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Biomedical subjects

O Hansen

Publications and source records attributed to O Hansen.

At least 127 records · Page 7Linked to original sources
PubMed1991

Identification of cases of myocardial infarction: hospital discharge data and mortality data compared to myocardial infarction community registers.

Identification of incident myocardial infarction (MI) cases in a defined population using hospital discharge data and mortality data in combination has been suggested. This method of case identification was compared to that of use of MI community registers set up in accordance with principles adopted in a World Health Organization collaborative programme. The comparison comprised data for four Swedish cities over a number of years. On average 81% of incident hospital-treated cases below 65 years of age identified through MI community registers were found by the retrospective use of the method based on hospital discharge data and mortality data. Of hospital-treated cases identified by the latter method, 83% were also found by the MI community registers. For cases fulfilling the diagnostic criteria employed by the MI community registers this proportion would be higher, probably 87%-92%. Several reasons for cases being missed by either method were suggested by the results. According to the findings of this study, the case identification of the method based on hospital discharge data and mortality data seems to be somewhat less efficient compared to use of MI community registers. This may be of importance in descriptive epidemiological studies, but is of less significance in analytical studies. The relative efficiency of the former method could be improved by a more reliable system for the recording of hospital discharges. If supplemented by a validation procedure, it could yield sufficiently accurate data for many epidemiological applications at a fairly low cost.

Acute Disease↗
PubMed1991

Metabolic, hemodynamic, and electrocardiographic responses to increased circulating adrenaline: effects of pretreatment with class 1 antiarrhythmics.

In order to study the effects of treatment with class 1 antiarrhythmics on the metabolic, hemodynamic, and electrocardiographic responses to adrenaline, 12 healthy volunteers were infused on four occasions, after pretreatment with placebo, disopyramide, mexiletine, and flecainide, respectively, with adrenaline at a rate producing serum adrenaline concentrations comparable with those seen in acute myocardial infarction. After pretreatment with placebo adrenaline caused significant falls in serum potassium, serum magnesium, serum calcium, and serum phosphate and a significant increase in blood glucose. Adrenaline also caused a significant increase in heart rate and systolic blood pressure and a significant fall in diastolic blood pressure. On the electrocardiogram a significant prolongation of QTc duration and a flattening of the T-wave amplitude were seen. Pretreatment with disopyramide had no effect on the hemodynamic response to adrenaline but caused a significant prolongation of Qtc duration before the adrenaline infusion. Pretreatment with mexiletine was associated with a significantly greater fall in serum potassium during adrenaline infusion, and pretreatment with flecainide with a greater fall in serum magnesium, as compared with placebo pretreatment Flecainide also caused a significant prolongation of the QRS duration before adrenalin infusion, and after all the active pretreatments a prolongation of QRS duration was seen during adrenaline infusion. The metabolic and hemodynamic changes during adrenaline infusion may not only reduce the antiarrhythmic efficacy of antiarrhythmics but may also increase the risk of proarrhythmic effects in a clinical setting. These results may help to explain why treatment with antiarrhythmics seems to be without beneficial effect on mortality in post-myocardial infarction patients.

Adult↗
PubMed1990

Systemic cytotoxic therapy of basal cell carcinoma. A review of the literature.

Fifty-five cases of systemic, cytotoxic therapy of patients with basal cell carcinoma have been reported in 53 patients in the English literature since the first report in 1960. Cytotoxic therapy without cis-platinum was used in 28 cases, resulting in only one partial response. On the contrary, 17 out of 22 evaluable patients (77%) responded to systemic treatment with cis-platinum-containing regimens. In 10 patients (45%) complete disappearance of the tumor was noted. These patients survived for a median time of more than 22 months (range 4+ to 51+ months). Although the experience is limited, the use of cis-platinum-containing regimens seems justified in the rare instances of metastatic disease, or when local treatment fails. When the primary tumor is very large, pretreatment with cis-platinum alone or in combination might be of value.

Adult↗
PubMed1990

Metabolic, electrocardiographic, and hemodynamic responses to increased circulating adrenaline: effects of selective and nonselective beta adrenoceptor blockade.

