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Query: UMLS:C0037315 (sleep apnea)
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About 1.5 million Australians are shift workers. Shift work is associated with adverse health, safety and performance outcomes. Circadian rhythm misalignment, inadequate and poor-quality sleep, and sleep disorders such as sleep apnoea, insomnia and shift work disorder (excessive sleepiness and/or insomnia temporally associated with the work schedule) contribute to these associations. Falling asleep at work at least once a week occurs in 32%-36% of shift workers. Risk of occupational accidents is at least 60% higher for non-day shift workers. Shift workers also have higher rates of cardiometabolic diseases and mood disturbances. Road and workplace accidents related to excessive sleepiness, to which shift work is a significant contributor, are estimated to cost $71-$93 billion per annum in the United States. There is growing evidence that understanding the interindividual variability in sleep-wake responses to shift work will help detect and manage workers vulnerable to the health consequences of shift work. A range of approaches can be used to enhance alertness in shift workers, including screening and treating sleep disorders, melatonin treatment to promote sleep during the daytime, and avoidance of inappropriate use of sedatives and wakefulness-promoters such as modafinil and caffeine. Short naps, which minimise sleep inertia, are generally effective. Shifting the circadian pacemaker with appropriately timed melatonin and/or bright light may be used to facilitate adjustment to a shift work schedule in some situations, such as a long sequence of night work. It is important to manage the health risk of shift workers by minimising vascular risk factors through dietary and other lifestyle approaches.
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PMID:Sleep loss and circadian disruption in shift work: health burden and management. 2413 59

Sleep disorders in physicians who perform shift work can result in increased risks of health problems that negatively impact performance and patient safety. Even those who cope well with shift work are likely to suffer from sleep disorders. The aim of this manuscript is to discuss possible causes, contributing factors and consequences of sleep disorders in physicians and to identify measures that can improve adaptation to shift work and treatment strategies for shift work-associated sleep disorders. The risk factors that influence the development of sleep disorders in physicians are numerous and include genetic factors (15 % of the population), age (> 50 years), undiagnosed sleep apnea,, alcohol abuse as well as multiple stress factors inherent in clinical duties (including shift work), research, teaching and family obligations. Several studies have reported an increased risk for medical errors in sleep-deprived physicians. Shift workers have an increased risk for psychiatric and cardiovascular diseases and shift work may also be a contributing factor to cancer. A relationship has been reported not only with sleep deprivation and changes in food intake but also with diabetes mellitus, obesity, hypertension and coronary heart disease. Nicotine and alcohol consumption are more frequent among shift workers. Increased sickness and accident rates among physicians when commuting (especially after night shifts) have a socioeconomic impact. In order to reduce fatigue and to improve performance, short naps during shiftwork or naps plus caffeine, have been proposed as coping strategies; however, napping during adverse circadian phases is less effective, if not impossible when unable to fall asleep. Bright and blue light supports alertness during a night shift. After shiftwork, direct sunlight exposure to the retina can be avoided by using dark sunglasses or glasses with orange lenses for commuting home. The home environment for daytime sleeping after a night shift should be very dark to allow endogenous melatonin secretion, which is a night signal and supports continuous sleep. Sleep disorders can be treated with timed light exposure, as well as behavioral and environmental strategies to compensate for sleep deprivation. Fatigue due to sleep deprivation can only be systematically treated with sleep.
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PMID:[Sleep disorders among physicians on shift work]. 2521 42

The respiratory stimulant caffeine is the most frequently used xanthine (theophylline or aminophylline) for the treatment of apnea in premature infants. It decreases but does not eliminate apnea. In most cases such decreases is insufficient to prevent the use of artificial ventilation. Progesterone is a respiratory stimulant in adult mammals including human, and it decreases sleep apnea in menopausal women. Whether progesterone as an adjunct to caffeine therapy could be effective in further reducing the frequency of apnea in premature infants is not known because its respiratory effect in newborns has not been well studied. Using rat pups at different postnatal ages, we first determined whether the respiratory stimulant effects of acute caffeine (10 mg/kg, i.p.) or progesterone (4 mg/kg i.p.) are age dependent. These studies showed that caffeine enhances the ventilatory response to hypoxia in 1 and 4 days-old rats while it decreases apnea frequency in 12-days-old. In contrast, progesterone enhances the ventilatory response to hypoxia in less than 7-days-old but decreases apnea in 1-day-old rats. Preliminary experiments show that administration of progesterone (4 mg/kg i.p.) to newborn rats that are chronically treated with caffeine (mimicking its clinical uses - 7.5 mg/kg once/day by gavage) enhances the respiratory stimulant effects of caffeine. Surprisingly, acute injection of progesterone enhances apnea frequency and reduces hypoxic ventilatory response in 12-day-old rats.
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PMID:An Overview on the Respiratory Stimulant Effects of Caffeine and Progesterone on Response to Hypoxia and Apnea Frequency in Developing Rats. 2630 83

