The results of the operative treatment in 33 patients suffering from pelviureteral obstruction and of the follow-up control using ultrasonography and renography are presented. A reduced radiation exposure and diminished treatment costs are the results of this changed diagnostic and therapeutic strategy.

Adolescent↗

PubMed1989

[Percutaneous nephrostomy and temporary immunosuppression in treatment of idiopathic retroperitoneal fibrosis (Ormond disease)].

Our experiences in the diagnostics, treatment and follow-up-course of 10 patients suffering from idiopathic retroperitoneal fibrosis are reported. The ureterolysis and temporary nephrostomy, initially as percutaneous nephrostomy, and a long-term immunosuppressive therapy is the treatment of choice. In the follow-up control ultrasonography and computerized tomography are valuable and the prognosis of the disease quoad functionem is good.

Adult↗

PubMed1988

High yield enzymatic conversion of intravascular leukotriene A4 in blood-free perfused lungs.

Experiments to investigate the fate of intravascularly administered leukotriene (LT) A4, an unstable intermediate of LT generation, were performed in isolated, ventilated, and blood-free perfused rabbit lungs. LT extracted from the lung effluent were separated by different reverse phase and straight phase HPLC procedures as methylated and nonmethylated compounds. Identity of eluting LT was confirmed by UV spectrum analysis and immunoreactivity. Pulmonary artery injection of 75 to 300 nmol of LTA4 resulted in the rapid appearance of cysteinyl-LT as well as LTB4 in the recirculating perfusate. The yield of these enzymatically generated LTA4 metabolites vs non-enzymatic hydrolysis products (6-trans-LTB4, 5-trans-epi-LTB4, 5,6-dihydroxyeicosatetraenoic acids) ranged above 90%. Experiments with application of tritiated LTA4 showed exclusive origin of the detected LT from the exogenously applied precursor. The time course of cysteinyl-LT appearance in the perfusate suggested metabolism of LTC4 via LTD4 to LTE4, whereas there was no evidence for LTB4 omega-oxidation. In the dose range of LTA4 used, the enzymatic conversion of this LT precursor did not approach saturation. Collectively, these data indicate that the intact pulmonary vasculature contains a hitherto not described capacity for enzymatic conversion of intravascularly offered LTA4 to both cysteinyl-LT and LTB4. This may be of biological significance for a putative transcellular biosynthesis of LT in the pulmonary microcirculation upon contact with LTA4 feeder cells, such as activated granulocytes.

Animals↗

PubMed1988

The hemolysin of Escherichia coli.

Many strains of E. coli elaborate a hemolysin which is responsible for the zone of beta-hemolysis surrounding bacterial colonies on blood agar. The significance of this cytolysin as a determinant of bacterial pathogenicity has been established in animal models with the use of genetically engineered, isogenic bacterial strains. An analogous role in human infections has been inferred from the high association of hemolysin production with disease. Studies at a molecular genetical level have defined 4 genes that are required for the synthesis, post-translational modification and secretion of the hemolysin. The structural gene hlyA encodes for a 107-110,000 polypeptide, which must be modified in an unknown manner to its active form by the product of the neighboring hlyC gene. Genes hlyB and hlyD encode for proteins that export the molecule to the extracellular medium. The signal for secretion is contained in the C-terminal portion of the toxin molecule. The secreted hemolysin attacks plasma membranes of target mammalian cells by inserting as a monomer into the bilayer and generating hydrophilic transmembrane pores of approximately 2 nm effective diameter. The pores display a marked selectivity for cations over anions and pore-opening is dependent on the presence of a correct transmembrane potential. Binding to a membrane target does not require the presence of a specific receptor, and pores may be generated in planar lipid membranes consisting solely of phosphatidylcholine. Pore formation in nucleated cells can trigger secondary reactions such as stimulation of arachidonate metabolism with release of lipid mediators, probably initiated by passive influx of extracellular Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Effects of alpha-tocopherol, its carboxylic acid chromane compound and two novel antioxidant isoflavanones on prostaglandin H synthase activity and autodeactivation.

