There is abundant and growing evidence that oxidative stress is an important factor in the propagation of endothelial dysfunction [1]. Recently, Hirsch, et al. reported that flow-mediate brachial artery dilation (FMD) is blunted in early compared to late morning postwaking hours, and independently predicts long-term adverse CVE in healthy subjects [2]. Transient endothelial dysfunction has been reported after mental and physical stress [3,4]. Most of the systemic processes that invoke endothelial dysfunction entail stress-induced activation of intracellular oxidative signaling, with secondary modulation of LDL oxidation, NO bioavailability, and vascular inflammatory gene expression [5]. We examined the effect of three sequential night shifts, with the accompanying inevitable stresses and lifestyle changes, on endothelial function by the FMD changes and the oxidative stress as the mechanism in apparently healthy medical personnel. The study group consisted of 22 healthy, female nurses (30.1± 4.1 years of age). None of the nurses had a history of coronary artery disease, diabetes mellitus, or hypertension. None of the nurses had a historyof usingherbalmedications or vitamins. The studywas approved by the Institutional Review Board of the Gwangju Veterans Hospital and all participants signed informed consent forms before the study. Endothelial function was examined twice in each subject: (1) on a regular workday (with no previous or subsequent night shift, and thus defined as the baseline measurement of FMD) and (2) after three sequential night shifts. All examinationswere performed in themorning (8 A.M.) under identical conditions in a temperature-controlled room. During the study, the participants in the no chocolate group were asked to substitute the chocolate with foods of similar energy and macronutrient composition. After the shift, nurses completed a questionnaire regarding the shift, including the number of hours slept, coffee consumption (number of cups drunk during the shift), and cigarette smoking. Endothelial function was examined non-invasively in the brachial artery using high-resolution ultrasound by standard methods (Sequoia 512; Acuson,Mountain View, CA, USA). The concentration of NOx (NO2 and NO3) was measured by using a nitrogen monoxide (NO) analyzer (model 7050; Antek Co., Guelph, Ontario, Canada). We calculated the concentration of NOx of the sample from a standardized curve, which was made by integrating values of a detector after injecting 50 μL of nitrous solution (1.63 nM,16.3 nM, and 163 nM) in theNO analyzer. The FMD (control and after three sequential night shifts) were compared using Student's t-test for paired data variance. Two tailed pb0.05 was considered significant. Systolic blood pressure at rest was slightly lower after the shift (from 105.00 ±8.89 to 102.50±9.11 beats/min, p=0.021), but there were no significant changes in diastolic blood pressure, heart rate, and BMI after 3 sequential night shifts compared with baseline measurements. The FMDwas significantly decreased after the sequential night shifts compared with baseline measurements (from 13.33±3.53% to 7.62±2.38%, pb0.001) (Fig. 1). There was no significant change in hsCRP after 3 sequential night shifts compared with baseline measurements. However, NOx was significantly decreased after 3 sequential night shifts compared with baseline measurements (from 176.1± 65.1 mmol/dL to 131.8±72.1 mmol/dL, p=0.033) (Fig. 1). By multivariate stepwise regression analysis, the decrease in FMD after shiftwork was independently related to a longer history of shift work (r=0.67, p=0.02). But, there was no correlation between changes in NOx and FMD before and after 3 sequential night shifts (r=−0.218, p=0.356). Our results are in agreement with a previous study which showed that working a 24-hour shift resulted in deterioration of the FMD [5]. Thus, night shift work might be a stressor that deteriorates the FMD, but the precise mechanism is unknown. We reasoned that oxidative stress might be the cause of endothelial dysfunction. One of the important results of production of oxygen radicals is reduced bioactivity by loss of NO. A decrease in the bioavailability of NO has important pathophysiologic effects in atherosclerosis, hypertension, and diabetic vascular disease [6]. Our study showed a significant
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May 8, 2012
Hossein Fakhrzadeh + 7
Open Access