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Aim and objective. The aim of the study was to analyse, while controlling for identified covariates, the effects of morningness-eveningness on sleep quality for shift nurses. Background. Shift nurses had greater difficulty falling asleep or staying asleep, thus resulting in higher rates of retiring from hospital. Existing research has addressed the effects of manpower demand and personal preferences on shift assignment; however, the concept of endogenous rhythms is rarely considered. Methods. This analysis included 137 nurses between the ages of 21-58. Nurses completed the Horne and Ostberg questionnaire to assess morningness-eveningness and the Pittsburgh Sleep Quality Index (PSQI) questionnaire to measure self-reported sleep quality over the last month. The 18-point Chinese version had a Cronbach's reliability coefficient of 0·79 overall and 0·86 respectively. This study analysed correlates of sleep quality by comparing the groups with better or worse sleep quality according to the median of PSQI. Univariate and multivariate analyses were used for the risk factors of worse sleep quality. Results. The result showed that the strongest predictor of sleep quality was morningness-eveningness not the shift schedule or shift pattern for nurses under controlling the variable of age. Greater age and longer years employed in nursing significantly decreased the risk of worse sleep quality. The confounding age factor was properly controlled; evening types working on changing shifts had higher risk of poor sleep quality compared to morning types. Conclusions. Morningness-eveningness was the strongest predictor of sleep quality under controlling the variable of age in shift nurses. Implications for clinical practice. Our results suggested that determining if nurses were attributed to morning or evening types is an important sleep issue before deciding the shift assignment. [ABSTRACT FROM AUTHOR]

Objectives: Long-term hypoxia results in hemodynamic breakdown in patients in the intensive care unit; however, intermittent hypoxia causes hypertension in individuals with sleep apnea. The objective of this study was to explore the sequential cardiovascular neural alterations in response to acute hypoxic apnea.Design: The authors conducted a prospective, randomized animal study.Setting: The study was conducted in a university animal laboratory.Methods: A programmable apnea model was developed in anesthetized rats, in which a 20-sec period of apnea was produced and subsequently divided into the early (2.0 to 7.9 secs), middle (8.0 to 13.9 secs), and late apneic phases (14.0 to 19.9 secs) and immediate reventilatory phase (20.0 to 25.9 secs).Results: Evident hypoxia developed during 20-sec apnea. Arterial pressure increased in the early apneic phase and returned to control level in the middle phase. Significant hypotension developed in the late apneic phase and deteriorated in the reventilatory phase. Interbeat interval increased mildly along the apneic event. The increase of pressure in the early and middle phases was inhibited by propranolol (1.0 mg/kg intravenously [iv]) but was provoked by phentolamine (2.5 mg/kg iv). The decrease of pressure in the late and reventilatory phases was reversed, at least in part, by phentolamine. Atropine (0.5 mg/kg iv) did not produce discernible effects in the arterial pressure. The increase of interbeat interval was suppressed by propranolol. Power spectral analysis of arterial pressure variability demonstrated significant increases of the low-frequency (sympathetic vasomotor activity) and normalized high-frequency (cardiac sympathetic modulation) power after reventilation.Conclusion: Although the sympathetic activity is excited during and after a hypoxic apnea, the immediate pressor effect is related to an inotropic response of cardiac sympathetic regulation, whereas the negative chronotropic and subsequent depressor effect is associated with a failure in the cardiovascular response to sympathetic excitation. [ABSTRACT FROM AUTHOR]