Antimicrobial efficacy and inactivation kinetics of a novel LED-based UV-irradiation technology.

BACKGROUND: Ultraviolet (UV)-light-emitting diodes (UV-LEDs) are energy efficient and of special interest for the inactivation of micro-organisms. In the context of the coronavirus disease 2019 pandemic, novel UV technologies can offer a powerful alternative for effective infection prevention and control. METHODS: This study assessed the antimicrobial efficacy of UV-C LEDs on Escherichia coli, Pseudomonas fluorescens and Listeria innocua, as well as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), human immunodeficiency virus-1 (HIV-1) and murine norovirus (MNV), dried on inanimate surfaces, based on European Standard EN 17272. RESULTS: This study found 90% inactivation rates for the tested bacteria at mean UV-C doses, averaged over all three investigated UV-C wavelengths, of 1.7 mJ/cm2 for E. coli, 1.9 mJ/cm2 for P. fluorescens and 1.5 mJ/cm2 for L. innocua. For the tested viruses, UV doses <15 mJ/cm2 resulted in 90% inactivation at wavelengths of 255 and 265 nm. Exposure of viruses to longer UV wavelengths, such as 275 and 285 nm, required much higher doses (up to 120 mJ/cm2) for inactivation. Regarding inactivation, non-enveloped MNV required much higher UV doses for all tested wavelengths compared with SARS-CoV-2 or HIV-1. CONCLUSION: Overall, the results support the use of LEDs emitting at shorter wavelengths of the UV-C spectrum to inactivate bacteria as well as enveloped and non-enveloped viruses by exposure to the appropriate UV dose. However, low availability and excessive production costs of shortwave UV-C LEDs restricts implementation at present, and supports the use of longwave UV-C LEDs in combination with higher irradiation doses.

Formation of even-numbered hydrogen cluster cations in ultracold helium droplets.

Neutral hydrogen clusters are grown in ultracold helium nanodroplets by successive pickup of hydrogen molecules. Even-numbered hydrogen cluster cations are observed upon electron-impact ionization with and without attached helium atoms and in addition to the familiar odd-numbered H(n)(+). The helium matrix affects the fragmentation dynamics that usually lead to the formation of overwhelmingly odd-numbered H(n)(+). The use of high-resolution mass spectrometry allows the unambiguous identification of even-numbered H(n)(+) up to n approximately = 120 by their mass excess that distinguishes them from He(n)(+), mixed He(m)H(n)(+), and background ions. The large range in size of these hydrogen cluster ions is unprecedented, as is the accuracy of their definition. Apart from the previously observed magic number n=6, pronounced drops in the abundance of even-numbered cluster ions are seen at n=30 and 114, which suggest icosahedral shell closures at H(6)(+)(H(2))(12) and H(6)(+)(H(2))(54). Possible isomers of H(6)(+) are identified at the quadratic configuration interaction with inclusion of single and double excitations (QCISD)/aug-cc-pVTZ level of theory.

Collisions between tunable halo dimers: exploring an elementary four-body process with identical bosons.

We study inelastic collisions in a pure, trapped sample of Feshbach molecules made of bosonic cesium atoms in the quantum halo regime. We measure the relaxation rate coefficient for decay to lower-lying molecular states and study the dependence on scattering length and temperature. We identify a pronounced loss minimum with varying scattering length along with a further suppression of loss with decreasing temperature. Our observations provide insight into the physics of a few-body quantum system that consists of four identical bosons at large values of the two-body scattering length.

[Realistic early and late results after otosclerosis surgery and presentation of a technique involving almost no complications]. / Realistische Früh- und Spätresultate nach Otosklerosechirurgie und Präsentation einer weitestgehend komplikationsfreien Technik.