The natural antioxidant alpha-tocopherol has repeatedly been described to inhibit platelet aggregation and thromboxane formation, whereas its influence on prostaglandin H synthase in vivo and in vitro is a matter of controversy. In the present study the effects of different antioxidative compounds on ram vesicular gland microsomal prostaglandin H synthase activity were investigated in vitro: d,l-alpha-tocopherol, its carboxylic acid chromane compound (Trolox), phytol, alpha-tocopherol-acetate and two novel antioxidative isoflavanones, obtained by methylation and/or hydrogenation of naturally occurring isoflavones from fermented soybeans (6,7-dihydroxy-4'-methoxyisoflavanone and 6,7,4'-trihydroxyisoflavanone). Alpha-tocopherol, -acetate and phytol revealed no significant influence on the enzyme activity when applied in concentrations up to 1 mM. Trolox (100-1000 mu mumol/l) and the two isoflavanones (5-50 and 10-100 mumol/l) dose-dependently augmented the initial rate of oxygen consumption and the total oxygen uptake during prostaglandin H synthase incubation with arachidonic acid (AA). In parallel, these compounds increased the formation of prostaglandin E2 and F2 alpha from 14C-labelled AA, and they markedly protected the prostaglandin H synthase from rapid autodeactivation as revealed by repetitive application of AA in small doses. We suggest that these compounds serve as cosubstrates to which the oxidizing equivalents are transferred which arise during the hydroperoxidase reaction of the enzyme.

Animals↗

PubMed1988

Diseases of the intrapetrous carotid artery.

In the early years of skull base surgery, total tumor removal was often deemed impossible due to involvement of the intrapetrous carotid artery. In contrast, previously considered unresectable lesions may be removed totally in selected cases, with reasonable expectation of successful treatment at the present time. Current techniques and operative exposures, when modified to accommodate the problem of intracranial extensions of tumor and when approached with neurosurgical collaboration, permit the removal of many of these difficult tumors. This retrospective study of 33 patients treated over the past 5 years offers a critical analysis of our treatment, and a categorization of abnormalities known to affect this anatomic region containing the vessel.

Adenocarcinoma↗

PubMed1988

Extended pterional decompression of the orbit: an alternative treatment in endocrine orbitopathy.

Extended pterional decompression was performed in seven orbits. The indication was optic neuropathy in six orbits and corneal ulceration in one. As compared to ethmoidectomy, advantages of the pterional approach seem to be the preservation of the motility of the eye and the lack of paranasal sinus complications. We consider the pterional approach to be appropriate for decompression of endocrine orbitopathies that do not respond to conservative measures.

Corneal Diseases↗

PubMed1988

Bacterial exotoxins and endothelial permeability for water and albumin in vitro.

Effects of Staphylococcus aureus alpha-toxin and Pseudomonas aeruginosa cytotoxin on the permeability of an endothelial monolayer were studied. Porcine pulmonary artery endothelial cells were grown on a polycarbonate membrane, mounted in a chamber, and exposed to a continuous hydrostatic pressure of 10 cmH2O. On application of this trans-endothelial pressure, endothelial monolayer became "sealed," i.e., the filtration rate for water decreased and the reflection coefficient for albumin increased, reaching a plateau after 1-2 h. Sealed monolayer had a hydraulic conductivity of 2.1 X 10(-6) cm.s-1.cmH2O and an albumin reflection coefficient of 0.73. Permeability of the monolayer was increased on addition of an excess of EDTA and reversed on readdition of calcium. Within 60-90 min after addition of 1 microgram/ml alpha-toxin, the filtration rate increased 75-fold, and the albumin reflection coefficient dropped to 0.20. These changes in permeability were accompanied by cell retraction and formation of large intercellular gaps between endothelial cells. Effects of alpha-toxin were abolished by preincubation with neutralizing antibodies and by inhibitors of calmodulin function. Pseudomonas aeruginosa cytotoxin (25 and 50 micrograms/ml) also increased the permeability of the endothelial monolayer, but it was only about one-third as effective as alpha-toxin.

