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Biomedical subjects

J Neumann

Publications and source records attributed to J Neumann.

At least 217 records · Page 12Linked to original sources
PubMed1989

[A historico-social approach to the medical scientific theory of Ludwik Fleck (1896-1961)].

Ludwik Fleck has shown in his discussion of the logical empirism of the Vienna Circle that his concept of reality presupposes an unproven logico-structural correspondence between the world and the formal logical structure of language, i.e. between reality and thought. Upon this questionable foundation he proceeds to develop his own position concerning the theory of medical science. He claims that scientific knowledge is at no time exempt from cultural, historical and social conditions, of which scientific knowledge itself is a function. These conditions find expression in the style of thought of a particular epoch ("Denkstil") as well as in the interaction of the participating scientists ("Denkkollektiv"). Flecks merits for having explicated the conditionality of the process of scientific knowledge over against positivistic thought have been honourably elaborated in many studies. The present study offers an analysis of the manner in which the Fleck position attempts to serve as an explanation of change in the content and style of thought in history. It will be made clear that these changes and developments can only be explained as the result of the interaction and competition among the collectives of scientists and thinkers. Fleck deprives his socio-historical position of its logical foundation by radicalizing these conditions in such a manner that they become fundamental determinants of human thought generally and for the individual scientist particularly. As a consequence, from the perspective in which the thought of the individual is thus determined, he can neither establish a convincing theory for changes in thought in history nor for the human relations obtaining within the collective of scientists and thinkers.

Austria↗
PubMed1988

Increase in myocardial Gi-proteins in heart failure.

The contractile response and myocardial content of Gi-proteins were examined in cardiac preparations from explanted hearts of four different patients with end-stage heart failure. Three patients had idiopathic dilated cardiomyopathy and one patient had inflammatory heart disease. Preparations from patients with idiopathic dilated cardiomyopathy showed reduced contractile response to the cAMP-increasing agent isoprenaline and an increase in myocardial Gi-proteins, compared with preparations from non-failing hearts. Therefore it is conceivable that an increase in myocardial Gi-proteins is causally related to heart failure due to idiopathic dilated cardiomyopathy. In the preparation from the patient with inflammatory heart disease the contractile response to isoprenaline was not reduced and likewise content of Gi-proteins was not changed.

Cardiomyopathy, Dilated↗
PubMed1988

The effects of roxatidine acetate (HOE-760) on 24-hour intragastric acidity in healthy volunteers: comparison with ranitidine and placebo.

In a series of double-blind randomized studies in normal volunteers using continuous intragastric pH monitoring, the effects of different dosage regimens of roxatidine, a new H2-receptor antagonist, were compared with placebo and ranitidine. Roxatidine acetate, 75 mg twice daily, decreased median 24 h gastric acidity from pH 1.6 to 3.2 and median nocturnal acidity from 1.5 to 3.0. Roxatidine acetate, 150 mg at bedtime, raised median 24 pH of the same 17 subjects to 2.4 and nocturnal pH to 5.9. In another series of experiments, 150 mg roxatidine acetate at bedtime was as effective as ranitidine 300 mg nocte raising median nocturnal pH (14 volunteers) from 1.4 to 6.65 compared to 6.7, respectively. However, when drugs were taken after the evening meal (post cenam nocte, pcn) roxatidine acetate 150 mg was less potent than ranitidine 300 mg with median night-time pH rising from 1.3 to 3.2 and 4.0, respectively, in 28 volunteers. Roxatidine acetate 300 mg pcn raised the pH to 4.9 suggesting that roxatidine is 1-2 times as potent as ranitidine, on a milligram-for-milligram basis.

Adolescent↗
PubMed1988

Adenosine inhibits the positive inotropic effect of 3-isobutyl-1-methylxanthine in papillary muscles without effect on cyclic AMP or cyclic GMP.

