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C Emmeluth

Publications and source records attributed to C Emmeluth.

18 recordsLinked to original sources
PubMed2006

Rotationally resolved infrared spectrum of the Li+-D2 cation complex.

The infrared spectrum of mass selected Li(+)-D(2) cations is recorded in the D-D stretch region (2860-2950 cm(-1)) in a tandem mass spectrometer by monitoring Li(+) photofragments. The D-D stretch vibration of Li(+)-D(2) is shifted by -79 cm(-1) from that of the free D(2) molecule indicating that the vibrational excitation of the D(2) subunit strengthens the effective Li(+)cdots, three dots, centeredD(2) intermolecular interaction. Around 100 rovibrational transitions, belonging to parallel K(a)=0-0, 1-1, and 2-2 subbands, are fitted to a Watson A-reduced Hamiltonian to yield effective molecular parameters. The infrared spectrum shows that the complex consists of a Li(+) ion attached to a slightly perturbed D(2) molecule with a T-shaped equilibrium configuration and a 2.035 A vibrationally averaged intermolecular separation. Comparisons are made between the spectroscopic data and data obtained from rovibrational calculations using a recent three dimensional Li(+)-D(2) potential energy surface [R. Martinazzo, G. Tantardini, E. Bodo, and F. Gianturco, J. Chem. Phys. 119, 11241 (2003)].

Journal Article↗
PubMed2001

Ragout-jet FTIR spectroscopy of cluster isomerism and cluster dynamics: from carboxylic acid dimers to N2O nanoparticles.

Direct absorption supersonic jet Fourier transform spectroscopy provides a panoramic view of the dynamics of molecular clusters over the entire IR spectral range. The new and generally applicable ragout-jet technique compensates for the sensitivity limits inherent in the incoherent FTIR approach by the use of synchronized giant gas pulses expanding into a large vacuum buffer. A modification based on fragmented interferograms is proposed and demonstrated, by which the spectral resolution can be extended to the limit of the available FTIR spectrometer. The power of the method is illustrated for two classes of compounds. For acetic acid and its isotopomers, the supersonic jet spectra of dimers and oligomers are investigated for the first time, concentrating on the very complex OH/CH stretching domain and on the more regular C=O/C-O stretching range. Issues of cluster isomerism, hydrogen exchange tunneling, anharmonic resonances, intermolecular Franck-Condon sequences, methyl group substitution and cluster coating with argon are explored. For the more weakly interacting nitrous oxide, stretching fundamentals and combination bands of clusters in the 1-3 nm range are studied as a function of composition. Surface vibrations are investigated in detail and modeled quantum mechanically. The semiempirical AM1 approach is found to provide a remarkably accurate description of the cluster structure, energetics and dynamics.

Algorithms↗
PubMed2001

Renal effects of nitric oxide synthase inhibition in conscious water-loaded dogs.

The renal effects of the nitric oxide (NO) synthase inhibitor nitro-L-arginine methyl ester (L-NAME) were investigated in conscious dogs undergoing sustained water diuresis and replacement of urinary sodium losses. Experiments were performed with and without additional extracellular volume expansion (isotonic saline, 2% body wt). L-NAME (10 microg. kg(-1). min(-1)) infused during water diuresis decreased urine flow (2.5 +/- 0.2 to 1.5 +/- 0.3 ml/min), free water clearance (1.9 +/- 0.2 to 1.0 +/- 0.2 ml/min), and sodium excretion (4.0 +/- 1.7 to 2.1 +/- 0.6 micromol/min). Arterial blood pressure increased from 112 +/- 2 to 126 +/- 3 mmHg, but creatinine clearance did not measurably change. Plasma endothelin and vasopressin concentrations and plasma renin activity (PRA) were unchanged. Urinary endothelin concentration increased (3.4 +/- 0.8 to 6.2 +/- 1.7 pg/ml), but the excretion rate remained constant. L-Arginine infusion (0.6 mg. kg(-1). min(-1)) along with L-NAME abolished the renal effects but not the blood pressure increase. Volume expansion increased urine flow (2.5 +/- 0.4 to 5.7 +/- 0.5 ml/min) and sodium excretion (3.8 +/- 1.6 to 76.5 +/- 14.5 micromol/min). L-NAME attenuated the renal effects of volume expansion: urine flow increased to 2.8 +/- 0.7 ml/min and sodium excretion to 34 +/- 17 micromol/min. PRA decreased with control volume expansion but not during L-NAME. Urinary endothelin levels were elevated by L-NAME, decreased with volume expansion in all series, but excretion rate remained constant. Infusion of L-arginine partially reversed these effects of L-NAME. The results demonstrate that NO synthase inhibition increases blood pressure and blunts the renal responses to water and saline loading.

