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  • 1
    ISSN: 1433-8580
    Keywords: RDS ; Surfactant ; Substitution ; Fluorocarbon ; DPPC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Respiratory distress syndrome (RDS) is characterized by quantitative and qualitative disturbances of surface active substances (surfactant). Therefore, intratracheal surfactant substitution is a favored subject of clinical investigations. In our study we tried to inflate and stabilize lungs in two steps: first, lungs were rinsed with a fluorocarbon and, second, artificially ventilated with a dipalmitoylphosphatidylcholine (DPPC) aerosol, the mean component of surfactant. Sixteen isolated fetal minipig lungs of day 95 (85% of the total gestation period) were used. From one pair of lungs one lung served as control (group 1), whereas the other was treated with DPPC (group II). In both groups the lungs were rinsed first with a fluorocarbon (FC-72, surface tension 12 mN/m). This maneuver was followed by an artificial ventilation with an aerosol of either salt solution (group I) or DPPC (group II) for 40 min. To characterize lung mechanics, static pressure volume curves were registered at 0, 20, and 40 min after fluorocarbon lavage. Airway opening pressure (pi), end-inspiratory volume (vi), and weightspecific end-inspiratory lung compliance (ci) were investigated. As biochemical parameters of the lungs we determined phospholipidphosphate content and DPPC, sphingomyelin (SM), and lysophosphaditylcholine (LPC) of the lung tissue. Significant differences were found with regard to phospholipidphosphate and DPPC content. No difference was seen in static pressure volume diagrams at the end of the investigation period.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 188 (1988), S. 425-432 
    ISSN: 1433-8580
    Keywords: Fluorocarbon ; Surfactant ; Substitution ; RDS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In our present study we tried to inflate and stabilize isolated immature lungs of fetal minipigs in gestation age of 95 days (= 85% of total normal gestation period) with different fluorocarbons. Based on our previous experiences, the immature lungs at day 95 are almost non inflatable with air [25–27, 29–31]. For our experiments we used fluorocarbon 43 (FC-43) with a surface tension of 16 mN/m and fluorocarbon 72 (FC-72) with a surface tension of 12 mN/m. Eighteen fetal immature lungs were used. In group 1 the lungs were rinsed with FC-43; in group 2 the rinse solution was FC-72, and in group 3 the lungs were untreated. After removing the fluorocarbon, in the case of groups 1 and 2, the lungs were artificially ventilated. Pressurevolume (p–v) curves were registered in the beginning (immediately after FC lavage), after 10 and 20 min of artificial ventilation. Airway opening pressure (pi) and weight-specific end-inspiratory lung compliance (ci) were investigated. Statistically significant differences in weight-specific end-inspiratory compliance were found between FCgroups and untreated group 3, but no stabilization could be seen during the investigation period of 20 min. No statistically significant improvement in weightspecific end-inspiratory compliance was observed between group 1 and 2, although the compliances of group 2 with FC-72 were better than those of group 1 with FC-43 in three p-v diagrams registered in the beginning and after 10 and 20 min of artificial ventilation (Table 2). In airway opening pressure there were no statistically significant differences to be observed between the investigated groups, but the opening pressures of group 2 with FC-72 at 0, 10, and 20 min were always better than those of other groups (Table 1). No significant differences were also seen in wet/dry weight ratio, in content of lipid phosphorus and of phospholipids (dipalmitoylphosphatidylcholine, sphingomyelin, and lysophosphatidylcholine) (Table 3). The data presented here suggest that fluorocarbons facilitate transient the inflation of immature lungs. However, for further permanent stabilization the additional replacement of surfactant phospholipids seems to be necessary.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Der Anaesthesist 44 (1995), S. 613-623 
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Endotracheale Intubation ; Ösophageale Tubusfehllage ; Kapnometrie ; Oesophageal-Detector-Device ; Rettungsdienst ; Key words Endotracheal intubation ; Oesophageal ET tube malposition ; Capnometry ; Oesophageal detector device ; Emergency medical system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Oesophageal malposition of an endotracheal tube is among the leading causes of anaesthesia incidents. While clinical manoeuvres for detection of tube malposition are unreliable, monitoring (i.e. capnography) can prevent such incidents. The problem is particularly important in prehospital care, where capnography is not (yet) widely available. We tested three devices used for differentiating oesophageal from endotracheal intubation: 1. Non-CO2dependent Oesophageal Detector Device (ODD) as described by Pollard and Wee, 2. Semi-quantitative chemical disposable capnometer EasyCAP (Nellcor), 3. Non-quantitative infrared miniaturised capnometer MiniCAP (MSA). Methods. 50 anaesthetised minipigs were intubated with a Magill tube. An identical additional tube was placed in the oesophagus. The cuffs of both tubes were inflated. Unexperienced personel (students, laborary technicians) were asked to determine the position of one of the tubes by using one of the devices according to the randomisation plan. The decision had to be taken within 30 s. Using the ODD, the proband first injected 100 ml air into the lung (or stomach) and then tried to aspirate the same volume. EasyCAP and MiniCAP were used according to manuals. Results. Each device was used 25 times with a tracheal tube and 25 times with an oesophageal tube. All tube position identifications were correct. When ventilating the oesophagus/stomach for capnometric control, regurgitation into the tube occurred six times (five times with the EasyCAP and once with the MiniCAP). In these cases, the decision was based on this occurrence and not on the display of the device. While using the ODD no regurgitation occurred. Conclusion. These devices are useful for preclinical practice. According to the literature and our experience, the ODD is superior for the initial control of tube position, especially in cardiac arrest. Capnometry is needed, however, for continuous control of ventilation.
