Diseases of the respiratory system. Respiratory failure.
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Presence of chloramphenicol in the growth medium for mycelia of Aspergillus oryzae was without effect on the oxidative activity, respiratory control, or P/O ratio of isolated mitochondria. The mitochondria oxidized Krebs cycle intermediates even in the presence of cyanide at the concentration markedly inhibiting the normal mitochondrial oxidation. However, the P/O ratio during the mitochondrial oxidation decreased by about 1.0 on addition of cyanide. The c-type cytochromes, shown to occur in large amounts than in normal mitochondria (Wakiyama and Ogura, 1972), were suggested to act as electron carriers in this cyanide-resistant oxidation. A novel pigment, demonstrated only in the mitochondria prepared from chloramphenicol-treated mycelia by a CO-difference spectrum, was presumed to be the terminal oxidase of the respiration in the presence of cyanide.
The respiratory system is described as a feedback control system. The controller consists of the peripheral chemoreceptors and the central chemosensitive structures, the respiratory centre in the medulla oblongata and the thorax-lung pump which they drive. The controlled system is comprised of three compartments (lung, brain and the remaining tissue) connected by the blood circulation. The controlled values are arterial pH and arterial O2 partial pressure and cerebral extracellular pH. Earlier models have been improved by: (1) the dead space description, (2) the thermodynamic formulation of the CO2 dissociation equation and the simple but accurate O2 dissociation equation of the blood, (3) the alteration of the CO2 dissociation equation for the brain and the remaining tissue to accommodate recent results, (4) the application of the one-receptor-theory of central chemosensitivity, (5) the pH dependence of brain circulation, (6) the bicarbonate exchange between blood and extracellular fluid of the brain and (7) the introduction of variable circulation times. Respiratory and metabolic disturbances of the respiratory system are analyzed. The mathematical formulation of the respiratory system is a differential difference equation system. In the steady state the experimental results are reproduced fairly well. A slight discrepancy is found in the simulation of metabolic acidosis. Apparently we have assumed the sensitivity of the peripheral chemoreceptors to be too large so that the respiratory response is not correctly predicted. In the numerical solution there is an overshoot in the on-transient and a damped oscillation in the off-transient of the alveolar CO2 partial pressure during respiratory acidosis. We have varied the parameters to make deviations small. The best agreement seems to result, if the central threshold is near the normal extracellular pH of the brain. A further deviation from experimental findings is that the cerebral CO2 and H+ concentration, the blood circulation of the brain, the alveolar O2 partial tension and the ventilation show a slight oscillation in the off-transient. Except for these discrepancies the experimental results, especially the stability of the extracellular pH of the brain, are reproduced fairly well. During hypoxia there are deviations form the experimental results if the central residual activity is constant and the central threshold deviates from the normal extracellular pH of the brain. But if the central residual activity is pH dependent and if the central threshold is equal to the normal extracellular pH of the brain, then the time course of VE and the other variables agree fairly well with experimental results. There is also a good correspondence between the theoretical and experimental data during hyperoxia. During metabolic acidosis the time constant of the bicarbonate exchange between blood and extracellular fluid of the brain is important. If a time constant of one minute is assumed, then the predicted and the experimental results correspond sufficiently well.
The translocation of fibrous dusts through the respiratory system is discussed on the basis of human and experimental data obtained with the transmission electron microscope. Comparison of the characteristics (numerical and mass concentrations, sizes, types) of asbestos fibers retained in different locations of the respiratory system in humans exposed to asbestos has shown that there is no relationship between the numerical concentrations in lung parenchyma and those in parietal pleura. Moreover, almost al fibers encountered in the pleura were ultimate, short fibrils of chrysotile. The animal data are from rats injected intrapleurally with different types of fibers (chrysotile, crocidolite and glass fibers) and sacrificed at different times. There was a progressive increase in the number and mass of fibers translocated into lung parenchyma from the pleural cavity that was particularly obvious after 90 days. After this time, the mean length of fibers, especially chrysotile, increased, indicating that more long fibers are retained in alveolar tissue than short fibers.