Animals↗
PubMed1998

Mechanism of vasopressin natriuresis in the dog: role of vasopressin receptors and prostaglandins.

Renal effects of physiological amounts of vasopressin were studied in conscious dogs during servocontrolled overhydration (2% body wt). During infusion of vasopressin (50 pg . min-1 . kg body wt-1), plasma vasopressin concentration increased to 2.30 +/- 0.20 pg/ml compared with 0.12 +/- 0.03 pg/ml during control (water diuresis). With vasopressin infusion, urine flow was significantly lower (0.30 +/- 0.10 ml/min) and sodium excretion (UNaV) was significantly higher (58.0 +/- 15.8 micromol/min) than without vasopressin (4.6 +/- 0.4 ml/min and 14.4 +/- 4.1 micromol/min, respectively). Deamino-[Cys1,D-Arg8]vasopressin, a V2 receptor agonist (4 pg . min-1 . kg-1), mimicked the antidiuretic response (0.20 +/- 0.03 ml/min) without changing UNaV (9.7 +/- 4.4 micromol/min). Indomethacin given during arginine vasopressin (AVP) infusion suppressed prostaglandin E2 excretion, intensified the antidiuresis (0.10 +/- 0.02 ml/min), and abolished the natriuresis (13.4 +/- 3.7 micromol/min). During AVP infusion, UNaV was highly correlated (r = 0.85) with prostaglandin E2 excretion. Blood pressure, glomerular filtration rate, plasma atrial natriuretic peptide concentration, and the rate of proximal tubule reabsorption (derived from lithium clearance) were similar in all series. The data indicate that, in the dog, physiological amounts of vasopressin can induce natriuresis, probably through activation of non-V2 receptors and the intrarenal synthesis of prostaglandins.

Animals↗
PubMed1996

Plasma endothelin in congestive heart failure: effect of the ACE inhibitor, fosinopril.

OBJECTIVES: The study evaluates the influence of treatment with the angiotensin-converting enzyme inhibitor, fosinopril, on the plasma endothelin level in patients with congestive heart failure, and the relationship between plasma endothelin and clinical study parameters (bicycle exercise test, echocardiography, heart failure score and blood pressure). METHODS: Plasma endothelin was measured in 34 patients with moderately severe congestive heart failure at randomisation in the fosinopril/placebo-controlled study 'Fosinopril Efficacy and Safety Trial' and at the end of the 12-week study period. RESULTS: The patients had elevated pre-treatment plasma endothelin concentrations (3.5 +/- 1.2 pg/ml, mean +/- s.d., n = 34) compared with healthy volunteers (2.0 +/- 0.4 pg/ml, n = 21, P < 0.0001). Treatment with fosinopril for 12 weeks lowered plasma endothelin from 3.5 +/- 1.2 to 2.5 +/- 0.7 pg/ml (m = 18, P < 0.005), in contrast to the non-significant increase in the placebo-treated group 3.5 +/- 1.3 to 4.3 +/- 2.4 pg/ml, n = 16). A multiple regression analysis for baseline study parameters, demonstrated a significant relationship between plasma endothelin and exercise test duration and a composite heart failure score classification (r = 0.53, P < 0.001). CONCLUSIONS: Treatment of patients with congestive heart failure with the angiotensin-converting enzyme inhibitor, fosinopril, reduce the elevated plasma endothelin level to normal values. The relation between plasma endothelin and clinical parameters indicates that endothelin may play a pathophysiological role in the progression of congestive heart failure.

Aged↗
PubMed1996

Plasma endothelin in congestive heart failure: a predictor of cardiac death?

