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Biomedical subjects

M Priesnitz

Publications and source records attributed to M Priesnitz.

7 recordsLinked to original sources
PubMed1994

Effect of BAY x 7195, an oral receptor antagonist of cysteinyl-leukotrienes, on leukotriene D4-induced bronchoconstriction in normal volunteers.

Leukotrienes (LT) have been proposed to play an important role in the pathogenesis of asthma. This paper reports the results of two studies investigating the effect of BAY x 7195, a new oral receptor antagonist of cysteinyl-leukotrienes, on LTD4-induced bronchoconstriction in healthy male volunteers. Using a double-blind, placebo-controlled, crossover design, volunteers received 250 mg (n = 6; study 1) and 100 and 500 mg (n = 6; study 2) of BAY x 7195. Bronchoprovocation with nebulized LTD4 was performed 2 (250 mg) and 2 and 8 (100 and 500 mg) h p.a. The specific airway's conductance (SGaw) was used to assess the airway's response. Blood samples to determine plasma concentrations of BAY x 7195 were taken at the end of bronchoprovocation. BAY x 7195 showed no effect on baseline lung function. Compared to placebo, the different doses of BAY x 7195 increased the concentration of LTD4 needed to produce a 35% decrease in SGaw 2 h p.a. between 1- and 23-fold. Eight hours p.a., 100 and 500 mg caused shifts in the concentration-response curve of between 1- and 13-fold. There was no predictive relationship between plasma concentrations of BAY x 7195 and the response to LTD4 challenge. However, there was a relationship between dose and effect. No relevant adverse effects were reported. In conclusion, the present results suggest that BAY x 7195 is an effective LTD4-receptor antagonist in man.

Administration, Inhalation↗
PubMed1992

[Multiple evanescent white dot syndrome].

A 38-year-old male patient experienced a unilateral visual acuity decrease to 20/60 and showed white dots at the level of the retinal pigment epithelial interface characteristic of multiple evanescent white dot-syndrome. Fluorescein angiography demonstrated early hyperfluorescent defects and some late staining. In spite of improvement of the visual acuity and the alterations of the fundus, an enlargement of the blind spot and some sharply demarcated depigmentations of the retinal pigment epithelium remain. This case shows, that already at the beginning of symptoms the characteristic white dots may be present. Enlargement of the blind spot and depigmentations of the retinal pigment epithelium may remain as defects after multiple evanescent white dot-syndrome.

Adult↗
PubMed1991

Fibrin degradation product D-dimer in the diagnosis of pulmonary embolism.

The study objective was to determine the specificity and sensitivity of plasma concentrations of D-dimer, a fibrin degradation product, as a marker for ongoing thrombotic and thrombolytic events in pulmonary embolism. A prospective study was performed in 74 patients with suspected pulmonary embolism who appeared in the emergency room with dyspnea and/or chest pain. The presence of pulmonary embolism was established by positive findings either in pulmonary angiography or lung scan. D-dimer concentrations were determined in all patients. In 11 patients with positive pulmonary angiography, D-dimer concentrations were monitored for 6-12 days. D-dimer concentrations were determined by a quantitative enzyme-linked immunoassay. Plasma probes of 26 patients (16 with/10 without positive pulmonary angiography) were re-assayed with a semiquantitative latex agglutination assay. D-dimer levels were significantly higher in patients with pulmonary embolism (greater than 1000 ng/mL in 41 out of 43) than in those without (less than 1000 ng/mL in all 21 patients) (p less than 0.01). The sensitivity and specificity for the ELISA were found to be 95% and 100%, respectively, for establishing the diagnosis of pulmonary embolism. In the latex assay the values were 81% and 60%, respectively. It is concluded that in patients with dyspnea and/or chest pain, determination of D-dimer in plasma by ELISA adds a valuable tool to the noninvasive diagnostic procedure for pulmonary embolism. From the time-course of D-dimer values we conclude that this assay might be valuable up to at least 6 days after symptom onset. The assay, however, is unreliable in malignancies or after surgery.

Adult↗
PubMed1985

Follow-up of prostaglandin plasma levels after acute myocardial infarction.

Prostaglandin plasma levels are elevated in patients with transient myocardial ischemia. We measured 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane (B2(TXB2) in venous blood of 32 patients with myocardial infarction on the first, third, and seventh days. TXB2 and 6-keto-PGF1 alpha levels in these patients (up to 117 +/- 237 pg/ml and 96 +/- 105 pg/ml mean +/- SD, respectively) differed significantly from levels in normal control subjects (10 +/- 12 pg/ml and 4 +/- 7 pg/ml mean +/- SD, respectively) (p less than 0.01). Prostaglandin values remained elevated from day 1 through day 7. In most patients, 6-keto-PGF1 alpha levels prevailed over those of TXB2. In a subgroup suffering from cardiac arrhythmias, the ratio of 6-keto-PGF1 alpha/TXB2 was inverse. It is concluded that prostaglandin generation is increased for at least 7 days after myocardial infarction. A disturbed ratio of 6-keto-PGF1 alpha/TXB2 in favor of the latter might be associated with cardiac arrhythmias in myocardial infarction.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Pressure effects and uptake of platelet-activating factor in isolated rat lung.

The aim of this study was, first, to examine pressure effects of platelet-activating factor (PAF) on pulmonary vasculature and bronchi in isolated perfused and ventilated rat lungs and, second, to investigate pulmonary uptake of tritium-labeled PAF injected into the pulmonary artery. Four different perfusates were used: Krebs-Ringer solution (KRS) and KRS with 0.2, 2.0, and 4% albumin. In the KRS, perfusion and inflation pressure increased by 100 and 47%, respectively, after 100 micrograms PAF. By increasing the albumin concentration, the pressure effects were reduced significantly (P less than 0.01). These changes were paralleled by increasing tritium outflow rates (15.9 +/- 3.6, 49.7 +/- 12.5, 78.3 +/- 8.7, 87.8 +/- 2.6%, respectively). Comparable changes in tritium outflow rates (19.2 +/- 3.9, 38.2 +/- 7.2%) occurred when tracer amounts of labeled PAF were injected, but, in KRS with 2.0 and 4.0% albumin, tritium outflow was significantly lower (52.8 +/- 8.0 and 60.8 +/- 11.8%, respectively). Pressure effects are related to extraction rates. Both pressure effects and extraction rates depend on binding to the albumin in the perfusion medium used. PAF might act on smooth muscle tissue of the pulmonary vasculature. Inflation pressure increases are probably due to concomitant occurrence of edema.

Animals↗
PubMed1984

Prostaglandin production in patients with pulmonary embolism.

Release of prostaglandins (PG's) after experimental pulmonary embolism has been reported. Therefore, prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were determined in venous plasma of 21 patients with acute pulmonary embolism. Venous plasma levels were followed up for one week after admission. Arterial and mixed-venous PG levels were additionally determined in 6 patients with acute pulmonary embolism prior to pulmonary angiography. Venous levels were substantially elevated (PGE2 16-1300, PGF2 alpha 48-592, TXB2 1-247, 6-ketoPGF1 alpha 1-248 pg/ml), differing significantly from normal controls (p less than 0.001). PG's remained elevated throughout the 7-day postadmission study period. No significant arterial-venous PG differences were detected, though 6-keto-PGF1 alpha and TXB2 levels were somewhat higher in arterial blood. There was no correlation between clinical data (blood pressure, mean pulmonary artery pressure, etc.) and PG levels. These data suggest that elevated prostaglandin levels are probably not, or only in part, responsible for the cardiopulmonary changes that occur in patients with acute pulmonary embolism.

6-Ketoprostaglandin F1 alpha↗