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Biomedical subjects

F Nielsen

Publications and source records attributed to F Nielsen.

At least 37 records · Page 2Linked to original sources
PubMed1992

Plasma lipoproteins and renal function during simvastatin treatment in diabetic nephropathy.

The aim of this study was to assess the effect of simvastatin on plasma lipoproteins and renal function in hypercholesterolaemic Type 1 (insulin-dependent) diabetic patients with diabetic nephropathy. Twenty-six hypercholesterolaemic (total cholesterol greater than or equal to 5.5 mmol/l) Type 1 diabetic patients with nephropathy were enrolled in a double-blind randomized placebo-controlled study for 12 weeks. The active treatment group (n = 14) received simvastatin (10-20 mg/day) for 12 weeks while the remaining 12 patients received treatment with placebo. The results during simvastatin treatment (baseline vs 12 weeks): total cholesterol 6.6 vs 4.8 mmol/l (p less than 0.01), LDL-cholesterol 4.25 vs 2.57 mmol/l (p less than 0.01) and apolipoprotein B 1.37 vs 1.06 mmol/l (p less than 0.01). HDL-cholesterol, and apolipoprotein A-I remained unchanged. Total cholesterol, LDL-cholesterol, HDL-cholesterol, apolipoprotein A-I, apolipoprotein B remained unchanged during placebo treatment. Albuminuria measured during the simvastatin and the placebo treatment (baseline vs 12 weeks) (the data are logarithmically transformed before analysis because of their positively skewed transformation; geometric mean (x/divided by antilog SE) is indicated) was 458 (x/divided by 1.58) vs 393 (x/divided by 1.61) and 481 (x/divided by 1.62) vs 368 (x/divided by 1.78 micrograms/min (NS). Glomerular filtration rate during simvastatin and placebo treatment (baseline vs 12 weeks) was 64 vs 63 and 72 vs 74 ml.min-1.1.73 m-2, respectively. Two patients receiving simvastatin treatment were withdrawn, one due to gastrointestinal side effects and one due to myalgia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Myocardial perfusion at fatal infarction: location and size of scintigraphic defects.

In a consecutive study of myocardial scintigraphy in acute ischemic syndrome, four patients had 99mTc-hexamibi injected intravenously before they developed fatal cardiogenic shock. Planar scintigraphy was performed after death. Slices of the hearts after autopsy were analyzed for scintigraphic and pathoanatomic abnormalities. Location of perfusion defects in planar views of the heart was in good agreement with the scintigraphied, sliced sections. The extent of infarction judged from inspection and formasan staining was much smaller (7%-40% and 6%-43% of the total slice area) than found at scintigraphy, where 83%-92% of the myocardium showed ischemia as defined by a 99mTc-hexamibi uptake below an arbitrary limit on half maximum uptake. Myocardial hypoperfusion might thus aggravate the functional impairment at myocardial infarction and lead to cardiogenic shock.

Aged↗
PubMed1989

[A study of cardiac vagal function in chronic alcoholics].

Reduced cardiac vagal tonus is correlated to sudden cardiac death and occurrence of arrhythmia, particularly in patients with ischemic heart disease. In patients with diabetic neuropathy increased frequencies of silent myocardial ischaemia and silent myocardial infarctions have been found, in addition. The object of the present investigation was to assess whether chronic alcoholics have lowered cardiac vagal tonus. The cardiac vagal tonus was assessed by means of a sensitive non-invasive method in which the variations in the pulse rate during six deep respirations were registered on the basis of the R to R interval in the ECG. Fourteen alcoholics and fourteen healthy controlled individuals participated in the investigation. The medians of the variations in the two groups were 15 and 25 beats per minute, respectively. The difference was statistically significant. No significant differences were observed in alcoholics with or without clinical evidence of polyneuropathy. This investigation thus suggests that ethanol has a toxic effect on the cardiac vagal function.

Adult↗
PubMed1989

Transient neonatal diabetes mellitus in a pair of twins.

The occurrence of transient neonatal diabetes mellitus in male twins with almost identical courses of illness is reported. A trial with chlorpropamide treatment of twin A had no obvious influence on the insulin consumption or on duration of treatment. Very low values of plasma C-peptide and serum proinsulin with no detectable insulin antibodies supports the theory of delayed maturation of the beta-cell.

Chlorpropamide↗
PubMed1988

Papillary muscle rupture as a first event in acute myocardial infarction.