Twelve healthy male volunteers were given adrenaline infusions, 0.05 microgram/kg body weight/minute over one hundred twenty minutes (min), in order to achieve serum adrenaline concentrations comparable with those seen in acute myocardial infarction. The infusions were given on three occasions, at intervals of at least four weeks. Before the infusions the subjects were given, in random order, two days' pretreatment with placebo, a beta-1-selective adrenoceptor blocker (atenolol), or a nonselective beta blocker (propranolol) with each subject receiving each pretreatment. Six of the volunteers also had a fourth adrenaline infusion, after two days' pretreatment with a beta-2-selective beta blocker, ICI 118551. Adrenaline increased heart rate by 11 beats/min, increased systolic blood pressure by 10 mmHg, and decreased diastolic blood pressure by 15 mmHg. These changes were partly prevented by atenolol. Propranolol and ICI 118551 partly prevented the rise in systolic blood pressure but differed from atenolol in their effects on heart rate and diastolic blood pressure, causing falls in heart rate by 7 beats/min and 12 beats/min respectively, secondary perhaps to increases in diastolic blood pressure by 13 mmHg and 17 mmHg respectively. Adrenaline caused a prolongation of QTc duration by 0.03 second and a flattening of the T-wave amplitude by 1.04 mm. These changes in cardiac repolarization were partly inhibited by atenolol, but the effects of propranolol and ICI 118551 were greater, each causing a reduction of QTc and an increase in T-wave amplitude. During adrenaline infusion S-potassium declined by 0.60 mmol/L, S-magnesium by 0.05, S-calcium by 0.10, and S-phosphate by 0.24, but S-free fatty acids increased nearly threefold. All these changes were statistically significant and were presumably mediated mainly by the beta-2-adrenoceptor, for they were blocked more effectively by the beta-2-adrenoceptor blockers than by the selective beta-1-adrenoceptor blocker. B-glucose increased by 4.1 mmol/L, the increase being practically unaffected by the different pretreatments. These adrenaline-induced hemodynamic, electrocardiographic, and metabolic changes may predispose to arrhythmias and impair cardiac performance after a myocardial infarction. Nonselective beta blockers may be more effective in blocking the electrocardiographic and metabolic effects, but beta-1-selective beta blockers may have hemodynamic advantages.

Adrenergic beta-Antagonists↗
PubMed1990

Effect of prophylactic sucralfate suspension on stomatitis induced by cancer chemotherapy. A randomized, double-blind cross-over study.

We have studied whether mouth-swishing with sucralfate, a well-known gastric mucosal protective agent, may be used as prophylaxis against chemotherapy-induced stomatitis. Using radioactively labelled sucralfate we found that 20-30% was still bound to the oral mucosal lining 2 1/2 h after mouth-swishing. Forty patients receiving cisplatin and continuous infusion with 5-fluorouracil (5-FU) for 5 days entered a double-blind placebo-controlled cross-over study. Among 23 evaluable patients a significant reduction (p = 0.04) in an objective score of edema, erythema, erosion and ulcerations was seen during treatment with sucralfate. Patient preference favored sucralfate, but this preference failed to reach statistical significance (p = 0.06). Seven patients were inevaluable for reasons not associated with the study treatment. However, ten patients did not complete the study since the swishing procedure aggravated chemotherapy-induced nausea. An equal rate of non-compliance was seen with sucralfate and placebo. To overcome this problem, the oral medication should have a neutral taste, the solution should not be swallowed after the swishing, which should not be started until the nausea had ceased.

Adult↗
PubMed1989

Characterization of fatty acid interaction with ouabain and vanadate binding to (Na+ + K+)-activated ATPase.

The candidateship of unsaturated fatty acids as endogenous ouabain-like factors was studied. Binding of the artificial ligand vanadate at the intracellular phosphorylation epitope of membrane-bound Na+/K+-ATPase was unaffected by linoleic and arachidonic acid. In the (Mg2+ + Pi)-facilitated system for ouabain binding they were characterized as noncompetitive inhibitors of cardiac glycoside binding, however. The ouabain binding capacity as well as the affinity decreased and the ouabain dissociation rate was accelerated by fatty acids. In the presence of vanadate for facilitation of ouabain binding an increase in ouabain affinity was seen. It is concluded that elementary criteria for the characterization of unsaturated fatty acids as ouabain-like factors are not fulfilled. The ratio between E2-subconformations of Na+/K+-ATPase with different ouabain affinities may be changed by incorporation of fatty acids in the lipid membrane.

