Human obesity is characterized by profound alterations in the hemodynamic and metabolic states. Whether these alterations involve sympathetic drive is controversial. In 10 young obese subjects (body mass index, 40.5 +/- 1.2 kg/m2, mean +/- SEM) with normal blood pressure and 8 age-matched lean normotensive control subjects, we measured beat-to-beat arterial blood pressure (Finapres technique), heart rate (electrocardiogram), postganglionic muscle sympathetic nerve activity (microneurography at the peroneal nerve), and venous plasma norepinephrine (high-performance liquid chromatography). The measurements were performed in baseline conditions and, with the exception of plasma norepinephrine, during baroreceptor stimulation and deactivation caused by increases and reductions of blood pressure via intravenous infusions of phenylephrine and nitroprusside. Baseline blood pressure and heart rate were similar in obese and control subjects. Plasma norepinephrine was also similar in the two groups. Muscle sympathetic nerve activity, however, was 38.6 +/- 5.1 bursts per minute in obese subjects and less than half that level in control subjects (18.7 +/- 1.3 bursts per minute), the difference being highly statistically significant (P < .02). Muscle sympathetic nerve activity and heart rate were reduced during phenylephrine infusion and increased during nitroprusside infusion, but the changes were about half as great in obese subjects as in control subjects. Thus, even in the absence of any blood pressure alteration, human obesity is characterized by a marked sympathetic activation, possibly because of an impairment of reflex sympathetic restraint. This may be involved in the high rate of hypertension and cardiovascular complications seen in obesity.
In obese normotensive subjects, a reduction in body weight induced by a hypocaloric diet with normal sodium content exerts a marked reduction in sympathetic activity owing to central sympathoinhibition. This can be due to the consequences of an increased insulin sensitivity but also to a restoration of the baroreflex control of the cardiovascular system with weight loss.
Abstract-Essential hypertension, obesity, and congestive heart failure are characterized by an increase in muscle sympathetic nerve activity. Whether in these conditions skin sympathetic nerve activity is also increased has never been systematically examined, however. In 10 untreated mild essential hypertensive, 12 untreated normotensive obese, 10 mild (New York Heart Association class II) heart failure, and 10 normotensive lean healthy control subjects, we measured beat-to-beat arterial blood pressure (Finapres technique), body mass index, and postganglionic sympathetic nerve activity in skeletal muscle and skin areas (microneurographic technique, peroneal nerve). The muscle and skin nerve measurements were made in a randomized sequence. All data were obtained with the subject supine in a quiet, semidark environment at constant temperature over two periods of 30 minutes each, separated by a 20-to 30-minute interval. Blood pressure was increased only in hypertensive and body mass index only in obese subjects. Muscle sympathetic nerve activity quantified as bursts/min was markedly and significantly (PϽ.01) greater in essential hypertensive (33.3Ϯ1.7), obese (42.2Ϯ2.8), and congestive heart failure subjects (55.8Ϯ4.3) in comparison with control subjects (23.9Ϯ1.6). This was the case also for muscle sympathetic nerve activity, quantified as bursts per 100 heart beats. In contrast, skin sympathetic nerve activity (bursts per minute) was superimposable in hypertensive, obese, heart failure, and control subjects, its ability to increase being documented in all four groups by the marked response to an acoustic stimulus. Thus, in various diseases, muscle but not skin sympathetic activity is increased, with the sympathetic activation not being uniformly distributed over the whole cardiovascular system. (Hypertension. 1998;31[part 1]:64-67.)Key Words: hypertension, essential Ⅲ obesity Ⅲ heart failure Ⅲ sympathetic nervous system Ⅲ reflex M icroneurographic studies have provided evidence that different mechanisms are involved in the regulation of muscle sympathetic nerve activity, ie, that while the former is under baroreflex and humoral control, the latter is mainly modulated by thermoregulatory and emotional factors. [1][2][3][4] This provides a physiological background to the recent finding that in severe heart failure, ie, a condition known to be characterized by a baroreflex impairment and neurohumoral abnormalities, 5-7 sympathetic activation can be detected via microneurography in the muscle but not in the skin nerve areas.8 It remains unsettled, however, whether the different behavior of muscle and skin sympathetic nerve activity reported in heart failure is peculiar to this condition or is a finding commonly observed in other abnormal states characterized by muscle sympathetic activation and reflex and humoral alterations.To obtain conclusive information on this issue, we systematically used the microneurographic technique to assess muscle and skin nerve activity in (1) essential hypertensive patients in which sev...