Cardiogenic shock caused by papillary muscle rupture in acute myocardial infarction is potentially reversible by surgical treatment. A case of inferior myocardial infarction in a 56-year-old previously healthy man is reported, in which the first event was papillary muscle rupture. The patient was in shock and had a mitral insufficiency murmur. The diagnosis was made by echocardiography and ventriculography. A St. Jude valve was implanted, and the patient was discharged in good health. It is suggested that routine echocardiography be carried out on patients with sudden cardiogenic shock, when a mitral murmur is present.

Heart Rupture↗
PubMed1987

Characterization of binding equilibrium data by a variety of fitted isotherms.

Experimental binding equilibrium data, resulting from measurement of ligand binding to macromolecular carriers, are usually described by fitting of binding constants. These constants are often highly variable, as illustrated in the present paper by two examples, binding of salicylate to human serum albumin and of oxygen to hemoglobin. In order to avoid over-interpretation of binding constants it is pointed out that the best-fit solution, obtained by least-squares fitting, may be supplemented by several, e.g. thirty, acceptable solutions. It is further shown how the 30 sets of acceptable binding constants, plotted as Klotz' affinity profiles, can serve for evaluation of cooperative effects.

Algorithms↗
PubMed1987

Bradykinin in carcinoid syndrome.

Bradykinin concentrations in peripheral venous blood were measured in seven patients with carcinoid syndrome. The diagnosis was based on typical symptoms and raised urinary excretion of 5-hydroxy-3-indole acetic acid; the carcinoid tumour was verified histologically. Two patients were flushing constantly and the other patients had flushing attacks two to 10 times daily. Several blood samples were taken at weekly intervals from six of seven patients. During 30 sampling procedures the patients were flushing during sampling in 12 instances. Bradykinin was measured by a sensitive solid phase radioimmunoassay technique. Blood bradykinin concentration was normal in all patients. Bradykinin is unlikely to be the vasoactive mediator of flushing.

Aged↗
PubMed1986

Laurate binding to human serum albumin. Multiple binding equilibria investigated by a dialysis exchange method.

Multiple binding of laurate (n-dodecanoate) to human serum albumin was studied by a kinetic dialysis method. With this method the concentration of unbound ligand can be determined by measuring the rate of exchange of radioactive label across a dialysis membrane under conditions of equilibrium. Determination of the rate constant of exchange, in the absence of albumin, revealed that laurate does not change its state of aggregation over a concentration range from 0.1 microM to 500 microM, indicating the prevalence of a monomer. Binding of laurate to albumin, at pH 7.5, 37 degrees C, was investigated through 220 determinations of binding equilibria in the range of 0-10 mol laurate/mol albumin, corresponding to a concentration range of unbound laurate from 1 nM to 0.1 mM. Binding data were analyzed in terms of stepwise binding. Considering the stochastic errors of the experimental data, we generated a variety of possible (equal goodness of fit) solutions to the stoichiometric binding equation. This analysis resulted in reasonably well-defined values for the first two step constants, with an indication of negative interaction. The variation of the higher step constants excluded any mechanistic conclusions, although the binding isotherms, defined by these varying sets of binding constants, fitted the experimental data well within a chosen probability limit.

Dialysis↗
PubMed1986

Converting enzyme inhibition in mild and moderate essential hypertension. II.

In 24 patients with mild/moderate essential hypertension, we studied the effects of captopril with/without hydrochlorothiazide (Htz) on blood pressure, the renin-angiotensin system, blood bradykinin concentration (BBK), plasma volume, exchangeable sodium and glomerular filtration. Daily captopril doses of 75 and 150 mg were equally effective in reducing the blood pressure. Addition of Htz caused further blood pressure reductions. Nineteen patients attained a diastolic blood pressure less than or equal to 90 mmHg. Angiotensin converting enzyme inhibition with captopril led to a fall in plasma concentrations of angiotensin II (PAII) and renin substrate, and an increase in plasma concentrations of renin and angiotensin I. Patients starting with Htz had a higher PAII and subsequently a larger fall in blood pressure on captopril than untreated patients. BBK remained unchanged, indicating that the hypotensive action of captopril does not involve an accumulation of circulating kinin. Body fluid volumes and renal function were not affected by the various treatment regimens.

Adult↗
PubMed1986

Lack of effect of nifedipine on counterregulatory mechanisms in essential hypertension.