Although the modern technique of otosclerosis surgery introduced by John Shea on 1st May 1956 has already been used throughout the world for almost fifty years it has not been possible to bring in line the differing opinions of surgeons concerning the optimum operation technique, the problems of the fenestration of the footplate, material and form of stapes replacement prosthetics and kind and place of their anchoring on the incus. Moreover, there is considerable disagreement among surgeons on a realistic evaluation of the findings of early and late results. During the last few decades otosclerosis surgery has become the hallmark of modern ear surgery and has been practiced in very highly specialized departments as well as in outpatient departments. The author, who has been very active in otosclerosis surgery since 1959-since 1979 with a modified personal technique-, wishes to prove that it is both meaningful and essential to modify the operation technique further, which is based on his own experiences and on more than 100 international publications. In this paper he presents his modified method, which has been tested on 1800 ears since 1979, as well as the results, achieved in this way.

Pregnancy-induced sympathetic overactivity: a precursor of preeclampsia.

BACKGROUND: Preeclampsia has been shown to constitute a state of sympathetic overactivity. However, it remains unclear if the sympathetic activity precedes preeclampsia or represents only a secondary phenomenon. To further investigate this issue, we performed a prospective study in pregnant women considered to be at increased risk for preeclampsia owing to preeclampsia during a preceding pregnancy. MATERIALS AND METHODS: Twenty-two women with a history of preeclampsia were longitudinally studied on three occasions: twice during pregnancy (M1: 22 +/- 4, M2: 33 +/- 5 weeks) and once postpartum (M3: 26 +/- 6 weeks postpartum). We measured muscle sympathetic nerve activity (MSNA), forearm blood flow, and blood pressure at rest and during reactive hyperaemia after forearm occlusion. RESULTS: At M1 and M2, none of the subjects was hypertensive, however, muscle sympathetic nerve activity levels were significantly augmented, compared with their postpartum values (M1: 21 +/- 9, M2: 29 +/- 14, M3: 9 +/- 5 bursts min(-1); P < 0.05). Forearm vascular resistance did not significantly change from M1 through M3 (M1: 16 +/- 9, M2: 15 +/- 7, M3: 16 +/- 7 U; P = NS). Gestational muscle sympathetic nerve activity values did not differ significantly among the subjects with subsequent preeclampsia compared with those who remained normotensive [with preeclampsia (n = 6): M1: 21 +/- 5, M2: 27 +/- 6, M3: 7 +/- 4 bursts min(-1); without preeclampsia (n = 16): M1: 21 +/- 11, M2: 30 +/- 16, M3: 9 +/- 6 bursts min(-1); P = NS]. CONCLUSION: Invariably, all women at risk for preeclampisa showed a pregnancy-induced increase in MSNA (pregnancy-induced sympathetic overactivity, PISO), which normalized after delivery. Most importantly, PISO is not necessarily associated with peripheral vasoconstriction and hypertension. Furthermore, only a subset of patients developed preeclampsia later on. Therefore, we hypothesize that PISO constitutes a precursor of preeclampsia which is physiologically compensated for by vasodilating mechanisms, leading to preeclampsia only when they fail.

Influence of antihypertensive medication on aldosterone and renin concentration in the differential diagnosis of essential hypertension and primary aldosteronism.

OBJECTIVE: Antihypertensive drugs influence the neurohumoral cardiovascular system and the concentration of hormones involved in blood pressure regulation. Little is known, however, about the extent to which various antihypertensive drugs influence cardiovascular hormone concentrations and thus disturb the differential diagnosis of hypertension in clinical practice. In this study we compare the impact of different antihypertensive medicaments on the renin-angiotensin-aldosterone system in patients with essential hypertension who are screened for primary aldosteronism. DESIGN AND SUBJECTS: We analysed serum aldosterone (SAC) and plasma renin concentration (PRC) in 37 normotensive controls, 144 hypertensive patients with essential hypertension, and 19 patients with primary aldosteronism. Patients were on different treatment regimens such as single drug or combination therapy with beta-blockers, angiotensin-converting enzyme (ACE) inhibitors or angiotensin II subtype 1 (AT1) receptor antagonists, calcium channel blockers, spironolactone and no treatment. RESULTS: In patients with essential hypertension, beta-blocker therapy (n = 47) led to a highly significant suppression of renin, whereas serum levels of aldosterone were not significantly altered. ACE inhibitors and AT1 receptor antagonists (n = 55) decreased aldosterone levels only to a minor extent. Calcium channel blockers (n = 23) had no significant influence on SAC or PRC. In patients with primary aldosteronism treated with spironolactone (n = 8), renin escaped suppression and reached very high levels. CONCLUSION: Beta-blockers and aldosterone antagonists have the strongest impact on the renin-angiotensin system. The decrease in renin concentration by beta-blockers leads to an increase in the ratio of aldosterone to renin, and thus to false-positive results in patients with essential hypertension. Calcium channel blockers, and probably also ACE inhibitors and AT1 receptor antagonists alone or in combination, may be continued during screening for primary aldosteronism by determination of renin and aldosterone concentration.

