We assessed the activity of the sympathetic nervous system during undisturbed nocturnal sleep and periods of wakefulness directly before and after sleep in healthy young men. Changes induced by periods of rapid eye movement and by morning awakening, both periods reported to demonstrate an enhanced risk for the onset of cardiovascular diseases, were of particular interest. In 13 healthy men (age, 18 to 35 years), blood for determination of epinephrine and norepinephrine was drawn every 7 minutes between 9:30 PM and 8:30 AM with the subjects resting in a strictly horizontal position. Lights were switched off at 11 PM until awakening at 7 AM. At 8:30 AM, subjects stood up and a final blood sample was drawn. Sleep was monitored somnopolygraphically, and heart rate and blood pressure were continuously measured. Average epinephrine but not norepinephrine concentrations were significantly lower during nocturnal sleep than during wakefulness before and after sleep. In parallel, heart rate and blood pressure declined significantly during sleep. During rapid eye movement sleep, both epinephrine and norepinephrine concentrations were significantly lower than during sleep stages 1 and 2 and slow-wave sleep. Whereas epinephrine concentrations gradually began to increase after morning awakening, norepinephrine levels were not significantly enhanced. However, standing up at the end of the experiment sharply increased norepinephrine concentrations by 180%, whereas epinephrine levels were less enhanced (46%) by the change of body position. This study suggests that the decrease in the activity of the sympathoadrenal branch of the sympathetic nervous system is probably due to an entrainment to the sleep-wake cycle, whereas the low activity of the noradrenergic branches depends mainly on horizontal body position during nocturnal sleep. The activities of the sympathoadrenal and noradrenergic branches of the sympathetic nervous system seem to be downregulated during rapid eye movement sleep. Awakening itself selectively enhances epinephrine levels. Subsequent orthostasis activates both the sympathoadrenal and, most prominently, the noradrenergic branches of the sympathetic nervous system.

Context An outbreak of Shiga toxin-producing enteroaggregative Escherichia coli (STEC O104:H4) infection with a high incidence of hemolytic uremic syndrome (HUS) occurred in Germany in May 2011. Antibiotic treatment of STEC infection is discouraged because it might increase the risk of HUS development. However, antibiotic therapy is widely used to treat enteroaggregative E coli infection. In the German outbreak, a substantial number of patients received prophylactic azithromycin treatment as part of a therapeutic regimen with the C5 antibody eculizumab.Objective To analyze the duration of bacterial shedding in patients with STEC infection who did and did not receive oral azithromycin therapy.Design, Setting, and Patients At a single center in Lü beck, Germany, 65 patients with STEC infection, including patients with HUS as well as STEC-infected outpatients without manifestation of HUS, were investigated between May 15 and July 26, 2011, and were monitored for a mean of 39.3 days after onset of clinical symptoms. Main Outcome Measure Carriage of STEC after azithromycin therapy.Results Twenty-two patients received oral azithromycin and 43 patients did not receive antibiotic treatment. Among antibiotic-treated patients, long-term STEC carriage (Ͼ28 days) was observed in 1 of 22 patients (4.5%; 95% CI, 0%-13.3%) compared with 35 of 43 patients (81.4%; 95% CI, 69.8%-93.0%) who were not treated with antibiotics (PϽ.001). All 22 patients receiving azithromycin treatment had at least 3 STECnegative stool specimens after the completion of treatment, and no recurrence of STEC was observed in these patients. As proof of principle, 15 patients who initially were not treated with antibiotics and were long-term STEC carriers were treated with oral azithromycin given for 3 days and subsequently had negative stool specimens. ConclusionTreatment with azithromycin was associated with a lower frequency of long-term STEC O104:H4 carriage.

Intranasal administration of some peptides has been shown to directly influence central nervous functions, thus pointing to a nose-brain pathway for these substances in humans. The present study investigated whether intranasal administration of angiotensin II (ANG II) affects central nervous functions of cardiovascular control in a different way from intravenously administered ANG II. In a balanced cross-over design 12 healthy men were treated with ANG II intravenously (2.5 g), ANG II intranasally (400 g), and placebo. Angiotensin II, vasopressin, norepinephrine, and epinephrine plasma levels were assessed every 10 min; blood pressure, heart rate, and systemic vascular resistance were measured by a Dinamap, and by continuous, noninvasive body plethysmography. Also, feelings of activation and mood were measured. Intranasal and intravenous administration invoked equivalent increases in plasma levels of ANG II, and induced an acute rise in blood pressure of comparable size and duration. However, subsequent blood pressure profiles differed dependent on intravenous and intranasal ANG II administration; after intravenous ANG II administration blood pressure remained enhanced at an intermediate level, but it returned to normal or even decreased below normal levels after intranasal ANG II administration. Intranasal ANG II also counteracted the decrease in norepinephrine levels observed after intravenous administration of ANG II. Intranasal but not intravenous ANG II enhanced plasma concentrations of vasopressin. This diverging pattern of effects bears similarities with effects of intracerebroventricular administration of ANG II in animals, suggesting that the effects after intranasal administration reflect a direct central nervous action of ANG II. Am J Hypertens 1998;11:971-977

Although shiga toxin-producing Escherichia coli (STEC)-HUS induced by O104:H4 was a life-threatening acute disease, follow-up showed a good recovery of organ function in all patients. Whereas kidney function recovered even after longer duration of dialysis, chronic hypertension developed after severe HUS with neurological symptoms and could not be prevented by the extended therapy.

No abstract