L ong-term prospective studies have recently shown that bariatric surgery significantly reduces the risk of death in severely obese patients.1 This has been confirmed by retrospective analyses of a large cohort of obese individuals in whom surgery-related reductions in body weight were associated with a significant reduction in death rate compared with obese individuals followed under dietary and medical treatment. [2][3][4] It is a widespread belief that the protective effect of bariatric surgery in obese patients may perhaps be related to a reduction of body weight per se but that the concomitant improvement of the array of risk factors commonly associated with obesity, for example, alterations in lipid and glucose metabolism, is likely to play a major role. [5][6][7] In this context, however, little attention has to date been given to whether bariatric surgery is also associated with the improvement of another adverse phenomenon of obesity (ie, sympathetic activation). 8,9 The only information available comes from 3 studies that assessed sympathetic tone by making use of spectral analysis of heart rate signal or 24-hour norepinephrine urinary excretion [10][11][12] (ie, approaches that display major intrinsic limitations not allowing to provide any direct insight on the effects of the intervention on central sympathetic outflow, as the microneurographic technique only allows to achieve 13 .) The issue has pathophysiological and clinical relevance because sympathetic activation has been shown to be an adverse prognostic factor in several clinical conditions.14-17 Furthermore, evidence has been obtained that sympathetic overdrive may cause or worsen insulin resistance, 18,19 thus contributing to a common metabolic alteration in obesity.Abstract-Weight loss improves insulin sensitivity and exerts sympathomodulatory effects. No data, however, are available on the effects of the weight loss induced by vertical sleeve gastrectomy on sympathetic neural drive, insulin sensitivity, and their reciprocal cross talks. In 10 severe obese hypertensives (age, 54.0±2.3 years [mean±SEM]), we measured sphygmomanometric blood pressure, heart rate, body mass index, homeostatic model assessment index, plasma leptin, muscle sympathetic nerve traffic (microneurography), and baroreflex sensitivity (vasoactive drug technique). Measurements were performed 2 to 3 days before surgery and repeated 6 and 12 months after the procedure. Ten matched hypertensive obeses not undergoing gastrectomy served as controls. Six months after bariatric surgery, a significant (P<0.05) reduction in body mass index (−9.1±1.4 kg/m 2 ), sphygmomanometric systolic blood pressure (−10.2±4.5 mm Hg), heart rate (−11.0±2.4 bpm), homeostatic model assessment index (−3-3±1.3 AU), plasma leptin (−53.6±8.8 μg/L), and muscle sympathetic nerve traffic (−15.0±3.4 bursts/100 heart beats) was observed. The weight loss, the plasma leptin reduction, and the sympathetic inhibition were maintained after 12 months, whereas homeostatic model assessment index showed a tendency ...
BackgroundAcute gastroenteritis is a common cause of morbidity and mortality in humans worldwide. The rapid and specific identification of infectious agents is crucial for correct patient management. However, diagnosis of acute gastroenteritis is usually performed with diagnostic panels that include only a few pathogens. In the present bicentric study, the diagnostic value of FilmArray™ GI panels was assessed in unformed stool samples of patients with acute gastroenteritis and in a series of samples collected from pediatric patients with heamorragic diarrhea. The clinical performance of the FilmArray™ gastrointestinal (GI) panel was assessed in 168 stool samples collected from patients with either acute gastroenteritis or hemorragic diarrhea. Samples showing discordant results between FilmArray and routine methods were further analyzed with an additional assay.ResultsOverall, the FilmArray™ GI panel detected at least one potential pathogen in 92/168 (54.8%) specimens. In 66/92 (71.8%) samples, only one pathogen was detected, while in 26/92 (28.2%) multiple pathogens were detected.The most frequent pathogens were rotavirus 13.9% (22/168), Campylobacter 10.7% (18/168), Clostridium difficile 9.5% (16/168), and norovirus 8.9% (15/168). Clostridium difficile was identified only in patients with acute gastroenteritis (p < 0.01), while STEC was detected exclusively in patients with hemorragic diarrhea (p < 0.01). In addition, Campylobacter spp., Salmonella spp., EPEC and E. coli producing Shiga-like toxin were more frequently detected in patients with hemorragic diarrhea (p < 0.05). The overall percent agreement calculated in samples was 73.8% and 65.5%, while 34.5% were discordant. After additional confirmatory analyses, the proportion of discordant samples decreased to 7.7%. Rotavirus and astrovirus were the most frequently unconfirmed pathogens.ConclusionIn conclusion, the FilmArray™ GI panel has proved to be a valuable new diagnostic tool for improving the diagnostic efficiency of GI pathogens.
Estrogen administration has a number of favorable cardiovascular effects, and recent evidence suggests that these include an increase in arterial distensibility. Whether this is also the case for the physiological changes in estrogen production during the menstrual cycle has never been determined, however. In 21 premenopausal healthy women, we continuously measured radial artery diameter and blood pressure by an echo-tracking device and a beat-to-beat finger device, respectively. Arterial distensibility was calculated as distensibility/blood pressure curve. The measurements were made during the follicular, ovulatory, and luteal phases of the menstrual cycle. As expected, compared with the follicular phase, plasma estradiol, follicle-stimulating hormone, luteinizing hormone, and prolactin were increased in the ovulatory phase, whereas progesterone was increased in the luteal phase, together with antidiuretic hormone. Radial artery distensibility was increased in the ovulatory and reduced in the luteal phase, the changes being independent of the small, concomitant blood pressure changes. The arterial wall stiffening seen in the luteal phase was associated with a reduction in the flow-dependent endothelial dilatation of the radial artery as assessed by the hyperemia after short-term ischemia of the hand. Thus, the natural menstrual cycle is characterized by alterations in radial artery distensibility. The mechanisms responsible for this phenomenon remain to be clarified. It is possible, however, that the greater arterial distensibility of the ovulatory phase is due to an estrogen-dependent reduction in vascular smooth muscle tone, whereas the arterial stiffening of the luteal phase depends on vascular smooth muscle contraction due to more complex hormonal phenomena, ie, an endothelial impairment due to estrogen reduction but also to an increase in progesterone and antidiuretic hormone levels.