Ratio of serum aldosterone to plasma renin concentration in essential hypertension and primary aldosteronism.

The ratio of serum aldosterone to plasma renin activity (PRA) has been proposed as sensitive screening method in the diagnosis of primary aldosteronism under random conditions. However, the method for determination of renin activity is hampered by the necessity of ice cooling during storage and transport. The present study was therefore conducted to examine the ratio of serum aldosterone to plasma renin concentration (ARR) and its usefulness in diagnosis of primary aldosteronism under ambulatory conditions and given antihypertensive medication. 146 patients with arterial hypertension who consecutively attended the outpatient clinic were studied prospectively. Patients with secondary hypertension besides primary aldosteronism were not included in the series. 37 normotensive patients served as control. Also, 17 patients with known primary aldosteronism were retrospectively examined. Among the hypertensive group 2 patients with Conn's syndrome were newly detected (1.4%). ARR was 7.92 +/- 6.04 [pg/ml]/[pg/ml] in normotensive controls (range from 2.03 to 26.98), 14.61 +/- 18.50 [pg/ml]/[pg/ml] in patients with essential hypertension (n = 144, range from 0.41 to 115.45) and 155.92 +/- 127.84 [pg/ml]/[pg/ml] in patients with primary aldosteronism (n = 19, range from 6.75 to 515). 17 of the 19 patients with Conn's syndrome had an ARR of more than 50. Under ongoing drug treatment this represents a sensitivity of 89% and a specificity of 96%. Sensitivity decreased to 84% and specificity increased to 100% when a second criteria (aldosterone > or = 200 pg/ml) was included. In summary, ARR using renin concentration is a useful screening parameter for primary aldosteronism.

Cardiovascular effects of beta-blockers with and without intrinsic sympathomimetic activity. A comparison between celiprolol and metoprolol.

BACKGROUND: Celiprolol, a newer beta-blocking agent, has been reported to have vasodilatory capacity which may be due to partial beta-2-receptor agonistic activity or to alpha-receptor antagonistic or central sympathoinhibitory effects. METHODS: To more critically assess the physiologic effects of celiprolol, we measured sympathetic nerve activity to muscle (MSNA), forearm blood flow (FBF), blood pressure (BP), central venous pressure, and heart rate (HR) in 10 normal volunteers at rest, during unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP), and during a cold pressor test (CPT). Responses were compared with those seen with metoprolol and with placebo, i.e. each subject was studied three times. RESULTS: Celiprolol did not alter resting levels of hemodynamics, FBF, and MSNA nor did it alter responses to LBNP or the CPT. In contrast, metoprolol produced significant decreases of FBF and HR, and increases of forearm vascular resistance and BP, but had also no effect on responses to the applied stress tests. CONCLUSIONS: The lack of peripheral vasoconstriction seen after acute administration of celiprolol is most likely due to its partial beta-2-receptor agonistic effect and does not seem to be due to a central or reflex action or to an alpha-blocking effect. Both beta-blockers do not impair fundamental neural mechanisms involved in circulatory homeostasis.

Long-term results after microvascular decompression in essential hypertension.

