Biomedical subjects

S Hansen-Schmidt

Publications and source records attributed to S Hansen-Schmidt.

5 recordsLinked to original sources

PubMed1995

[Calciphylaxis].

HISTORY AND CLINICAL FINDINGS: Acute, zigzag-shaped livid skin markings developed on both thighs of a 55-year-old woman who had been on dialysis for 6 years. Within 7 days these areas increased in size to about 10 cm in diameter and contained central dry and painful necroses. On legs, lower arms and hands hard subcutaneous nodules were palpable with a diameter up to 3 mm. For many years the phosphate and parathormone levels, as well as alkaline phosphatase activity had been raised. The patient had often failed to follow treatment recommendations. TESTS: There were increased serum concentrations of calcium (2.8 mmol/l) and phosphate (1.78 mmol/l). The calcium phosphate ion product was 4.98 (mmol/l)2. Furthermore, there were raised levels of alkaline phosphatase (315 U/l) and parathormone (1076 ng/l, normal: 10-65). X-ray film of the hands showed soft tissue and arterial calcifications, while histological examination of a deep skin biopsy revealed calcium phosphate emboli of the main vessels. TREATMENT AND COURSE: Excision of the cutaneous necroses was followed by parathyroidectomy at which only three parathyroid glands were identified and removed. The parathormone level fell postoperatively, but rose again after 4 weeks. The fourth parathyroid gland was then found and removed, after which the parathormone level fell below measurable levels. The skin ulcers healed completely 4 weeks after the second operation.

Calciphylaxis↗

PubMed1989

Effects of low-dose atenolol on postural and postprandial changes in heart rate, blood pressure, venous plasma catecholamines, and plasma renin activity.

The administration of a single dose of atenolol 50 mg 1 h before a standard 3100 kJ cold meal in fasting healthy subjects reduced the supine preprandial heart rate and systolic blood pressure, and blunted the postural and postprandial rises in mean heart rate and systolic blood pressure relative to placebo. It did not affect the preprandial supine diastolic blood pressure, nor the postural rise and postprandial drop in diastolic blood pressure. Preprandial administration of atenolol blunted the postural and postprandial rises in mean plasma renin activity, and it enhanced the rise in plasma noradrenaline during eating in the sitting position, and the postprandial concentrations of noradrenaline. The findings do not permit the conclusion that beta 1-adrenergic stimulation was the predominant cause of these atenolol-responsive changes.

Adult↗

PubMed1989

Time course and nature of postprandial haemodynamic changes in normal man.

The present study describes the nature and time course of the cardiovascular and neuro-endocrine changes that followed a standard 3100 kJ cold meal in 12 supine and fasting normal men who were studied in a balanced cross-over design. Heart rate, blood pressure, systolic time intervals and estimates of cardiac performance by impedance cardiography were measured every 10 min up to 4 h after eating. Eating caused a rapid and short-lasting increase in systolic blood pressure, estimated stroke volume and maximum velocity of impedance changes. Eating also caused a rapid and more protracted decrease in diastolic and mean blood pressure, PEP-i, QS2-i and estimated systemic vascular resistance with an increase in heart rate and estimated cardiac output. In the later phase of the profiling a drop in LVET-i was also observed. The differences vs. fasting were statistically significant and judged to be biologically relevant. Venous plasma noradrenaline rose during eating as a consequence of the postural change, but eating itself did not alter venous plasma noradrenaline, and plasma adrenaline even tended to decrease. This reflects both the roughness of venous catecholamines in estimating adrenergic changes and the complexity of the underlying mechanisms and related reflexes.

Adult↗

PubMed1989

SK&F 86466, a novel alpha-adrenolytic drug: effects on heart rate, blood pressure, and neuroendocrine function in supine resting position and in response to postural and cold stimulation in normal humans.

SK&F 86466 is a novel alpha-adrenoceptor blocking drug shown in preclinical profiling to have relative selectivity for the pre- and postjunctional alpha 2-adrenoreceptor. In the present clinical study, the effects of single oral doses of 10, 25, and 50 mg SK&F 86466 on supine and stimulated circulatory and neuroendocrine function were assessed in eight normal subjects studied in a placebo-controlled balanced cross-over design with the drugs administered in double-blind fashion. SK&F 86466 caused a dose-related increase in stimulated (postural and cold challenge) and supine plasma norepinephrine (NE) concentrations. This increase was associated with an increase in supine heart rate (HR) and plasma renin activity and orthostatically stimulated HR, with little increase in systolic blood pressure (SBP) and no increase in diastolic blood pressure (DBP). Assuming that no changes occurred in catecholamine clearance, SK&F 86466 thus appeared to have a prejunctional alpha 2-adrenoreceptor blocking effect, which was countered by a post-junctional alpha-adrenoreceptor blocking effect at the level of the resistance vessels, whereas this latter effect did not alter the pressor responses to cold and postural challenge.

Adrenergic alpha-Antagonists↗

PubMed1988

Postprandial haemodynamic changes: a source of bias in cardiovascular research affected by its own methodological bias.

The effects of heart rate and systolic and diastolic blood pressure of eating a 3100 kJ cold meal were assessed in eight young normal subjects studied in a randomised and balanced crossover study. Blood pressure was measured simultaneously and in the same arm by auscultation of the fossa cubitalis (Korotkoff I, IV, and V), by an automated device with a microphone over the brachial artery (equivalent to Korotkoff I and V), and by graphical analysis of these microphone signals (equivalent to Korotkoff I and IV). Eating caused a rise in mean heart rate, a small rise in systolic blood pressure, and a decrease in diastolic blood pressure, which was overestimated when Korotkoff V rather than Korotkoff IV endpoints were considered. Both the automated device and the graphical analysis yielded acceptable overall quantitative agreement with the auscultatory method. Both alternative methods allowed similar postprandial blood pressure trends to be detected, but the quantitative agreement in estimating the postprandial effects was far less optimal. Eating therefore was shown to cause changes that might distort and confuse the interpretation of cardiovascular data in studies in which subjects are allowed to eat. This source of bias itself appeared to be affected by its own methodological bias.

Adult↗