Sleep deprivation is common in Western societies and is associated with increased cardiovascular morbidity and mortality in epidemiological studies. However, the effects of partial sleep deprivation on the cardiovascular system are poorly understood. In the present study, we evaluated 13 healthy male volunteers (age: 31 ± 2 yr) monitoring sleep diary and wrist actigraphy during their daily routine for 12 nights. The subjects were randomized and crossover to 5 nights of control sleep (>7 h) or 5 nights of partial sleep deprivation (<5 h), interposed by 2 nights of unrestricted sleep. At the end of control and partial sleep deprivation periods, heart rate variability (HRV), blood pressure variability (BPV), serum norepinephrine, and venous endothelial function (dorsal hand vein technique) were measured at rest in a supine position. The subjects slept 8.0 ± 0.5 and 4.5 ± 0.3 h during control and partial sleep deprivation periods, respectively (P < 0.01). Compared with control, sleep deprivation caused significant increase in sympathetic activity as evidenced by increase in percent low-frequency (50 ± 15 vs. 59 ± 8) and a decrease in percent high-frequency (50 ± 10 vs. 41 ± 8) components of HRV, increase in low-frequency band of BPV, and increase in serum norepinephrine (119 ± 46 vs. 162 ± 58 ng/ml), as well as a reduction in maximum endothelial dependent venodilatation (100 ± 22 vs. 41 ± 20%; P < 0.05 for all comparisons). In conclusion, 5 nights of partial sleep deprivation is sufficient to cause significant increase in sympathetic activity and venous endothelial dysfunction. These results may help to explain the association between short sleep and increased cardiovascular risk in epidemiological studies.

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Abstract-We used microneurography to measure muscle sympathetic nerve activity (MSNA) in 25 hypertensive subjects and correlated these results with the presence or absence of signs of neurovascular compression (NVC) at the rostral ventrolateral (RVL) medulla on MRI. Subjects were divided into 3 groups based on MRI findings: NVC Ϫ , no MRI evidence of NVC (Nϭ9); NVCϩcontact, image showing artery in contact but not compressing the RVL medulla (Nϭ8); and NVCϩcompression, image showing arterial compression of the RVL medulla (Nϭ8). The MSNA measurements were performed at rest, after a hypothermic stimulus, and during isometric exercise. The MSNA during rest in the NVCϩcompression group was significantly higher than that in the NVCϩcontact and NVC Ϫ groups (30.4Ϯ3.4 versus 17.5Ϯ1.1 and 21.4Ϯ3.2 spikes per minute, respectively). However, the blood pressure in the NVCϩcompression group was slightly but not significantly higher than that in the other 2 groups (183Ϯ7/115Ϯ8, 174Ϯ6/108Ϯ7, and 171Ϯ5/ 110Ϯ5 mm Hg, respectively). The increases in MSNA, blood pressure, and heart rate during the cold pressor and isometric exercise tests were similar. Our results show that, although resting MSNA is elevated in patients with true NVC of the RVL medulla, patients without NVC or with arterial contact but not overt compression of the RVL medulla have similar MSNA. These findings are important for identifying, among hypertensive patients with NVC, individuals who may have associated physiological repercussions, such as increased sympathetic activity. Key Words: sympathetic nervous system Ⅲ magnetic resonance imaging P rimary hypertension in humans has a high prevalence worldwide and is considered to be multifactorial and polygenic. Central sympathetic activation has been implicated in the pathogenesis of hypertension (HTN), although its mechanisms still remain unclear. 1 Neurovascular compression (NVC) is a neuroanatomical anomaly of the brain stem classically associated with neurological diseases, such as hemifacial spasm and neuralgia of the trigeminal and glossopharyngeal nerves. NVC has also been related to neurogenic HTN when occurring at the rostral ventrolateral (RVL) medulla, 2 a region identified as an important efferent pathway of the sympathetic nervous system. [3][4][5] Various techniques for identifying NVC at RVL medulla in humans have been described since the first intraoperative reports by Jannetta and Gendell. 6,7 Currently, MRI is the most effective method for studying details of the brain stem and surrounding vessels involved in NVC. In some studies, the frequency of signs of NVC has ranged from 7% to 22.2% in nonhypertensive subjects, from 11% to 16.6% in subjects with secondary HTN, and from 74% to 90% in subjects with primary HTN. 8 -11 These data suggest that NVC may be associated with primary HTN and not secondary to prolonged exposure to high blood pressure (BP). Other studies, which used different means of assessment, revealed no difference in the frequency of NVC in populations with and without primary HTN...

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Background: Endothelial function has been extensively evaluated at the arterial bed in several cardiovascular scenarios. Venous endothelial dysfunction, however, has not been thoroughly explored particularly in heart failure (HF). Aims: To characterize venous endothelial function in severe HF. Methods and results: Venous endothelial function was evaluated by the dorsal hand vein technique using a tripod holding a linear variable differential transformer. Dorsal hand veins were pre-constricted with phenylephrine and dose-response curves were constructed after acetylcholine and sodium nitroprusside administration. Maximum vasodilator response to acetylcholine, a marker of endothelium-dependent venodilation, was significantly lower (47 ± 53% versus 102 ± 54%, respectively, p = 0.0004) in HF (n = 27) patients compared to healthy controls (n = 20). No difference in the endothelium-independent venodilator response was observed (p = 0.87). Maximum vasodilator response to acetylcholine was also significantly lower on admission compared to the response immediately before hospital discharge in patients with acute decompensated HF (p b 0.01). Improvement in venous endothelial function paralleled weight loss (mean difference of − 3.8 kg, p b 0.01) and improvement in the 6-minute walk test (mean difference of 107 m, p b 0.01). There was no significant change in angiotensin-converting enzyme inhibitor or beta-blocker use during hospital stay. Conclusions: HF patients experience marked endothelium-dependent venous dysfunction with partial recovery during in-hospital management.