BACKGROUND AND PURPOSE: In 1998, 8 patients with severe, intractable arterial hypertension and MR tomography-demonstrated neurovascular contact of a looping artery at the root entry zone of cranial nerves IX and X, causing neurovascular compression, underwent neurosurgical decompression. The short-term results showed a normalization of blood pressure with a markedly reduced antihypertensive drug regimen in 7 patients. To determine the longer-term outcome concerning blood pressure and secondary organ damage after neurovascular decompression, we studied these 8 operated patients prospectively for a mean follow-up of 3.5 years after surgical intervention. METHODS: Eight hypertensive patients who had undergone microsurgical decompression were monitored every 6 months after surgery to assess blood pressure (by 24-hour ambulatory pressure readings) and the need for antihypertensive medication. To evaluate secondary organ damage, echocardiographic assessment of left ventricular hypertrophy, fundoscopic assessment of hypertensive lesions, and analysis of renal function and proteinuria were done. RESULTS: Three of the 8 operated patients remained normotensive in the long-term period with decreased antihypertensive medication. Two patients required gradual increases of antihypertensive medication after the first postoperative year, after which arterial blood pressure levels were 10% to 15% lower than preoperative levels. Three patients suffered serious cardiovascular and renal complications, with the incidence of lethal intracerebral hemorrhage in 1 patient and end-stage renal disease in 2 patients, of whom 1 experienced sudden cardiac death. CONCLUSIONS: The long-term results verify that microsurgical decompression is a successful alternative therapy in a certain subgroup of patients with arterial hypertension due to neurovascular compression. However, the relevance of the looping artery in the other cases, who did not improve, is not clear. Prospective studies to elucidate the pathophysiological role of neurovascular abnormalities and arterial hypertension are needed.

Vascular reactivity in patients with preeclampsia and HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome.

OBJECTIVE: Early structural and functional changes in the systemic vasculature have been proposed to play a major pathogenetic role in preeclampsia and HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome. The aim of the study was to determine vascular reactivity in patients with preeclampsia with and without HELLP syndrome with respect to those in healthy pregnant control subjects. STUDY DESIGN: Forearm blood flow was measured by strain gauge plethysmography with the venous occlusion technique in 12 hypertensive patients with HELLP syndrome, in 8 patients with preeclampsia without HELLP syndrome, and in 8 healthy normotensive pregnant control subjects. To determine vascular reactivity the forearm blood flow was measured at baseline and after forearm occlusion for a period of 5 minutes (reactive hyperemia). The investigations were repeated 4 to 6 months post partum. Forearm vascular resistance was calculated as the ratio of mean arterial pressure to forearm blood flow. RESULTS: Mean arterial pressure at rest was elevated in patients with preeclampsia (116 +/- 20 mm Hg) and in patients with HELLP syndrome (110 +/- 16 mm Hg) with respect to healthy pregnant control subjects (86 +/- 10 mm Hg; P <.05). Forearm blood flow at rest was not statistically different in patients with preeclampsia (5.1 +/- 2.6 mL/min per 100 mL) and with HELLP syndrome (4.7 +/- 1.5 mL/min per 100 mL) with respect to pregnant control subjects (5.9 +/- 3.1 mL/min per 100 mL); however, forearm vascular resistance at rest was elevated in patients with preeclampsia (25.9 +/- 9.5 units; P <.05) and in patients with HELLP syndrome(24.6 +/- 6.9 units; P <.05) with respect to healthy control subjects (17.0 +/- 6.1 units). During reactive hyperemia the peak forearm blood flow, which is an indicator of maximal vasodilatory capacity, was impaired in patients with preeclampsia (21.9 +/- 8.2 mL/min per 100 mL; P <.05) but not in patients with HELLP syndrome (37.4 +/- 17.5 mL/min per 100 mL) and healthy control subjects (44.9 +/- 15.0 mL/min per 100 mL). Consequently, minimum forearm vascular resistance was higher in women with preeclampsia (6.1 +/- 1.9 units) than in both women with HELLP syndrome (3.5 +/- 1.6 units) and the control subjects (2.8 +/- 2.4 units). CONCLUSION: Despite similarly elevated forearm vascular resistances at rest in patients with HELLP syndrome and in patients with preeclampsia, forearm vascular resistance during reactive hyperemia did not differ significantly from that in healthy control subjects in the women with HELLP syndrome but was increased in women with preeclampsia. Vasodilatory reactivity thus is reduced in preeclampsia but not in HELLP syndrome, which suggests different alterations of the vasculature.