BACKGROUND: Endothelin is a potent vasoconstrictor, with growth-promoting and possible cardiotoxic and arrhythmogenic properties. This study investigates the association between increased plasma endothelin in congestive heart failure and prognosis. METHODS AND RESULTS: Forty-four patients with congestive heart failure showed increased plasma endothelin concentrations (mean +/- SD, 3.7 +/- 1.7 pg/mL; n = 44) compared with healthy volunteers (2.0 +/- 0.4 pg/mL, n = 21, P < .00003). Plasma endothelin increased with the severity of the disease. All patients were followed for an average of 17 months (range, 2-25 months). Cardiac mortality was 27% (8 of 30 patients) in the group with plasma endothelin concentrations above 3 pg/mL and 0% (0 of 14 patients) in the group with plasma endothelin concentrations below 3 pg/mL (P < .05). In contrast, separation of patients based on different New York Heart Association groups and ejection fractions revealed no significant difference regarding this endpoint. CONCLUSIONS: Increased plasma endothelin concentrations in patients with congestive heart failure appears to serve as a predictor of cardiac death.

Adult↗
PubMed1996

Natriuresis caused by increased carotid Na+ concentration after renal denervation.

The renal effects of a selective estimated 3 mM increase in the concentration of Na+ in blood perfusing the brain was investigated in conscious dogs with surgically denervated kidneys. In split-infusion experiments the concentration of Na+ in carotid plasma was increased by a bilateral carotid infusion of hypertonic NaCl combined with an infusion of distilled water into the caval vein. In control experiments the same load of NaCl and water was administered as an isotonic solution into the carotid and jugular vessels. Peak rate of Na+ excretion was significantly higher during split infusion (156 +/- 19 mumol/min) compared with control (89 +/- 14 mumol/min). Renal excretion of urodilatin increased in both series. Renal excretion of endothelin immunoreactivity increased significantly more during split infusion (20 +/- 6 pg/min) than during control (9 +/- 3 pg/min). It is concluded that the natriuretic response to minute increases in Na+ concentration of carotid plasma is intact after renal denervation. Furthermore, endothelin may be involved in the excess excretion observed.

Animals↗
PubMed1995

Venous plasma levels of endothelin-1 are not altered immediately after nitroglycerin infusion in healthy subjects.

Endothelin-1 and nitric oxide play an important regulatory role in the control of vascular smooth muscle tone. Nitroglycerin (NTG), a nitric oxide donating drug, may inhibit endothelin production. In this double-blind placebo-controlled crossover study, plasma levels of endothelin-1 were measured before and immediately (5-30 s) after 80 min infusion of NTG (glyceryl trinitrate) or saline in 12 healthy subjects. On two different days separated by at least 1 week, NTG in four different doses, 0.015, 0.25, 1.0, and 2.0 micrograms. kg-1. min-1, or placebo (isotonic saline) was infused successively for 20 min each dose. During the infusion blood pressure and heart rate were measured. NTG infusion significantly decreased systolic blood pressure from 112.4 to 103.4 mmHg and pulse pressure from 39.3 to 29.5 mmHg. Heart rate increased from 62.7 to 73.1 beats. min-1. No changes in endothelin-1 plasma levels were induced by NTG infusion (2.4 pg.ml-1 before NTG vs. 2.7 pg.ml-1 after NTG) and placebo infusion also did not affect plasma endothelin-1. It is concluded that venous plasma levels of endothelin-1 are not altered immediately after NTG infusion.

Adult↗
PubMed1994

Biphasic response of plasma endothelin-1 concentration to exhausting submaximal exercise in man.

The concentration of endothelin-1 in forearm venous plasma was measured in 10 healthy men at rest and during ergometer bicycling at 65% of maximal aerobic capacity until exhaustion (96 +/- 10 min, mean +/- SE). A control group of 10 comparable subjects rested for 2 h. Mean plasma endothelin-1 concentration at rest was 2.0 +/- 0.2 pg ml-1, n = 20. The concentration decreased significantly by 21% during the first 30 min of exercise, whereupon it increased so that the concentration after 60 min of exercise was no different from resting values. The change in endothelin concentration could not be explained by changes in plasma volume. Unspecific effects of catheterization or time could also not explain the change in endothelin-1, since in the 10 control subjects who did not exercise, plasma endothelin-1 did not change significantly over 120 min. It is concluded that the concentration of endothelin-1 in forearm venous plasma changes in a biphasic manner during prolonged exhaustive bicycle exercise in man. An initial decrease in concentration is followed by an increase restoring the concentration to resting values after 60 min exercise.