1 Adenosine and the adenosine receptor agonist (-)-N6-phenylisopropyladenosine (PIA) produced a small positive and negative inotropic effect, respectively, in isolated electrically driven papillary muscles of guinea-pigs. 2 Adenosine (100 mumol l-1) had no effect on cyclic AMP or cyclic GMP content. PIA (100 mumol l-1) slightly increased cyclic AMP. 3 In the presence of 3-isobutyl-1-methylxanthine (IBMX; 60 mumol l-1), which increased force of contraction 2 fold, adenosine and PIA exerted strong negative inotropic effects. PIA was more potent than adenosine (mean IC25 2.1 and 168 mumol -1, respectively). 4 In contrast, the nucleosides did not affect the increase in force of contraction produced by elevating extracellular Ca2+ concentration. 5 The IBMX-antagonistic effects of adenosine and PIA were not accompanied by modification of the IBMX-induced increase in cyclic AMP and cyclic GMP. 6 The effects of adenosine and PIA on force of contraction were accompanied by a partial reversal of the IBMX-induced increase in the maximal rate of depolarization of slow action potentials. 7 It is concluded that adenosine and PIA are able to attenuate the positive inotropic effect of a phosphodiesterase inhibitor. This effect is unlikely to be due to a reduction of the IBMX-induced increase in cyclic AMP content. It is conceivably due to an inhibition of the stimulant action of cyclic AMP on slow Ca2+ channels leading to the reduction of the slow inward current which in turn reduces force of contraction.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Double blind comparison of the effects of cimetidine, ranitidine, famotidine, and placebo on intragastric acidity in 30 normal volunteers.

Continuous measurement of 24 hour intragastric acidity was carried out in 30 normal volunteers during treatment with placebo, cimetidine 800 mg, ranitidine 300 mg, and famotidine 40 mg in a double blind study. Medication was taken after the evening meal (post cenam nocte, PCN). Median 24 hour acidity decreased with all H2-receptor antagonists from 25.1 mmol/l on placebo to 10 mmol/l (-60.1%) during cimetidine, to 3.2 mmol/l (-87.25%) during ranitidine and to 2.5 mmol/l (-90.0%) during famotidine treatment (p less than 0.0005). All drugs significantly inhibited night time acidity but only famotidine decreased acidity during the late morning compared with placebo. Significantly greater acid reduction was seen with famotidine and ranitidine compared with cimetidine but no difference was found between famotidine and ranitidine.

Cimetidine↗
PubMed1988

Continuous intravenous infusions of famotidine maintain high intragastric pH in duodenal ulcer.

Three double blind crossover studies were carried out to assess the ability of primed infusions of famotidine to raise intragastric pH over 24 hours in 12 duodenal ulcer patients. pH was measured continuously using intragastric electrodes and solid state recording devices. The studies compared the effects of placebo, famotidine 10 mg bolus injection iv followed by continuous infusions of 3.2 mg/h and 4 mg/h in random order. Gastric acidity decreased significantly with both dose regimens (p less than 0.0005) but the effects of either dosage were similar. During fasting median pH rose from 1.35 to 7.1 and 7.05 respectively. During the day, when standard meals were taken, median pH rose from 1.30 to 4.3 and 3.65 respectively. Despite continuous infusions the H2-antagonist was less effective during this time. The latter finding raises questions about gastric secretory control during the day when food is eaten.

Adult↗
PubMed1988

The effects of roxatidine acetate on 24-hour intragastric acidity. Investigations in healthy volunteers and comparison with ranitidine and placebo.

In a series of double-blind randomised studies in normal volunteers with continuous intragastric pH monitoring, the effects of different dosage regimens of roxatidine acetate, a new H2-receptor antagonist, were compared with placebo and ranitidine. Roxatidine acetate 75 mg twice daily decreased median 24-hour gastric acidity from pH 1.6 to 3.2 and median nocturnal acidity from 1.5 to 3.0. Roxatidine acetate 150 mg at bedtime raised median 24-hour pH in the same 17 subjects to 2.4 and nocturnal pH to 5.9. In the second experiment, in 14 volunteers, roxatidine acetate 150 mg at bedtime was as effective as ranitidine 300 mg at night, raising median nocturnal pH from 1.4 to 6.65 compared to 6.7 for ranitidine. However, when drugs were taken after the evening meal (post cenam nocte; PCN) roxatidine acetate 150 mg was less potent than ranitidine 300 mg, with median night-time pH rising from 1.3 to 3.2 and 4.0, respectively, in 28 volunteers. Roxatidine acetate 300 mg PCN produced the greatest rise of pH, to 4.9, suggesting that the true potency ratio of the 2 drugs is between 1 and 2.

