On the mechanisms of adenosine induced pulmonary vasoconstriction in rats

The effect of adenosine on pulmonary vessels was studied in isolated perfused rat lungs. Drugs were administered intra-arterially in a fixed volume of 0.1 ml Krebs solution as bolus injections. Adenosine responses were obtained before and 10 min after drug injections. When applied in logarithmically increasing doses (1-100 micrograms/ml), adenosine caused dose-dependent increases in pulmonary perfusion pressure (e.g. pulmonary vasoconstriction) which were readily reversible. Challenging adenosine with quinidine, dihydroergocristine and cyproheptadine (2 micrograms/ml each) did not significantly alter adenosine responses. Pretreatment of lungs with 0.5 mM theophylline, 10 micrograms/ml indomethacin, 30 micrograms/ml tebokan (a PAF antagonist) or 1 microgram/ml methylene blue for 10 min, however, antagonized the vasoconstrictor effect of the drug significantly. From these experiments, it was concluded that the mechanisms underlying the pulmonary vasoconstrictor action of adenosine are complex, and that both types of purinoceptors, prostaglandins, PAF and other vascular endothelial hormones might be involved.     

Thermochemical investigation of binary liquid mixtures in glass-forming oxide systems

Methods and equipment successfully employed in high- temperature calorimetry to measure partial and integral enthalpies of mixing in liquid oxide systems are reviewed with special attention given to the drop-mixing method. This technique has been used to measure enthalpies of mixing in binary liq-uid mixtures composed of network forming oxides (e.g. SiO₂) and network modifying oxides (e.g. Na₂O). Results for the systems Na₂O-SiO₂ and Na₂O- B₂O₃ are presented graphically. Entropies of mixing were estimated by combining enthalpies with available data on Gibbs energies of mixing. Prominent thermochemical features of glass-forming oxide melts are pointed out. The observed thermodynamic behavior is discussed in relation to its structural basis.     

Fluorescence flow cytometry of human leukocytes in the detection of LDL receptor defects in the differential diagnosis of hypercholesterolemia

A flow-cytometric method with fluorescence-labeled monoclonal antibodies (MABs) against the low density lipoprotein (LDL) receptor (C7A MAB) or 3,3'-dioctadecylindocarbocyanin-iodide (DiI) LDL has been developed that allows the quantification of LDL receptors on leukocytes and the identification of patients with familial hypercholesterolemia (FH) within 48 hours. Leukocytes were isolated from 10 mL anticoagulated blood by density gradient centrifugation. To induce maximal expression of LDL receptors, mononuclear cells were preincubated with either phytohemagglutinine (PHA) or lipoprotein-deficient serum (LPDS). LPDS-treated monocytes provided a more homogeneous cell population with regard to LDL receptor activity than did the PHA-treated lymphocytes; they also provided a greater discrimination between the fluorescence of the receptor probes and cellular autofluorescence. The C7A MAB was able to compete for DiI LDL binding by about 40%. In competition with unlabeled LDL, DiI LDL revealed linear binding, indicating an affinity similar to native LDL. The binding characteristics of DiI LDL were also similar to 125I-LDL binding. LDL isolated from familial defective apolipoprotein B-100 was not able to compete for DiI LDL binding on monocytes, whereas native LDL reduced it by about 80%. In monocytes from FH heterozygous patients, the cellular mean fluorescence using either C7A MAB or DiI LDL at 4 degrees C was 30% to 70%; in FH homozygotes, cellular mean fluorescence was less than 20% of that in monocytes from normal individuals. In patients with familial defective apolipoprotein B-100 antibody binding was normal, but one patient's own LDL failed to compete with normal DiI LDL for 4 degrees C binding on U937 test monocytes. Patient monocytes having internalization defects showed normal 4 degrees C DiI LDL binding, but at 20 degrees C cell-associated fluorescence was reduced by about 40%. In our study 384 hypercholesterolemic patients (preselected according to serum cholesterol levels, clinical symptoms, and family history) were analyzed for LDL receptor expression using the C7A MAB-based assay. In 71.8% of the patients with cholesterol levels higher than 300 mg/dL, an LDL receptor deficiency was observed. Apolipoprotein E isoforms and lipoprotein[a] were found to be independent from the LDL receptor status. In some patients with high cholesterol levels but normal LDL receptor expression with the C7A MAB assay, LDL receptor defects could be diagnosed when either reduced binding or internalization of DiI LDL or familial defective apolipoprotein B-100 was detected.(ABSTRACT TRUNCATED AT 400 WORDS)     

Nontuberculous mycobacteriosis as a complication of the Swyer-James syndrome

The chest radiograph of a 35-year-old man with fatigue, exertional dyspnoea and haemoptyses revealed a cavity in the left upper lobe and a shrunken left lung with radiolucency greater than that on the right. Acid-fast rods in sputum were identified as Mycobacterium kansasii on culture. Scintigraphy showed a 9% residual perfusion on the left and abnormal ventilation, compatible with Swyer-James syndrome. This had favoured the development of a mycobacterial infection. There was also a decrease in ciliary function (rate of 4-7 Hz, normal: 10-11). Treatment, begun when tuberculosis had been suspected, was after sensitivity tests changed to a combination of rifampicin (600 mg), ethambutol (1600 mg) and protionamide (500 mg) daily. There was marked regression of the findings within 4 weeks, but treatment was prematurely stopped after 11 months. Two years later there was a recurrence which again responded well to the same drug regimen with additional sulphamethoxazole (1600 mg/d).