Animals↗
PubMed1989

Quantitative determination of Ca2+-dependent Mg2+-ATPase from sarcoplasmic reticulum in muscle biopsies.

The possibility of quantifying the total concentration of Ca2+-dependent Mg2+-ATPase of sarcoplasmic reticulum was investigated by measurement of the Ca2+-dependent steady-state phosphorylation from [gamma-32P]ATP and the Ca2+-dependent 3-O-methylfluorescein phosphatase (3-O-MFPase) activity in crude muscle homogenates. The Ca2+-dependent phosphorylation at 0 degree C (mean +/- S.E.) was 40.0 +/- 2.5 (n = 6) and 6.2 +/- 0.7 (n = 4) nmol/g wet wt. in rat extensor digitorum longus (EDL) and soleus muscle, respectively (P less than 0.001). The Ca2+-dependent 3-O-MFPase activity at 37 degrees C was 1424 +/- 238 (n = 6) and 335 +/- 56 (n = 4) nmol/min per g wet wt. in rat EDL and soleus muscle, respectively (P less than 0.01). The molecular activity calculated from these measurements amounted to 35 +/- 5 min-1 (n = 6) and 55 +/- 10 min-1 (n = 4) for EDL and soleus muscle respectively. These values were not different from the molecular activity calculated for purified Ca2+-ATPase (36 min-1). The Ca2+-dependent 32P incorporation in soleus muscle decreased in the order mice greater than rats greater than guinea pigs. In EDL muscles from hypothyroid rats at a 30% reduction of the Ca2+-dependent phosphorylation was observed. The Ca2+-dependent phosphorylation in vastus lateralis muscle from three human subjects amounted to 4.5 +/- 0.8 nmol/g wet wt. It is concluded that measurement of the Ca2+-dependent phosphorylation allows rapid and reproducible quantification of the concentration of Ca2+-dependent Mg2+-ATPase of sarcoplasmic reticulum. Since only 20-60 mg of tissue is required for the measurements, the method can also be used for biopsies obtained in clinical studies.

Animals↗
PubMed1989

S-Mg does not change inversely to S-FFA during acute stress situations.

The apparently divergent changes in serum magnesium (S-Mg) and serum free fatty acids (S-FFA) in stress situations associated with elevated levels of circulating adrenaline were studied experimentally in 12 healthy volunteers, who were each given three adrenaline infusions (0.05 micrograms/kg bw/min over one hundred twenty minutes). Before the adrenaline infusions the volunteers were treated for three days with either a non-selective beta-blocking agent (propranolol) or a beta-1-selective agent (atenolol) or with placebo. Six of the volunteers underwent a fourth adrenaline infusion after pretreatment with a beta-2-selective beta-blocking agent (ICI 118551). S-Mg and S-FFA were determined every fifteen minutes. After pretreatment with placebo, adrenaline infusion caused an increase in S-FFA from 0.22 +/- 0.20 mmol/L (mean +/- SD) to max 0.59 +/- 0.39 mmol/L after thirty minutes of adrenaline infusion (p less than 0.001). At one hundred twenty minutes S-FFA had decreased to 0.35 +/- 0.26 mmol/L. Thirty minutes after cessation of the adrenaline infusion, S-FFA had returned to the same level as before the infusion. S-Mg before the adrenaline infusion was 0.83 +/- 0.05 mmol/L, rose to 0.85 +/- 0.05 at fifteen minutes, and then decreased to 0.78 +/- 0.05 at one hundred thirty-five minutes (p less than 0.05). Pretreatment with atenolol did not change this pattern, although the changes in S-FFA and S-Mg were of a smaller magnitude but still statistically significant.

Acute Disease↗
PubMed1988

Traffic a source of lead exposure in childhood.

Experimental and observational data has long implicated automobile exhaust from leaded petrol as a major source of human lead exposure. The present study evaluates the association of individual traffic exposure with individual lead absorption. A case-referent study was carried out on 1302 out of 2412 children in the municipality of Aarhus - Denmark. Shed deciduous teeth were matched for sex and socioeconomic status. Individual lead sources were assessed by an interview. Information on former addresses and the data of address change was obtained as was information on the daily number of cars driving on all roads of the city. A traffic index was constructed describing the traffic density at the home. An association between high lead and high traffic density was found in the children at the age of 6 months to 2 years. This relationship was of a dose-response nature. The association was not account for by other possible major sources.