Abstract-Previous studies have shown that hypothalamic and hypophyseal factors are involved in the acute sympathoexcitation induced by a variety of laboratory stimuli. Whether a chronic condition of sympathetic activation, such as that characterizing human obesity, is also dependent on these factors has never been investigated. In 40 normotensive obese subjects ([meanϮSEM] age, 39.1Ϯ0.8 years) we measured blood pressure (Finapres), heart rate (ECG), and postganglionic muscle sympathetic nerve activity (MSNA) (microneurography). In 20 subjects measurements were repeated, according to a double-blind randomized sequence, after a midnight oral dose of dexamethasone (1 mg) (nϭ10) or placebo (nϭ10), while in the remaining subjects they were performed again after 1 week of a daily evening oral administration of 1 mg of dexamethasone (nϭ10) or placebo (nϭ10). The same protocol was performed in 16 age-matched lean normotensives. In both groups acute dexamethasone administration markedly reduced plasma cortisol (radioimmunoassay), without affecting hemodynamic and neural variables. In contrast to the acute administration, in obese subjects prolonged dexamethasone administration, although not affecting blood pressure and heart rate, significantly reduced both plasma cortisol (from 16.0Ϯ1.3 to 0.7Ϯ0.1 g/dL; PϽ0.01) and MSNA (from 59.5Ϯ2.8 to 39.6Ϯ2.9 bursts per 100 heartbeats; PϽ0.02; Ϫ33.1Ϯ4.1%). This was not the case in lean subjects, in which the dexamethasone-induced reduction in plasma cortisol was associated with a slight and nonsignificant MSNA decrease.In both lean and obese subjects, placebo administration caused no change in any variable. Thus, prolonged dexamethasone administration exerts in obese subjects marked sympathoinhibitory effects that are not detectable in lean individuals. This suggests that hypothalamic and hypophyseal factors substantially contribute to the sympathoexcitation of obesity. Key Words: obesity Ⅲ sympathetic nervous system Ⅲ hypothalamus Ⅲ hormones I n anesthetized rats or dogs, intracerebroventricular administration of corticotropin-releasing hormone (CRH) increases plasma levels of norepinephrine and elicits a sudden rise in blood pressure (BP) that is abolished by ganglionic blockade, thereby indicating origination from sympathoexcitation. 1,2 Furthermore, in conscious rats the sympathetic activation induced by stress is suppressed by acute blockade of CRH release by dexamethasone. 3 Finally, the acute increase in muscle sympathetic nerve activity (MSNA) that occurs in humans by administering alcohol intravenously or by increasing plasma insulin through a euglycemic clamp is also suppressed by a dose of dexamethasone capable of blocking corticotropin. 4,5 Thus, the activation of the sympathetic nervous system (as well as the related cardiovascular effects) acutely occurring in response to a number of laboratory stimuli appears to be mediated at least in part by centrally secreted peptides and possibly also by the intervention of the hypothalamus-hypophysis axis.Whether the dependence ...
Obesity is characterized by a number of cardiovascular alterations, and whether these alterations involve arterial compliance is unknown. In 12 young, obese, normotensive subjects (age, 23.9 +/- 1.3 years; mean +/- SEM) and 12 age- and sex-matched lean control subjects we measured blood pressure, radial artery diameter, and radial artery compliance continuously over the systodiastolic pressure range with a Finapres device and recently developed echo-tracking device. Measurements were obtained at baseline and after prolonged ischemia, that is, when diameter and compliance are increased. Blood pressure values were normal in both groups (obese subjects: 109.2 +/- 4.9/68.2 +/- 2.7 mm Hg; lean control subjects: 108.2 +/- 4.1/60.7 +/- 3.8 mm Hg), but in addition to a marked increase in body mass index (38.5 +/- 0.8 versus 23.1 +/- 0.9 kg/m2, P < .01), obese subjects showed a slight and nonsignificant increase in heart rate (71.1 +/- 3.2 versus 66.7 +/- 3.3 beats per minute, P = NS), increases in left ventricular wall thickness and left ventricular mass index (121.5 +/- 4.8 versus 103.4 +/- 3.3 kg/m2, P < .01), no changes in plasma renin activity and plasma norepinephrine (compared with normal values), and a marked reduction in total body glucose uptake (glucose clamp technique). Obese subjects showed radial artery diameter and compliance values that were greater than those seen in control subjects throughout the systodiastolic pressure range. The differences were 13% (P < .05) and 96% (P < .01), respectively, and both diameter and compliance remained higher in obese than lean subjects after forearm ischemia. In obese and lean subjects baseline radial artery diameter values correlated highly with body weight, body surface area, and body mass index.(ABSTRACT TRUNCATED AT 250 WORDS)
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