Severely impaired baroreflex-buffering in patients with monogenic hypertension and neurovascular contact.

BACKGROUND: We identified a family with a monogenic syndrome of hypertension, brachydactyly, and neurovascular contact of the brain stem. Neurovascular contact of the ventrolateral medulla may lead to arterial hypertension by interfering with baroreflex function. METHODS AND RESULTS: In 5 patients with monogenic hypertension (18 to 34 years old), we conducted detailed autonomic function tests. Blood pressure during complete ganglionic blockade was 134+/-4.9/82+/-4.1 mm Hg and 90+/-6/49+/-2.4 mm Hg in patients and in control subjects, respectively. During ganglionic blockade, plasma vasopressin concentration increased 24-fold in control subjects and <2-fold in patients. In patients, cold pressor testing, hand-grip testing, and upright posture all increased blood pressure excessively. In contrast, muscle sympathetic nerve activity was not increased at rest or during cold pressor testing. The phenylephrine dose that increased systolic blood pressure 12.5 mm Hg was 8.0+/-2.0 microg in patients and 135+/-35 microg in control subjects before ganglionic blockade and 5.4+/-0.4 microg in patients and 13+/-4.8 microg in control subjects during ganglionic blockade. CONCLUSIONS: In patients with monogenic hypertension and neurovascular contact, basal blood pressure was increased even during sympathetic and parasympathetic nerve traffic interruption. However, sympathetic stimuli caused an excessive increase in blood pressure. This excessive response cannot be explained by increased sympathetic nerve traffic or increased vascular sensitivity. Instead, we suggest that baroreflex buffering and baroreflex-mediated vasopressin release are severely impaired.

Impact of aldosterone on left ventricular structure and function in young normotensive and mildly hypertensive subjects.

Left ventricular (LV) hypertrophy is an independent risk factor for cardiovascular morbidity and mortality. Experimental data revealed that elevated circulating aldosterone is associated with increased collagen accumulation resulting in myocardial fibrosis. To analyze whether aldosterone is also associated with cardiac structural and functional changes in humans, we examined the effects of aldosterone on LV structure and function before and after suppression of aldosterone by increasing oral salt intake. The study group comprised 26 normotensive male white healthy control subjects (age 26 +/- 3 years) and 31 male white subjects (age 25 +/- 3 years) with mild essential hypertension (World Health Organization stages I to II). Two-dimensional-guided M-mode echocardiography and 24-hour ambulatory blood pressure (BP) monitoring was performed in each subject. Simultaneously, we measured 24-hour urinary sodium excretion, 24-hour urinary aldosterone, and serum aldosterone concentration at baseline and after increasing oral salt intake to suppress aldosterone secretion. In all subjects LV mass correlated with body mass index (r = 0.42, p <0.001) and both 24-hour ambulatory systolic (r = 0.28, p <0.05) and diastolic (r = 0.25, p <0.05) BP. Changes in urinary sodium excretion correlated inversely with changes in serum aldosterone concentration (r = -0.28; p <0.05). Urinary aldosterone concentration after salt loading decreased in normotensive (10.98 vs 7.44 microg/24 hours; p <0.02) but not in hypertensive (9.34 vs 10.51 microg/24 hours; p = NS) subjects. Serum and urinary aldosterone levels at baseline were not related to LV structure or function. In contrast, after increasing oral salt intake, urinary aldosterone concentration was related to LV mass (r = 0.43; p <0.01) and impaired midwall fractional fiber shortening (r = -0.33; p <0.02) in all subjects, independent of 24-hour ambulatory BP. Subgroup analysis revealed that this was significant only in hypertensive (r = 0.46; p <0.01 and r = -0.44; p <0.02, respectively) but not in normotensive (r = 0.28 and -0.16; p = NS for both, respectively) subjects. Consistently, the greater serum aldosterone remained after increasing oral salt intake, the greater was LV mass (r = 0.35; p <0.01). The latter was found in hypertensive subjects (r = 0.44; p <0.02), independent of 24-hour ambulatory BP, but not in normotensive subjects (r = 0.025; p = NS). Inadequate suppression of aldosterone in response to an increase in oral salt intake is related to LV structural and functional changes in hypertensive subjects. Thus, our results support experimental data indicating that aldosterone affects LV structure and function in humans and that this effect is BP independent.