    Notes: Zusammenfassung Die ösophageale Tubusfehllage zählt zu den häufigen Ursachen schwerer Narkosezwischenfälle. Sie ist heute durch Kapnographie zuverlässig entdeckbar, Zwischenfälle sind daher prinzipiell vermeidbar. Da die quantitative Kapnometrie im Rettungsdienst (noch) nicht verfügbar ist, bleibt das Problem der Erkennung einer ösophagealen Tubuslage im präklinischen Bereich weiterhin akut. Im Tierversuch wurden 3 Geräte getestet, die zur präklinischen Überprüfung der Tubuslage eingesetzt werden: 1. CO 2 -unabhängiges „Öesophageal Detector Device“ nach Pollard und Wee, 2. Semi-quantitatives chemisches Einmalkapnometer EasyCAP (Nellcor, Idstein), 3. Nicht-quantitatives Miniaturinfrarotkapnometer MiniCAP III (MSA, Pittsburgh). Möglichkeiten und Grenzen der Geräte sowie Literatur hierzu werden diskutiert.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 298 (1967), S. 170-184 
    ISSN: 1432-2013
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Wirkung oberflächenaktiver Substanzen auf die Oberflächenkräfte der Lunge läßt sich am Verhalten des Druck-Volumen-Diagrammes erkennen. Wir registrierten statische Druck-Volumen-Diagramme (pV-Diagramme) isolierter Rattenlungen nach Entfernung (Entfilmung) und nach Einbringen (Befilmung) oberflächenaktiver Substanzen in die Lungen. Nach Spülung der Lungen mit Ringerscher Lösung und nach Spülung mit einem Detergens (Polysorbat) sahen wir Veränderungen der pV-Diagramme, die eine gesteigerte Oberflächenspannung in der Lunge anzeigten: Erhöhung des Entfaltungsdruckes bei steigendem, Instabilität und vorzeitige Volumenabnahme bei fallendem intrapulmonalem Druck, verringertes Kollapsvolumen. Diese Veränderungen waren durch nachfolgende Spülung mit oberflächenaktiver Substanz umkehrbar. Dabei war Dipalmitoyllecithin angenähert gleich wirksam wie aus Hundelungen gewonnene oberflächenaktive Substanz. Eine Ausnahme bildete der Entfaltungsdruck, der in unseren Versuchen durch Behandlung mit oberflächenaktiven Substanzen nur begrenzt zu beeinflussen war. Bei Anwesenheit von Polysorbat in der Lunge war die Befilmung weniger wirksam als nach Entfernung des Detergens. Anscheinend wird durch das Detergens die Oberflächenspannung der Subphase erniedrigt und die Filmspreitung oberflächenaktiver Substanzen gehemmt. Die Wirkung der Oberflächenstoffe scheint nicht an die Intaktheit des Alveolarepithels gebunden zu sein, da auch nach seiner Zerstörung durch Detergentien eine Befilmung mit oberflächenaktiven Stoffen möglich ist.
    Notes: Summary The effects of surfactants on the surface forces in the lung can be demonstrated by analysis of pressure-volume-diagrams. We recorded static pressure-volume-diagrams from isolated rat lungs after removing and replacing the surface active substance in the lungs. Rinsing of the lungs with Ringer's solution or with a detergent (Polysorbat) caused changes in the pressure-volume-diagrams which indicated an increased surface tension in the lungs. The pressure required to open the alveoli was increased, and when the lungs were deflated the alveoli became instable. The pressure at which collapse occured was higher and the lung volume at the end of collapse was lower than normal. These changes were reversed by a subsequent rinsing with surface active substances. Dipalmitoyl-Lecithin was almost as effective as surfactant prepared from dog lungs. The subsequent rinsing with surfactant however had little effect on the pressure required to open the alveoli, which remained at a high value. The replacement of the film was less effective in the presence of Polysorbat than after removal of the detergent. Apparently the surface tension of the subphase is lowered by the detergent and spreading of surfactant is inhibited. After destruction of epithelium by detergents it was possible to form a film of surface active substances. Therefore the influence of surfactant seems not to depend on an intact alveolar epithelium.
