closely similar amounts of adrenaline were released in response to splanchnic nerve stimulation in the presence and absence of exogenous ACTH. In the presence of ACTH the average mean output of noradrenaline (58 +/- 2 ng min-1 kg-1) was significantly less than that of adrenaline (102 +/- 4 ng min-1 kg-1; P less than 0.001), whereas the corresponding values were not significantly different in the absence of ACTH. 4. These results also confirm the fact that the fall in adrenal vascular resistance which occurs during splanchnic nerve stimulation is substantially reduced by ACTH, as is the rise in met5-enkephalin output. 5. It is concluded that the splanchnic innervation is capable of enhancing the secretion of adrenal glucocorticoids in response to ACTH under physiological conditions in the conscious calf.

Venous plasma levels of neuropeptide Y-like immunoreactivity (with chromatographic properties of synthetic neuropeptide Y) increased in parallel with catecholamines, heart rate and blood pressure during graded physical exercise in man. The plasma levels of neuropeptide Y correlated better with the levels of noradrenaline than adrenaline, suggesting release of a neural origin. Taken together with previous results, this suggests that neuropeptide Y is released together with noradrenaline upon sympathetic activation during physiological conditions in man. Determinations of plasma neuropeptide Y may therefore be valuable in the assessment of sympathetic nerve activity.

1. Changes in forearm blood flow to intra-arterial infusion of isoprenaline and the chronotropic response to intravenous boluses of isoprenaline were measured in 15 healthy volunteer subjects, eight younger than 25 years and seven older than 50 years. Intra-arterial blood pressure and basal plasma renin activity, adrenaline and noradrenaline were also measured. 2. Young subjects exhibited a greater increase in forearm blood flow than old subjects, to all four doses of isoprenaline used, a greater cardiac isoprenaline responsiveness (measured by the increase in heart rate; P less than 0.001) and a higher renin (P less than 0.02). 3. Resting values of blood pressure, forearm blood flow, adrenaline and noradrenaline were not significantly different in young and old subjects. In the latter, noradrenaline correlated with forearm blood flow (r = -0.77, P less than 0.05), forearm vascular resistance (r = 0.86, P less than 0.02) and mean arterial pressure (r = 0.83, P less than 0.02), whereas in the younger subjects forearm blood flow was related to adrenaline (r = 0.78, P less than 0.05). 4. These data provide evidence for an age-related parallel reduction in cardiac, peripheral vascular and renal beta-adrenoceptor-mediated responses.

OBJECTIVE

To test the relation between socioeconomic status (SES) and biomarkers of chronic stress, including basal cortisol, and to test whether these biomarkers account for the relation between SES and health outcomes.

METHODS

Cross sectional study using data from the 2000 social and environmental biomarkers of aging study (SEBAS).

METHODS

Taiwan.

METHODS

Nationally representative sample of 972 men and women aged 54 and older.

METHODS

Highest risk quartiles for 13 biomarkers representing functioning of the neuroendocrine system, immune/inflammatory systems, and the cardiovascular system: cortisol, adrenaline (epinephrine), noradrenaline (norepinephrine), serum dihydroepiandrosterone sulphate (DHEA-S), insulin-like growth factor 1 (IGF1), interleukin 6 (IL6), albumin, systolic blood pressure, diastolic blood pressure, waist-hip ratio, total cholesterol-HDL ratio, HDL cholesterol, and glycosylated haemoglobin; self reported health status (1-5) and self reported mobility difficulties (0-6).

RESULTS

Lower SES men have greater odds of falling into the highest risk quartile for only 2 of 13 biomarkers, and show a lower risk for 3 of the 13 biomarkers, with no association between SES and cortisol. Lower SES women have a higher risk for many of the cardiovascular risk factors, but a lower risk for increased basal readings of adrenaline, noradrenaline, and cortisol. Inclusion of all 13 biological markers does not explain the relation between SES and health outcomes in the sample.

CONCLUSIONS

These data do not support the hypothesis that chronic stress, via sustained activation of stress related autonomic and neuroendocrine responses, is an important mediator in the relation between SES and health outcomes. Most notably, lower SES is not associated with higher basal levels of cortisol in either men or women. These results place an increased burden of proof on researchers who assert that psychosocial stress is an important pathway linking SES and health.