The influence of long-term nifedipine treatment on body fluid compartments, renal function, the renin-angiotensin system, and the adrenergic system was studied in 18 patients with essential hypertension. A placebo period of 4 weeks was followed by a 6-week dose-titration period. Thereafter, the dose was kept constant for an additional 6 weeks (mean dose, 51 mg/day). As compared with placebo values, diastolic blood pressure decreased approximately 12% during nifedipine treatment. Plasma volume, extracellular fluid volume, and the ratio of plasma to interstitial fluid volume did not change significantly, either in the group as a whole or in a subgroup in which pedal edema developed. Plasma concentrations of epinephrine and norepinephrine increased slightly after 2 weeks of treatment, but they returned to control values after 6 weeks of therapy. Plasma concentrations of renin, angiotensin II, and aldosterone did not change significantly. Glomerular filtration rate and renal clearances of sodium and potassium were unchanged as well. These results indicate that long-term nifedipine treatment does not lead to activation of counterregulatory mechanisms, such as fluid retention or the renin-angiotensin or adrenergic systems. This may well be of importance for the antihypertensive efficacy of nifedipine treatment.

Adult↗
PubMed1985

Prominent ears: a follow-up study.

Following a minimum observation time of 14 months, 74 patients having undergone surgical correction of prominent ears were re-examined. The applied surgical technique was modified from Stenström and Warrer utilizing the scoring technique and subcutaneous mattress chrome catgut sutures for fixation. Satisfactory results were achieved in more than 95 per cent of the patients, when assessed by both the patient and the surgeon. Only few complications were revealed.

Adolescent↗
PubMed1985

Quinsy: a bilateral presentation.

Bilateral peritonsillar abscesses are rare and often not diagnosed until tonsillectomy. As the condition may create diagnostic problems and serious complications, a case history is presented. The importance of rapid otorhinolaryngological examination and treatment is stressed.

Adult↗
PubMed1985

Converting enzyme inhibition in mild and moderate essential hypertension. I. Acute effects on blood pressure, the renin-angiotensin system and blood bradykinin after a single dose of captopril.

The acute effects of 25 mg captopril on blood pressure, heart rate, components of the renin-angiotensin system and blood concentration of bradykinin were followed in a single-blind placebo study of untreated (group A, n = 15) and thiazide-treated (group B, n = 13) patients with mild or moderate essential hypertension. A drug-related fall in blood pressure was seen in both groups. The blood pressure reduction was more marked in group B than in group A. Heart rate remained unchanged. Plasma concentrations of angiotensin II decreased significantly with concurrent increases in plasma concentrations of renin and angiotensin I, indicating the in vivo inhibition of converting enzyme. Blood concentrations of bradykinin showed no systemic changes. The magnitude of blood pressure reduction was correlated both with the pretreatment levels and the concurrent decreases in plasma angiotensin II. Inhibition of angiotensin II formation can explain a large part of the acute hypotensive pharmacological action of captopril. Other vasoactive systems may be involved. The kallikrein-kinin system does not appear to participate as indicated by the unchanged concentrations of kinin in blood.

Adult↗
PubMed1985

The influence of nifedipine treatment on counter-regulatory mechanisms in essential hypertension.

The influence of nifedipine treatment on plasma (PV) and extracellular fluid volume (ECV), the ratio of plasma volume to interstitial fluid volume (PV:IF), glomerular filtration rate (GFR), renal clearances of Na+ and K+, plasma concentrations of renin (PRC), angiotensin II (pANG II), aldosterone (pAldo), adrenaline (PA) and noradrenaline (PNA) were studied in 18 consecutive patients with essential hypertension. A 4-week placebo period was followed by a 6-week dose-titration period (period A). Thereafter the dose was kept constant for an additional 6 weeks (period B), the mean dose being 51 mg/day. As compared with placebo, diastolic blood pressure (DBP) decreased from 105 +/- 7 to 93 +/- 9 mmHg at the end of period B. Extracellular fluid volume, PV, and PV:IF were not significantly changed at the end of period A or B, neither in the group as a whole nor in a subgroup, who developed pedal oedema. After 2 weeks on nifedipine, PA as well as PNA increased slightly but returned to control values after 6 weeks of therapy. Plasma renin concentration, pANG II, pAldo and GFR did not change significantly. Renal sodium handling was also unchanged. It is concluded that long-term nifedipine therapy (exceeding 6 weeks) does not lead to activation of counter-regulatory mechanisms such as fluid retention, activation of the renin-angiotensin system and the adrenergic system. Renal function is unaffected by nifedipine.

Adult↗