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  • 5
    ISSN: 1432-2013
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An Hundelungen wurden in drei verschiedenen Versuchsanordnungen die Beziehungen zwischen der Filtration von Flüssigkeit durch die Alveolar-Capillar-Schranke und dem kolloidosmotischen Druck des Blutplasmas untersucht. 1. An isolierten Lungenlappen, die von einem zweiten Hund aus durchblutet wurden, wurde durch fortlaufende Wägungen des Lappens die Druckdifferenz zwischen den Lungencapillaren und dem Alveolarraum bestimmt, bei dem weder Flüssigkeit aus der Capillare in den Alveolarraum filtriert noch aus dem Alveolarraum in die Capillare rückfiltriert wurde (kritischer transmuraler Druck entsprechend dem isogravimetrischen Druck nach Pappenheimer). Der kritische transmurale Druck war weitgehend unabhängig vom kolloidosmotischen Druck des Blutplasmas. Gleiche Verhältnisse ergaben sich auch bei Lungenlappen, deren Alveolarraum mit Ringerscher Lösung oder Blutplasma gefüllt war. 2. Am rechten Unterlappen wurde in situ bei offenem Thorax durch Veränderung der Drücke in der A. und V. pulmonalis der kritische transmurale Druck bestimmt. Bei Senkung des kolloidosmotischen Druckes des Blutplasmas durch Verdünnung des Blutes mit Ringerscher Lösung sank der kritische transmurale Druck im Verhältnis zur Senkung des kolloidosmotischen Druckes nur sehr wenig ab. 3. Bei Hunden mit geschlossenem Thorax wurde mit Hilfe eines in der Aorta ascendens liegenden Gummiballons der Druck in der V. pulmonalis erhöht. Die veränderte Absorption einer Strahlung, die aus einer 238Am-Quelle stammte, zeigte die Entwicklung eines Lungenödems an. Die Ödembildung war abhängig vom Druck in der A. pulmonalis und im linken Vorhof. Dagegen fanden wir nur eine sehr geringe Abhängigkeit der Ödembildung vom kolloidosmotischen Druck des Blutplasmas, wenn wir ihn durch Infusion von Ringerscher Lösung und nachfolgenden Bluttransfusionen veränderten. Nach diesen Ergebnissen kann man die Alveolar-Capillar-Schranke nur begrenzt als ein Ultrafilter betrachten.
    Notes: Summary The relationship between filtration of liquid through the alveolar-capillary barrier and the colloid-osmotic pressure of the blood plasma was investigated in lungs of the dog, using three different experimental approaches. 1. In isolated lung lobes perfused with blood from another dog the pressure difference between pulmonary capillaries and the alveolar space at which liquid was neither filtered from the capillaries into the alveolar space nor was refiltered from the alveolar space into the capillaries was determined by continuous monitoring of the weight of the lung lobe. This pressure difference, the critical transmural pressure (closely related to the isogravimetric pressure of Pappenheimer), was essentially independent of the colloid-osmotic pressure of the blood plasma. Similar behaviour was found in lung lobes filled with blood plasma. 2. In an open thorax preparation the critical transmural pressure for the right inferior lung lobe in situ was determined by variation of pressures in the pulmonary artery and vein. When the colloid-osmotic pressure of the blood plasma was decreased by dilution of the blood with Ringer solution, the critical transmural pressure decreased very little in comparison to the decrease of the colloid-osmotic pressure. 3. In dogs with closed thorax the pressure in the pulmonary veins was increased by means of a rubber balloon placed in the ascendent aorta. The consequent changes in the absorption of the radiation from an Am 238 source showed the development of lung oedema. The formation of the oedema was dependent upon the pressure in the pulmonary artery and in the left atrium. However, when the colloid-osmotic pressure of the plasma was changed by infusions of Ringer solution and subsequent blood transfusions, only a slight dependency of the oedema formation upon the colloid-osmotic pressure of the blood plasma was found. According to these results the alveolar-capillary barrier cannot be considered an ultrafilter without reservations.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 47 (1969), S. 190-197 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary In 29 patients with lymphogranulomatosis — the diagnosis was established by histology — blood-gas-studies were carried out during romm-air and oxygen-breathing. Alveolar-arterial O2-difference during room-air and O2-breathing and the venous admixture were calculated. Results: 1. The patients with lymphogranulomatosis without changes at the finger — or toenails — didn't show any difference to the normals of corresponding age. 2. In the patients with lymphogranulomatosis and changes at the nails the AaDO2 was higher as in the corresponding normal group. The AaDO2 in the normals during romm-air-breathing was 21.4 torr (SD ± 4.57), in patients with lymphogranulomatosis and nailchanges 36.5 torr (SD ± 7.3). 3. The venous admixture for patients with nail-changes was calculated with 7.54%, the Vva of the corresponding normal group was 3.53%. This difference is statistically significant. 4. The possible importance of vasoactive substances in the development of finger-clubbing is discussed.