Oxidative stress has been closely linked to the progressive cell damage associated with emerging non-communicable disease (NCDs). Early detection of these biochemical abnormalities before irreversible cell damage occurs may therefore be useful in identifying disease risk at an individual level. In order to test this hypothesis, this study assessed the relationship between a simple measure of redox status and lifestyle risk factors for NCDs, and the population-based risk score of Framingham. In a cross-sectional study design, 100 apparently healthy middle-aged males (n = 48) and females (n = 52) were asked to complete a comprehensive lifestyle assessment questionnaire, followed by body fat percentage and blood pressure measurements, and blood collection. The ratio of plasma total antioxidant capacity to hydroperoxide (TAC/HPX) was used as an index of redox balance. One-way ANOVA and multiple linear regression analysis were performed to analyse the association between TAC/HPX, lifestyle components and other plasma biomarkers. The TAC/HPX ratio was higher in males compared to females (t96 = 2.34, P = 0.021). TAC/HPX was also lower in participants with poor sleep quality (t93 = 2.39, P = 0.019), with high sleep apnoea risk (t62.2 = 3.32, P = 0.002), with high caffeine (F(2, 93) = 3.97, P = 0.022) and red meat intake (F(2, 93) = 5.55, P = 0.005). These associations were independent of gender. Furthermore, the TAC/HPX ratio decreased with increasing body fat percentage (F(2, 95) = 4.74, P = 0.011) and depression score (t94 = 2.38, P = 0.019), though these associations were dependent on gender. Importantly, a negative association was observed between TAC/HPX levels and the Framingham risk score in both males (r(45) = -0.39, P = 0.008) and females (r(50) = -0.33, P = 0.019) that was independent of other Framingham risk score components. Findings from this study suggests that a relatively simple measure of redox balance such as the TAC/HPX ratio may be a sensitive indicator of redox stress, and may therefore serve as a useful biomarker for assessing an individual's specific NCD risk linked to unhealthy lifestyle practices.
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PMID:Significant relationships between a simple marker of redox balance and lifestyle behaviours; Relevance to the Framingham risk score. 2910 74

It is known that adenosine and adenosine-5'-triphosphate (ATP) are excitatory mediators involved in carotid body (CB) hypoxic signaling. The CBs are peripheral chemoreceptors classically defined by O2, CO2, and pH sensors. When hypoxia activates the CB, it induces the release of neurotransmitters from chemoreceptor cells leading to an increase in the action potentials frequency at the carotid sinus nerve (CSN). This increase in the firing frequency of the CSN is integrated in the brainstem to induce cardiorespiratory compensatory responses. In the last decade several pathologies, as, hypertension, diabetes, obstructive sleep apnea and heart failure have been associated with CB overactivation. In the first section of the present manuscript we review in a concise manner fundamental aspects of purine metabolism. The second section is devoted to the role of purines on the hypoxic response of the CB, providing the state-of-the art for the presence of adenosine and ATP receptors in the CB; for the role of purines at presynaptic level in CB chemoreceptor cells, as well as, its metabolism and regulation; at postsynaptic level in the CSN activity; and on the ventilatory responses to hypoxia. Recently, we have showed that adenosine is involved in CB hypersensitization during chronic intermittent hypoxia (CIH), which mimics obstructive sleep apnea, since caffeine, a non-selective adenosine receptor antagonist that inhibits A2A and A2B adenosine receptors, decreased CSN chemosensory activity in animals subjected to CIH. Apart from this involvement of adenosine in CB sensitization in sleep apnea, it was recently found that P2X3 ATP receptor in the CB contributes to increased chemoreflex hypersensitivity and hypertension in spontaneously hypertension rats. Therefore the last section of this manuscript is devoted to review the recent findings on the role of purines in CB-mediated pathologies as hypertension, diabetes and sleep apnea emphasizing the potential clinical importance of modulating purines levels and action to treat pathologies associated with CB dysfunction.
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PMID:Purines and Carotid Body: New Roles in Pathological Conditions. 2931 23


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