Adult↗
PubMed1994

Natriuresis in conscious dogs caused by increased carotid [Na+] during angiotensin II and aldosterone blockade.

The renal response to a selective increase in the Na+ concentration of the blood perfusing the central nervous system was investigated in conscious dogs treated with the converting enzyme inhibitor enalaprilat and the aldosterone antagonist canrenoate. In split-infusion experiments the plasma [Na+] of carotid blood was increased (approx. 6 mM) by bilateral infusion of hypertonic NaC1. Concomitantly distilled water was infused into the v. cava making the sum of the infusions isotonic. In control experiments isotonic saline was infused at identical rates into all three catheters. Na+ excretion increased markedly in both series, 103 +/- 14 to 678 +/- 84 mumol min-1 during split-infusion and 90 +2- 14 to 496 +/- 74 mumol min-1 during the isotonic volume expansion. Peak rate of excretion, peak fractional sodium excretion, and cumulative sodium excretion were all significantly higher (P < 0.05) during split-infusion than during control experiments. Plasma vasopressin increased only during split-infusion (0.68 +/- 0.11 to 2.4 +/- 0.8 pg ml-1) while the increases in plasma atrial natriuretic peptide were similar in the two series. Urinary excretion of urodilatin (ANP95-126) increased significantly more during split-infusion (46 +/- 11 to 152 +/- 28 fmol min-1) than during the isotonic volume expansion (45 +/- 14 to 84 +/- 16 fmol min-1) (P < 0.05). It is concluded that the natriuretic mechanisms activated by a selective increase in the Na+ concentration of carotid blood and associated with increased excretion of urodilatin cannot be eliminated by blockade of the renin-angiotensin-aldosterone system.

Angiotensin II↗
PubMed1993

Elevated circulating plasma endothelin-1 concentrations in cirrhosis.

As endothelin-1 (ET-1), a potent vasoconstricting peptide, may play a role in the circulatory derangement and renal impairment in cirrhosis, the aim of the present study was to investigate plasma concentrations of ET-1 in different vascular beds in relation to clinical and biochemical parameters of liver function. Median brachial venous ET-1 concentrations were substantially higher in patients with cirrhosis (3.40 pg/ml, range: 1.25-7.84, n = 24) than in controls (1.53 pg/ml, range: 0.78-2.12, n = 11) (P < 0.00005). In patients with cirrhosis ET-1 was directly correlated to serum creatinine (r = 0.70, P < 0.0001) and aspartate aminotransferase (r = 0.44, P < 0.03) and negatively correlated to serum sodium (r = -0.58, P < 0.003). In patients who underwent liver vein catheterization (n = 8), no significant differences were found in ET-1 plasma concentration between the liver, renal, or femoral veins on the one hand and the femoral artery on the other (P > 0.1), indicating no major net elimination or release in the liver, kidney or lower limb. A significant negative correlation was found between systolic and diastolic blood pressures on the one hand and circulating ET-1 on the other (r = -0.71, P < 0.05). In conclusion, circulating ET-1 is elevated in cirrhosis and related to markers of systemic circulation and renal function, thus suggesting a role for ET-1 in the circulatory derangement and nephropathy in cirrhosis. Locations of major net elimination or release of ET-1 were not identified.

Adult↗
PubMed1992

Vasopressin and angiotensin II in the conscious dog: synergistic effects on renal excretory parameters?