ADP Ribose Transferases↗

PubMed1988

Pulmonary vasoconstrictor response to soluble fibrin in isolated lungs: possible role of thromboxane generation.

The blood coagulation system is activated regularly in severe forms of shock, polytrauma, and sepsis. Arising thrombin cleaves the fibrinopeptides A and B from fibrinogen, and it generates monomers of fibrin, which are initially kept in solution by the remaining excess fibrinogen. The effects of soluble fibrin (fibrin monomer/oligomer-fibrinogen complexes) and fibrinopeptides A and B were investigated in blood-free perfused, isolated rabbit lungs. Urea Tris buffer-dissolved fibrin monomers were injected into the pulmonary artery in the presence of circulating excess fibrinogen. In doses above 5 mg, the monomers consistently provoked a sharp rise in pulmonary artery pressure, which was followed by an elevated pressure plateau. Changing to fresh perfusate devoid of soluble fibrin did not restore the pressure to baseline, and a second administration of the soluble fibrin caused a pressor response larger than the first. Only a modest increase in lung weight (less than 2 g) was observed, and lung inflation pressure was not altered. The pressor responses were accompanied by a rapid release of thromboxane A2 and a more delayed release of prostaglandin I2 into the perfusion fluid. A significant correlation between the height of the fibrin-induced pressure rise and the amount of thromboxane release was noted. Inhibition of cyclooxygenase (indomethacin) suppressed the generation of both prostanoids, whereas inhibition of thromboxane synthetase (OKY-046 and imidazole) selectively blocked the liberation of thromboxane. All three inhibitors caused an immediate decline in pulmonary artery pressure, which had been previously elevated due to administration of soluble fibrin, and markedly reduced the pressor response evoked by a subsequent fibrin application in the same lung.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed1988

A highly sensitive gas chromatographic method does not detect exhalation of volatile hydrocarbons from isolated ventilated lungs under massive peroxidative stress.

Lung lipid peroxidation is thought to be a basic pathophysiological phenomenon responsible for pulmonary damage in different types of oxidant attack. Measurement of volatile hydrocarbons, especially ethane and pentane, produced during peroxidative degradation of polyunsaturated fatty acids and exhaled into an animal housing chamber, has attracted increasing interest for the monitoring of in vivo lipid peroxidation. However, this approach cannot distinguish between pulmonary exhalation of hydrocarbons generated in different organs or even the intestinum and pulmonary generation of these lipid peroxidation markers. In the present study we developed a respiration and hydrocarbon trapping system for isolated, ventilated, and perfused lungs that avoided rebreathing and allowed complete sampling and gas chromatographic separation and quantification of exhaled alkanes and alkenes (C1-C5) in the absence of background levels. Using an "artificial lung," the recoveries of exogenously administered hydrocarbons ranged between 80 and 95% with good reproducibility (SD between 1.7 and 9.6%). The detection limit of the system was approximately 3 fmol of each alkane or alkene/g wet lung weight.min. However, neither under basal conditions nor during massive peroxidative stress by the application of high doses of H2O2, FeCl3/ascorbate, paraquat, or ozone was any material with a retention time similar to that of hydrocarbons exhaled from isolated rabbit lungs. We conclude that under the experimental conditions employed, there is only insignificant generation of hydrocarbons in intact lungs.

Animals↗

PubMed1988

Potentiation of leukotriene production following sequestration of neutrophils in isolated lungs: indirect evidence for intercellular leukotriene A4 transfer.