Adolescent↗
PubMed1988

Assessment of intragastric acidity in man: modern aspects, reproducibility of intragastric pH-monitoring, and pharmacodynamic results obtained with H2-receptor antagonists.

Unlike other methods for assessing intragastric pH or total acid output, the reproducibility of ambulatory pH-monitoring is excellent but is critically dependent on the electrode system and the recording device. In three double-blind randomized studies in normal volunteers the effects of different dosage regimens of roxatidine acetate were compared with placebo and ranitidine. Roxatidine acetate, 75 mg twice daily, raised median 24-h gastric pH from 1.6 to 3.2 and median nocturnal pH from 1.5 to 3.0 Roxatidine acetate, 150 mg at bedtime, raised median 24-h pH to 2.4 and nocturnal pH to 5.9. Roxatidine acetate, 150 mg at bedtime, was as effective as ranitidine, 300 mg at night, in raising median nocturnal pH. However, when drugs were taken after the evening meal, 150 mg roxatidine acetate was less potent than 300 mg ranitidine or 300 mg roxatidine acetate.

Clinical Trials as Topic↗
PubMed1988

[Extracorporeal blood circulation in the unanesthetized free-moving rabbit--an animal model for biocompatibility studies].

The rabbit is suitable as a basis model for the extracorporal circuit (ECC) in long-term test (20 days). A decrease of the leucocytes and platelets is established already in the blank test qualified by catheter material and pumping influence. This effect can be compensated by the rabbit in long-term test. The typical decrease of the leucocytes and platelets does not show any significant alteration during many test days independent of the number of tests which were carried out in one rabbit (blank test and hemoperfusion). A hemoperfusion across activated carbon--independent of the albumin coating--leads to a significant decrease of the leucocytes in comparison to the blank test. This rabbit model is well-suitable for biocompatibility investigations respectively also for effective investigations of detoxication techniques taken as a basis of our results.

Animals↗
PubMed1987

Comparison of ranitidine 300 mg twice daily, 300 mg at night and placebo on 24-hour intragastric acidity of duodenal ulcer patients.

Continuous measurement of 24-hour intragastric acidity was performed in 12 duodenal ulcer patients in remission during treatment with placebo, ranitidine 300 mg nocte and ranitidine 300 mg b.d. Median 24-hour acidity was 79.4 mmol litre-1 during placebo treatment; it decreased to 28.2 mmol litre-1 during treatment with ranitidine 300 mg nocte and to 3.6 mmol litre-1 during treatment with ranitidine 300 mg b.d. The two regimens decreased intragastric acidity to a similar degree during the night, but significantly greater inhibition of daytime and 24-hour acidity followed use of ranitidine 300 mg b.d.

Adult↗
PubMed1987

Single dose treatment with H2 receptor antagonists: is bedtime administration too late?

Using ambulatory ph-metry, intragastric acidity was measured over three separate 24 hour periods in each of 12 healthy volunteers receiving either (a) placebo (1800 h and 2200 h), (b) 300 mg ranitidine (1800 h) and placebo (2200 h), or (c) placebo (1800 h) and 300 mg ranitidine (2200 h). Ranitidine was significantly more effective in decreasing 24 h median intragastric acidity when the drug was administered at 1800 h rather than at 2200 h. Median pH (and interquartile range) was 1.45 (1.4-1.7) on placebo, 2.55 (2.05-3.2) on ranitidine given at 2200 h and 3.35 (2.5-3.85) on ranitidine given at 1800 h (p less than 0.004). The total duration of highly acidic electrode readings (pH less than 1.5) over a 24 h period was reduced significantly by administering the H2-receptor antagonist at 1800 h compared with the later administration. It is suggested that treatment of duodenal ulcers by single administration of ranitidine in the early evening should be evaluated by clinical trial.

Adult↗