1. The renal effects of angiotensin II were investigated (a) with and without acute blockade of the effects of aldosterone and (b) with and without concomitant infusion of vasopressin. Angiotensin II (2 ng min-1 kg-1) and/or vasopressin (5 pg min-1 kg-1) was infused intravenously into conscious water-diuretic dogs and the effects were quantified by measurements of renal excretion of water, Na+ and K+, as well as determination of plasma renin activity and plasma levels of atrial natriuretic peptide and catecholamines. 2. Angiotensin II alone increased blood pressure by 7% (P < 0.05), decreased effective renal blood flow markedly and reduced urine flow and osmolar and free water clearances. Na+ and K+ excretion did not change significantly. Aldosterone blockade with canrenoate increased Na+ excretion by a factor of 10; subsequent infusion of angiotensin II decreased Na+ excretion by about 50%, the other renal effects being qualitatively similar to those seen without blockade. As expected, vasopressin also decreased diuresis and free water clearance substantially; however, the effect of combined infusion of angiotensin II and vasopressin was not compatible with the notion of additive effects of the two peptides. 3. Angiotensin II alone or in combination with vasopressin did not change the plasma concentrations of atrial natriuretic peptide, adrenaline, noradrenaline, or dopamine. Vasopressin alone exerted its antidiuretic effect without affecting plasma renin activity, plasma aldosterone concentration or renal excretion of Na+ and K+.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1992

Plasma endothelin-1 during central hypovolaemia in man.

Endothelin-1 (ET-1) is a potent vasoconstricting peptide with effect on resistance as well as capacitance vessels. We followed ET-1 in arterial plasma together with heart rate (HR), central venous pressure (CVP), mean arterial pressure (MAP), and thoracic electrical impedance (TI) in seven men during central hypovolaemia induced by 50 degrees head-up tilt. During tilting plasma ET-1 increased from 1.1 +/- 0.2 to 1.4 +/- 0.3 pmol l-1 (mean +/- SE) concomitant with an increase in total peripheral resistance (TPR) (from 15 +/- 2 to 25 +/- 3 mmHg min l-1) (P < 0.01), and HR (from 67 +/- 2 to 94 +/- 5 beats min-1) (P < 0.01) while MAP remained unchanged. CVP decreased (from 1.8 +/- 0.9 to -1.6 +/- 1.0 mmHg) (P < 0.01) during tilting and remained unchanged during sustained tilt despite further reduction of central blood volume as recorded by TI. Presyncopal symptoms occurred after 28 +/- 6 min associated with decreases in HR (to 70 +/- 6 beats min-1), MAP (from 90 +/- 3 to 52 +/- 4 mmHg) and TPR (to 11 +/- 2 mmHg min l-1) (P < 0.01). At this time plasma ET-1 reached its highest level of 1.6 +/- 0.3 pmol l-1 (P < 0.01). Data show that head-up tilt is associated with increased plasma concentrations of ET-1 which may play a role in maintaining vascular tone in situations with a reduced central blood volume.

Adult↗
PubMed1992

Effects, release and disposal of endothelin-1 in conscious dogs.

Cardiovascular and renal responses to a step-up infusion of endothelin-1 (ET-1) (1, 5, and 15 ng kg-1 min-1) were investigated in conscious dogs. In addition, the disappearance of ET-1 in arterial and central venous plasma after an infusion of 10 ng kg-1 min-1 was quantified, and the effects of vasopressin (AVP, 10 ng kg-1 min-1) and angiotensin II (AII, 2, 5, and 10 ng kg-1 min-1) on plasma ET-1 were investigated. The step-up infusion of ET-1 increased the plasma level from 3.6 +/- 0.3 to 243 +/- 23 pg ml-1. Concomitantly, arterial blood pressure increased and heart rate (HR) decreased dose-dependently. Diuresis, sodium, and potassium excretion did not change significantly. However, free water clearance increased during the infusion. Clearance of creatinine and excretion of urea decreased (39 +/- 4 to 29 +/- 3 ml min-1 and 87 +/- 16 to 71 +/- 14 mumol min-1, respectively). Decay curves for ET-1 in venous and arterial plasma were identical, and initial t1/2 was 1.1 +/- 0.1 min. Vasopressin increased arterial blood pressure (107 +/- 4 to 136 +/- 3 mmHg) beyond the infusion period and increased plasma ET-1 (85%). An equipressor dose of AII tended to decrease plasma ET-1. It is concluded that the lung is apparently not important in the removal of ET-1, that the disappearance of ET-1 follows a complex pattern, and vasopressin--in contrast to angiotensin II--is able to increase the plasma concentration of ET-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1992

Roles of cephalic Na+ concentration and urodilatin in control of renal Na+ excretion.