Child↗
PubMed1988

Quantitative determination of Na+-K+-ATPase and other sarcolemmal components in muscle cells.

A recurring problem in the characterization of plasma membrane enzymes in tissues and cells is whether the samples tested are representative for the entire population of enzyme molecules present in the starting material. Measurements of [3H]-ouabain binding, enzyme activity, and maximum transport capacity all indicate that the concentration of Na+-K+ pumps in mammalian skeletal muscle is high (300-800 pmol/g wet wt). Studies on Na+-K+-ATPase activity in isolated sarcolemma, however, generally give little or no information on total cellular enzyme concentration. Due to the low and variable enzyme recovery (0.2-8.9%), such subcellular preparations may, therefore, give misleading data on factors regulating Na+-K+-ATPase in heart and skeletal muscle cells. As the same isolation and purification procedures are used for the study of other sarcolemmal components (lipids, hormone receptors, enzymes, and other transport systems), this inadequate recovery has general implications for statements on regulatory changes in the sarcolemmal composition of muscle cells. On the other hand, complete quantification of Na+-K+-ATPase in muscle tissue can now be achieved using simple procedures and the entire material (intact muscle fibers, biopsies, and whole homogenates). Recent studies have shown that regulatory changes in the entire population of Na+-K+ pumps in muscle can be quantified in measurements of [3H]-ouabain binding, K+-activated 3-O-methylfluorescein phosphatase activity, as well as maximum ouabain suppressible Na+-K+ transport capacity.

Animals↗
PubMed1988

Adrenaline-induced changes in serum electrolytes, ECG, and blood pressure, with Ca-blockade pretreatment.

Adrenaline infusions (AI) (0.5 micrograms adrenaline per 10 kg body weight per minute over 120 minutes) were given weekly for three weeks to 20 healthy male volunteers aged twenty-one to thirty-eight years. The AI was given after three days' treatment with diltiazem (D), verapamil (V), or placebo (PI) in a single-blind fashion. After pretreatment with Pl, serum potassium (s-K) decreased from 3.93 +/- 0.30 mmol/L (M +/- SD) to 3.33 +/- 0.31 (P less than 0.001) with the greatest change 69.75 +/- 46.24 minutes after the start of the AI. Corresponding values for s-Mg were 0.84 +/- 0.06 to 0.78 +/- 0.05 (P less than 0.01) and 106.50 +/- 36.71 minutes, for s-Ca 2.40 +/- 0.07 to 2.30 +/- 0.08 (P less than 0.01) and 103.50 +/- 36.06 minutes, for s-P 1.05 +/- 0.17 to 0.91 +/- 0.17 (P less than 0.02) and 80.25 +/- 47.25 minutes, and for s-urate 344.79 +/- 50.55 to 329.26 +/- 47.80 (P greater than 0.05) and 63.95 +/- 46.05 minutes. After pretreatment with D, AI produced similar electrolyte changes as after Pl, but the rise in blood glucose was slightly more pronounced and the drop in s-urate less pronounced. The heart rate (HR) before AI after pretreatment with D was lower than after Pl, but the increase during the AI was of the same magnitude. The AI-induced changes in systolic (SBP) and diastolic (DBP) blood pressure after D did not differ significantly from those seen after Pl, and neither did QT and QTc, whereas the PR duration was prolonged (0.18 +/- 0.03 second) when compared with Pl (0.16 +/- 0.02) (P less than 0.05). Although the magnitude of the change in DBP was not influenced, V prolonged the time till the lowest DBP (48.95 +/- 26.38 minutes) when compared with Pl (31.50 +/- 29.16 minutes) (P greater than 0.05). The other variables followed the same pattern as for D. In conclusion AI in healthy volunteers produced a drop in s-K but in addition a drop in s-Mg and s-Ca, the latter appearing later than the drop in s-K. Pretreatment with diltiazem and verapamil did not influence the magnitude of these changes but reduced the drop in s-urate.

Adult↗