Relation between the renin-angiotensin-aldosterone system and left ventricular structure and function in young normotensive and mildly hypertensive subjects.

BACKGROUND: High angiotensin II levels in relation to the corresponding urinary sodium excretion have been found to modulate left ventricular (LV) structure in middle-aged hypertensive patients. To analyze whether such a relation between the renin-angiotensin-aldosterone system and left ventricular structure is already present in young individuals, we examined the changes of angiotensin II and aldosterone in response to increased salt intake and their relations to LV structure and function. METHODS: In 119 young (aged 26 +/- 3 years) patients with normal or mildly elevated blood pressure, we determined LV structure and function (2-dimensional guided M-mode echocardiography and pulse wave Doppler sonography) and 24-hour ambulatory blood pressure (SpaceLabs 90207). Dietary sodium intake as estimated by 24-hour urinary sodium excretion, plasma renin activity, angiotensin II, and aldosterone concentrations were measured first on a normal diet and second at high salt intake to determine the extent of the resulting suppression of the renin-angiotensin-aldosterone system. RESULTS: Body mass index (r = 0.43, P <.001) and both systolic (r = 0.24, P <. 01) and diastolic (r = 0.19, P <.05) 24-hour ambulatory blood pressure correlated with LV mass. No straightforward relation was found between LV structure and baseline angiotensin II or aldosterone concentration. The increase of sodium excretion at high salt intake was related to a physiologically expected decrease of angiotensin II and aldosterone levels in normotensive (r = -0.36, P <.01 and r = -0.32; P =.016, respectively) but not in hypertensive patients. Changes in angiotensin II or aldosterone concentration were not related to LV structure in either hypertensive or normotensive young individuals. However, changes in aldosterone secretion correlated with diastolic filling parameters in hypertensive patients (velocity-time integrals of the A over E wave: r = 0.32, P =.03; atrial contribution of LV filling: r = 0.33, P =. 025) but not in normotensive individuals. CONCLUSION: In contrast to middle-aged hypertensive patients, neither angiotensin II, aldosterone, nor their suppression in response to high salt intake were related to LV structure in young hypertensive patients. However, inadequate suppression of aldosterone after salt intake was associated with diastolic filling abnormalities in our young hypertensive patients, which may represent early changes in hypertensive heart disease and precede potential structural alterations.

Hyper-responsiveness to angiotensin II is related to cardiac structural adaptation in hypertensive subjects.