Granulocyte (polymorphonuclear leukocyte, PMN) sequestration in the microvascular bed with release of different mediators has been implicated in the pathogenesis of inflammatory and allergic disorders in many organs including the lung. In the present study, we investigated the profile and quantity of leukotriene (LT) generation in isolated blood-free perfused rabbit lungs, in isolated PMNs in vitro and in rabbit lungs, following administration of PMNs, mimicking pulmonary leukostasis. Following stimulation with increasing concentrations of the calcium ionophore A 23137 (0.1 to 2 mumol/L), LTs were detected in the buffer fluid by their chromatographic mobility in different high-performance liquid chromatography (HPLC) systems, by on-line peak spectrum analysis, and by post-HPLC radioimmunoassay (RIA). In isolated lungs, a dose-dependent generation of cysteinyl LTs greater than LTB4, in the complete absence of omega-oxidation products of LTB4 as well as nonenzymatic hydrolysis products of LTA4, was evoked. PMNs in vitro showed a typical profile of LT liberation (LTB4, 20-OH-, and COOH-LTB4, nonenzymatic LTA4 metabolites). In the model of pulmonary leukostasis, the presence of omega-oxidation products of LTB4 indicated metabolic integrity of the trapped PMNs. Nonenzymatic hydrolysis products of LTA4 were, however, not detected in the combined system, whereas the cysteinyl LTs increased markedly. This profile suggests intercellular transfer of PMN-derived LTA4 to lung cells in the microenvironment. In addition, at 2 mumol/L A23187, the sum of all LTA4-derived products surpassed the arithmetic sum of the isolated preparations more than threefold. This potentiation of an LT generation under conditions of pulmonary leukostasis may be of biologic significance for amplification of inflammatory events.

Animals↗

PubMed1988

[The significance of inflammatory mediators for the development and therapy of acute lung failure].

Explore the source record for details and available documents.

Arachidonic Acid↗

PubMed1988

[Mechanism of cell damage by E. coli hemolysin].

Many strains of E. coli elaborate a hemolysin which is responsible for the zone of beta-hemolysis surrounding bacterial colonies on blood agar. The significance of this cytolysin as a determinant of bacterial pathogenicity has been established in animal models with the use of genetically engineered, isogenic bacterial strains. An analogous role in human infections has been inferred from the high association of hemolysin production with disease. Studies at a molecular genetical level have defined 4 genes that are required for the synthesis, post-translational modification and secretion of the hemolysin. The structural gene hlyA encodes for a 107-110,000 polypeptide which must be modified in an unknown manner to its active form by the product of the neighboring hlyC gene. Genes hlyB and hlyD encode for proteins that export the molecule to the extracellular medium. The signal for secretion is contained in the C-terminal portion of the toxin molecule. The secreted hemolysin attacks plasma membranes of target mammalian cells by inserting as a monomer into the bilayer and generating a hydrophilic transmembrane pore of approximately 2 nm effective diameter. The pore displays a marked selectivity for cations over anions and pore-opening is dependent on the presence of a correct transmembrane potential. Binding to a membrane target does not require the presence of a specific receptor, and pores may be generated in planar lipid membranes consisting solely of phosphatidylcholine. Pore formation in nucleated cells can trigger secondary reactions such as stimulation of arachidonate metabolism with release of lipid mediators, probably initiated by passive influx of extracellular Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Serum alpha-tocopherol levels after high-dose enteral vitamin E administration in patients with acute respiratory failure.

Serum levels of tocopherols were measured in 5 healthy volunteers and in 14 patients with acute respiratory failure before and after onset of high-dose enteral vitamin E administration. The initial alpha-tocopherol levels did not differ between both groups (12.1 +/- 2.7 micrograms/ml in the volunteers and 11.3 +/- 3.5 micrograms/ml in the patients; mean +/- SD). After oral administration of 1 g d,l-alpha-tocopherylacetate per day the serum levels more than doubled within 1 day and reached a plateau between 22 and 30 micrograms/ml after 3 days in the volunteers. In contrast, application of even 3 g vitamin E/day by gastric tube in the patients with respiratory failure caused only a delayed increase of the serum levels with values nearly doubling after 5-10 days (6 patients), or there was no increase at all (8 patients). Serum alpha-tocopherol did not rise in patients without accompanying highmolecular weight formula diet and in patients with prolonged hemodynamic insufficiency and metabolic acidosis. The age of the patients, the fact of severe blood losses, hemodialysis and hemofiltration and the final outcome of death or survival appeared to be without influence on the response to enteral vitamin application. Neither in the volunteers nor in the patients with acute respiratory failure were there any detectable amounts of beta-, gamma- or delta-tocopherol or of alpha-tocopherolquinone or alpha-tocotrienol.

Acute Disease↗