Effects on renal function of an increase in the concentration of sodium in the blood supplying the head were investigated in water-diuretic conscious dogs in which the sodium and water contents were controlled by separate servo-mechanisms. A selective 2% increase in the sodium concentration of the carotid blood was achieved by a split-infusion technique including infusions of hypertonic saline into both carotid arteries and water into a jugular vein at rates making the combined infusate isotonic. This procedure caused a 34-fold increase in renal sodium excretion concomitant with a fourfold increase in the rate of urinary excretion of urodilatin. A comparable isotonic volume expansion (isotonic saline infusion into carotid arteries and jugular vein) caused a significantly smaller (13-fold) increase in urinary rate of excretion of sodium (P less than 0.02) and no increase at all in the excretion of urodilatin. It is hypothesized that cephalic sodium concentration receptors regulate the rate of excretion of sodium via urodilatin even under the present slightly hypotonic conditions.

Animals↗
PubMed1990

Increase in plasma sodium enhances natriuresis in response to a sodium load unable to change plasma atrial peptide concentration.

The influence of plasma sodium concentration in the control of sodium excretion was investigated in conscious, water-diuretic dogs. NaCl was infused for 60 min as a hypertonic or isotonic solution at a rate of 60 mumol NaCl min-1 kg-1 body wt. Plasma sodium concentration rose only during hypertonic infusion (P less than 0.05). Sodium excretion increased markedly with both infusions (hypertonic, from 2.4 +/- 0.6 to 105 +/- 27 mumol min-1; isotonic, from 3.9 +/- 1.3 to 58 +/- 17 mumol min-1). Fractional sodium excretion increased more during hypertonic than during isotonic infusion. Hypertonic infusion decreased diuresis from 3.1 +/- 0.5 to 1.3 +/- 0.6 ml min-1, while isotonic infusion elicited an increase from 3.9 +/- 0.5 to 7.2 +/- 0.7 ml min-1. Plasma renin activity and plasma aldosterone decreased markedly in both series (P less than 0.05), the relative changes in the two series being very similar. Central venous pressure increased (2.8 +/- 0.7 to 4.5 +/- 1.0 mmHg) during isotonic infusion but not significantly during hypertonic infusion. Arterial pressure, heart rate and plasma levels of atrial natriuretic peptide and catecholamines did not change measurably in either series. It is concluded that simultaneous increases in extracellular volume and sodium concentration cause a larger natriuretic response than a change in volume alone, and that a 40-fold increase in sodium excretion may occur without measurable changes in plasma atrial natriuretic peptide concentration.

Aldosterone↗
PubMed1987

Effects of atrial natriuretic peptides and furosemide in conscious dogs.

Effects of ANF(8-33) and Auriculin A on renal variables were investigated in conscious water-diuretic dogs. The two substances were injected intravenously (1.08 micrograms/kg in 3 min) or ANF(8-33) was infused (0.2 microgram/kg X min in 20 min). The effects were compared to those of an equinatriuretic dose of furosemide (1.0 microgram/kg X min). Injections caused increases in sodium excretion, diuresis, and osmolar clearance. No significant change in exogenous creatine clearance (CCREA) occurred. Infusion of ANF(8-33) decreased blood pressure by 14% (P less than 0.01) and increased sodium excretion by a factor of 10 (P less than 0.01). The natriuresis was a function of increases in diuresis and urinary sodium concentration, the latter by a factor of 6 (P less than 0.01). Diuresis and free-water clearance (CH2O) increased by 60% (P less than 0.01), but urine osmolality did not change significantly. After the infusion a significant decrease in PAH clearance (CPAH) (P less than 0.01) was observed. Filtration fraction (FF) did not change. The furosemide natriuresis appeared later than that of ANF without significant deviations in diuresis, CH2O, CCREA, CPAH, and FF; urine osmolality increased by 35% (P less than 0.01). The effects of ANF(8-33) differ from those of furosemide in several ways. First, the onset of natriuresis is faster, second, the natriuresis is associated by marked increases in diuresis and free-water clearance but not in urine osmolality; and third, natriuresis is followed by a reduction in renal blood flow. The rapid natriuresis of ANF can occur without changes in glomerular filtration rate.

Animals↗