We have studied three afibrinogenemic patients, who had only trace amounts of plasma and platelet fibrinogen as measured by radioimmunoassay, and demonstrate here that the residual aggregation observed in their platelet-rich plasma is dependent upon von Willebrand factor (vWF) binding to the platelet membrane glycoprotein (GP)IIb/IIIa complex. The abnormality of aggregation was more pronounced when ADP, rather than thrombin, collagen, or the combination of ADP plus adrenaline was used to stimulate platelets. With all stimuli, nevertheless, the platelet response was completely inhibited by a monoclonal antibody (LJP5) that is known to block vWF, but not fibrinogen binding to GPIIb/IIIa. Addition of purified vWF to the afibrinogenemic plasma resulted in marked increase in the rate and extent of aggregation, particularly when platelets were stimulated with ADP. This response was also completely blocked by LJP5. Addition of fibrinogen, however, restored normal aggregation even in the presence of LJP5, a finding consistent with the knowledge that antibody LJP5 has no effect on platelet aggregation mediated by fibrinogen binding to GPIIb/IIIa. Two patients gave their informed consent to receiving infusion of 1-desamino-8-D-arginine vasopressin (DDAVP), a vasopressin analogue known to raise the vWF levels in plasma by two- to fourfold. The bleeding time, measured before and 45 min after infusion, shortened from greater than 24 min to 12 min and 50 s in one patient and from 16 min to 9 min and 30 s in the other. Concurrently, the rate and extent of ADP-induced platelet aggregation improved after DDAVP infusion. The pattern, however, reversed to baseline levels within 4 h. The concentration of plasma vWF increased after DDAVP infusion, but that of fibrinogen remained at trace levels. We conclude that vWF interaction with GPIIb/IIIa mediates platelet-platelet interaction and may play a role in primary hemostasis.

Previous observations have shown that the effects of sympathetic stimulation and of tyramine were absent in the organs of animals treated with reserpine, but that they were restored by an infusion of noradrenaline. Observations are described showing that an infusion of adrenaline did not restore the pressor action of tyramine in the cat or in the rat, but that in the rat the pressor action was restored by an infusion of dopamine, or of (-)-dopa, or of m-tyrosine,or of phenylalanine. Observations are also described showing that the effect of postganglionic stimulation of the fibres to the nictitating membrane and to the iris was restored by an infusion of dopamine or of (-)-dopa; it was restored less well by an infusion of noradrenaline. An infusion of noradrenaline did not restore the action of tyramine on the denervated iris or on the denervated vessels of the cat's foreleg. An infusion of noradrenaline appeared to increase the effect of sympathetic stimulation of the hypogastric nerves to the uterus of the virgin cat about as much as an infusion of adrenaline. An infusion of noradrenaline restored the constrictor action of nicotine on the perfused vessels of the rabbit ear.

The primary aims of this paper were to examine the effect of heat stress on working memory, choice reaction time and mood state, and to investigate the relationship between heat induced changes in plasma concentrations of selected neurotransmitters and hormones, and cognition. Heat stress resulted in a deterioration of performance on a central executive task (random movement generation) but not on verbal and spatial recall, and choice reaction time tasks. Perceptions of vigour decreased and fatigue increased following exposure to heat stress. Plasma concentrations of cortisol and 5-hydroxytryptamine significantly increased following exposure to heat. Regression analyses showed that percent body mass loss and change from baseline (Delta) concentrations of cortisol, post-exposure to heat, were significant predictors of Delta random movement generation and Delta fatigue. A secondary purpose was to examine the effect of recovery on cognition and mood. Following recovery, the performance of the central executive task was poorer than pre-treatment. Mood states, catecholamines and 5-hydroxytryptamine concentrations returned to pre-treatment values, but cortisol fell to a level significantly lower. Regression correlations showed that Delta adrenaline and Delta scores, post-recovery, on the central executive task were significantly correlated. Delta noradrenaline correlated significantly with Delta fatigue. It was concluded that heat stress results in deterioration in the performance of central executive tasks and perceptions of mood state, and that this can be predicted by changes in body mass loss and plasma concentrations of the hormones cortisol and adrenaline.

BACKGROUND

Analysis of primary healthcare datasets offers the possibility to increase understanding of the epidemiology of acute uncommon conditions such as anaphylaxis, but these datasets remain under-exploited.

OBJECTIVE

To investigate recent trends in the recorded incidence, lifetime prevalence and prescribing of adrenaline for anaphylaxis in England.

METHODS

QRESEARCH is one of the world's largest national aggregated health databases containing the records of over nine million patients. We extracted data on all patients with a recorded diagnosis of anaphylaxis and calculated annual age-sex standardized incidence and lifetime period prevalence rates for each year from 2001-2005. We also analysed trends in adrenaline prescribing in those with a recorded diagnosis of anaphylaxis. National population figures were used to estimate numbers of people in England that have experienced anaphylaxis at some point in their lives.

RESULTS

The age-sex standardized incidence of anaphylaxis was 6.7 per 100,000 person-years in 2001 and increased by 19% to 7.9 in 2005. Lifetime age-sex standardized prevalence of a recorded diagnosis of anaphylaxis was 50.0 per 100,000 in 2001 and increased by 51% to 75.5 in 2005. Prescribing of adrenaline increased by 97% over this period. By the end of 2005 there were an estimated 37,800 people that had experienced anaphylaxis at some point in their lives.

CONCLUSIONS

Recorded incidence, lifetime prevalence and prescribing of adrenaline for anaphylaxis all showed substantial increases in recent years. An estimated 1 in 1,333 of the English population have at some point in their lives experienced anaphylaxis.