    Notes: Zusammenfassung Bei 29 Fällen mit histologisch gesicherter Lymphogranulomatose wurden blutgasanalytische Untersuchungen bei Luft- und reiner O2-Atmung durchgeführt. Aus den gewonnenen Daten konnten alveolar-arterielle Sauerstoffdruckdifferenz bei Luft- und Sauerstoffatmung sowie die Zumischung venösen Blutes zum arteriellen Blut berechnet werden. Es fanden sich folgende Ergebnisse: 1. Die Patienten mit Lymphogranulomatose ohne Nagelveränderungen unterschieden sich nicht gegenüber den altersentsprechenden Normalkollektiven. 2. Die Patienten mit Lymphogranulomatose und Nagelveränderungen zeigten eine deutlich höhere AaDO2 als das entsprechende Normalkollektiv. Für letzteres betrug die AaDO2 bei Luftatmung 21,4 Torr (SD ± 4,57), für die Patienten mit Uhrglasnägeln 36,6 Torr (SD ± 7,3). 3. Nach Atmung reinen Sauerstoffs ließ sich für die Patienten mit Uhrglasnägeln eine venöse Beimischung von 7,54% des Herzzeitvolumens, bei den vergleichbaren Normalpatienten nur eine venöse Beimischung von 3,53% des Herzzeitvolumens errechnen. Dieser Unterschied ist statistisch signifikant. 4. Die Rolle vasoaktiver Substanzen bei der Entstehung des klinischen Symptoms „Uhrglasnägel“ wird diskutiert.
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Lung 141 (1969), S. 186-189 
    ISSN: 1432-1750
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 304 (1968), S. 315-321 
    ISSN: 1432-2013
    Keywords: Lung ; Alveolar Surface Tension ; Aerobic Metabolism ; Breathing Mechanics ; Rat ; Lunge ; Alveoläre Oberflächenspannung ; Oxydativer Stoffwechsel ; Atemmechanik ; Ratte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung 1. Beatmet man isolierte Rattenlungen mit Drucken von 0–25 cm H2O (Überbeatmung), so zeigen sich im statischen Druck-Volumen-Diagramm Veränderungen, die auf eine Zunahme der Oberflächenspannung in den Lungenalveolen hinweisen. Läßt man die Lungen im Anschluß an die Beatmung 30 min im geblähten Zustand, so wiest das Verhalten despV-Diagramms auf ein Wiederabsinken der alveolären Oberflächenspannung hin, wenn die Versuche bei 37°C vorgenommen wurden, während eine derartige Änderung bei 20–24°C nur angedeutet nachzuweisen ist. 2. Wird der oxydative stoffwechsel durch Beatmung der Lunge mit N2 oder Vergiftung mit KCN ausgeschaltet, so zeigen sich prinzipiell sowohl während der Beatmung als auch in der Restitutionsphase die gleichen Verhältnisse, nur daß unter anoxischen Bedingungen die alveoläre Oberflächenspannung während der Beatmung noch etwas stärker ansteigt. Danach spielt der oxydative Stoffwechsel für die beobachteten Erscheinungen eine untergeordnete Rolle. 3. Wahrscheinlich wird durch die Überbeatmung der Oberflächenfilm in den Lungenalveolen mechanisch geschädigt, wobei ein Teil des oberflächenaktiven Materials inaktiviert wird. Eine Restitution könnte durch Wiederspreitung des inaktivierten Materials oder durch Übertreten von LAS aus den Alveolarzellen an die Alveolaroberfläche erfolgen.
    Notes: Summary The effect of ventilation on the lung alveolar lining layer has been demonstrated by analysis of pressure-volume diagrams. Ventilation of isolated rat lungs at intrapulmonary pressures of 0–25 cm H2O caused an increase of surface forces in the lungs. After ventilation was stopped the lungs were kept inflated at intrapulmonary pressures of 25 cm H2O up to 60 min. Subsequent analysis of the pressure-volume diagrams indicated a decrease of surface forces at 37°C while at 20–24°C only little recovery occurred. The influence of ventilation with N2 or poisoning with KCN on aerobic cell metabolism was investigated. The increase of surface forces was only slightly more pronounced by anoxia during lung-ventilation than in the above experiments. Aerobic cell metabolism, therefore, did not play an important role in our experiments. It is very likely that the decrease of surface activity following ventilation was caused by mechanical changes of the alveolar lining layer. We believe that, to some extent, the lung alveolar surfactant was inactivated. Recovery can be explained by new spreading of inactivated materials or by passage of lung alveolar surfactant from the alveolar cells to the alveolar surface.
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