BACKGROUND: Angiotensin II has been found to be a growth stimulating factor for myocardial cells. In humans, angiotensin II infusion causes vasoconstriction in systemic and renal vasculature and leads to aldosterone secretion. Our hypothesis was that hyper-responsiveness to angiotensin II is related to left ventricular mass in human essential hypertension. METHODS AND RESULTS: In 30 normotensive individuals and 30 subjects with mild essential hypertension (white men, mean age 26+/-3 years), the responsiveness to angiotensin II was assessed by measuring changes in mean arterial pressure, renal blood flow, glomerular filtration rate and aldosterone secretion in response to i.v. angiotensin II infusion (0.5 and 3.0 ng/kg per min). The provoked changes to angiotensin II infusion were similar in the normotensive and hypertensive group with the exception of an exaggerated increase in mean arterial pressure in hypertensives (14+/-5 versus 10+/-5 mm Hg, P<0.001 at 3.0 ng/kg per min angiotensin II). The increase in mean arterial pressure was correlated with left ventricular mass in hypertensive subjects (angiotensin II 0.5 ng/kg per min: r = 0.49, P<0.005; angiotensin II 3.0 ng/kg per min: r = 0.35, P<0.05); no such correlation was found in the normotensive group. After taking into account baseline mean arterial pressure and body mass index, the increase in mean arterial pressure to angiotensin II 0.5 ng/kg per min was still correlated with left ventricular mass (partial r = 0.50, P<0.01). Similarly, the change of glomerular filtration rate but not of renal blood flow in response to angiotensin II 0.5 ng/kg per min was correlated with left ventricular mass, (r = 0.42, P<0.02) in the hypertensive group but not in the normotensive one. This relationship remained significant even after taking baseline glomerular filtration rate, mean arterial pressure and body mass index into account (partial r = 0.43, P<0.05). CONCLUSION: Hyper-responsiveness to angiotensin II is related to an increased left ventricular mass in hypertensive subjects independent of blood pressure.

Angiotensin II stimulates left ventricular hypertrophy in hypertensive patients independently of blood pressure.

Angiotensin II (AII) is known to be a growth stimulating factor for myocardial cells. We examined whether an exaggerated responsiveness to AII might aggravate left ventricular (LV) hypertrophy in human essential hypertension. To determine the responsiveness to AII in humans, we examined changes in mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR) (steady state input clearance technique with para-aminohippurate and inulin, respectively) and aldosterone secretion to AII infusions (0.5 and 3.0 ng/kg/min) in 71 normotensive male and 48 hypertensive male subjects (age: 26 +/- 3 years; 24-h ambulatory blood pressure: 121 +/- 5/71 +/- 4 mmHg v 138 +/- 7/82 +/- 7 mmHg, P < .001). In addition, each patient underwent two-dimensional guided M-mode echocardiography at rest to assess cardiac structure and function. When given AII 3.0, a greater increase of MAP (13 +/- 7 v 17 +/- 8 mm Hg, P < .022) and a more marked decrease of RBF (-203 +/- 123 mL/min v -270 +/- 137 mL/min, P < .007) were found in hypertensives than in normotensives, whereas changes in GFR and aldosterone concentration were similar in both groups. Most important, changes in GFR to AII correlated with echocardiographically determined LV mass (normotensives: AII 0.5: r = 0.33, P < .006, AII 3.0: r = 0.28, P < .05; hypertensives: AII 0.5: r = 0.41, P < .006, AII 3.0: r = 0.32, P < .05). After taking baseline MAP and body mass index into account, the increase in GFR to AII 0.5 in hypertensives still correlated with LV mass (partial r = 0.37, P < .01). Inasmuch as the increase of GFR is a marker of the responsiveness to AII (related to vasoconstriction at the postglomerular site), our data suggest that increased sensitivity to AII is linked to LV hypertrophy in early essential hypertension, independently of the level of blood pressure.

[The autonomic nervous system and pre-eclampsia]. / Autonomes Nervensystem und Präeklampsie.

Alterations in the autonomic cardiovascular control have been implicated to play an important etiologic role in preeclampsia. Earlier assessments of sympathetic nervous system activity by measurements of urinary and plasma levels of catecholamines showed contradictory results, due to serious methodological problems. The microneurographic technique enables the assessment of sympathetic outflow to the vascular bed of skeletal muscles. By the use of this technique it has been shown that preeclampsia represents a state of sympathetic overactivity as compared to healthy pregnant women. Other studies have shown that exogenous stimulation of the celiac ganglion causes a HELLP-syndrome-like disease in pregnant rats and that preeclamptic human plasma increases norepinephrine release in isolated sympathetic neurons of chicken embryos. These data suggest that the autonomic nervous system may play a fundamental role in the etiology of preeclampsia.