Toluylene diisocyanate (TDI) has an uncommon importance in the production of irritation of respiratory system. In the last few years less volatile isocyanate compounds have been substituted for TDI. Commercial available diphenylmethane diisocyanate (MDI) and polymethylene polyphenyl isocyanate (PAPI) were analyzed in 1971. The analysis indicated the presence of 21% TDI in several samples. It is evident, with respect to the relatively high vapor pressure of TDI, that such impurities will be able to cause air concentrations in excess of the current threshold limit value (TLV) of 0.02 ppm. Liberation of TDI by heat from varnish insulinations is a difficult problem. This problem was described as "an old hazard in new guise". Especially, in a soldering process on polyurethane coated wire, excess of TLV is possible in unfavourable conditions. By the regulation that the concentration of TLV must not exceed 0.02 ppm and by the use of new non-volatile isocyanate the risk of acute and subacute intoxications has considerably subsided. Chronic irritations of respiratory system and asthma-like diseases, however represent still an unsolved problem.
Role of serotonin in the regulation of respiratory system function. Acta Physiol. Pol., 1978, 29 (2): 131--138. This study examined respiratory centre reflector excitability, the electrical activity of respiratory muscles, outer breathing, pH and arterial blood gas composition under conditions of experimentally induced serotonin excess or deficiency in 48 dogs. It was found that excess of serotonin in the animals leads a strenghthening of respiratory action in terms of increased respiratory centre bioelectrical excitability, muscular electrical activity and outer respiratory indices, such as frequence, volume and lung ventilation per min. In addition the pH of blood shifted to alkalic and oxygen tension of the blood increased while CO2 tension of the blood decreased.
Connective tissue macromolecules, glycosaminoglycans, glycoproteins, collagen, and elastin were isolated from different parts of the respiratory system and characterized. The materials included bronchiolar tissue, gas-exchange tissue, lung pleura, and tracheal mucosa. The similarity of the macromolecular composition of lung pleura and tracheal mucosa suggests a common cellular component in these structures. The high concentration of GAG and collagen in bronchiolar tissue is consistent with the cartilagenous nature of this tissue. Particularly interesting is the high content of heparin in all pulmonary structures, a relatively greater content of hyaluronic acid in gas-exchange tissue, and a high content of heparan sulfate and dermatan sulfate in vascular tissues. Elastin also occurs as a major fibrous structure. Although the biologic role of these connective tissue macromolecules has not been established, certain functional relationships are inferred.
Bovine respiratory anatomy and physiology were reviewed and considered in relationship to the pathogenesis of pulmonary disease. Factors which may predispose cattle to respiratory disease included a small physiological gaseous exchange capacity, greater basal ventilatory activity, and greater anatomical compartmentalization of the lung as compared with other mammals, a low level and atypical bioactivity of bovine lysozyme, and low numbers of macrophages within the alveolar lumen.
The experiments were carried out to observe certain functional changes in the respiratory system which develop in the early stage of aspiration pneumonia and to study the possibility of influencing these changes by application of artificial ventilation (IPPB) and/or administration of dehydrobenzperidol. The experiments were carried out on 32 mongrel dogs divided into 4 groups. Experimental Mendelson's syndrome was produced by instilling, during anaesthesia, hydrochloric acid solution of pH 1.5 in a dose of 4 ml/kg into the tracheobronchial tree. Immediately after anaesthesia and then 10 times at intervals of one hour after HCl instillation the following determinations were done: mean blood pressure, CVP, haematocrit, PO2 and PCO2 in arterial and mixed venous blood, and minute artifical ventilation. The veno-arterial blood shunt in the lungs, alveolo-arterial difference of oxygen partial pressure and the effective compliance were also determined. The chemical damage to the lungs by acid caused condensation of blood and a fall in CVP. These changes were due to fluid escape from the vessels especially in the pulmonary vascular tree. Disturbances in pulmonary gas exchange were a result of deficient ventilation of lung areas damaged primarily by acid and suffering secondarily from developing disturbances in pulmonary blood flow. Dehydrobenzperidol in a dose of 1 mg/kg applied as the only treatment in Mendelson's syndrome had the same favourable effect on pulmonary changes as controlled IPPB. The combination of controlled artificial ventilation and intravenous dehydrobenzperidol decreased the disturbances in pulmonary gas exchange in Mendelson's syndrome. This was possible because both factors exert a benficial effect on ventilation and perfusion preventing the development of oedema and atelectasis.
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The leech as a foreign body and parasite in the human respiratory tract occurs principally in the Mediterranean countries, in Africa and Asia. It reaches the respiratory tract when water is drunk directly from rivers, lakes, etc. Ignorance of this fact may cause diagnostic difficulties leading to errors in treatment. Anaemia and respiratory obstruction due to leeches cause danger to health and life, especially in children. Fatalities have been known. Treatment consists of endoscopic removal of the parasite, which may be technically difficult, especially when the leech is in the region of the larynx and thus presents dramatic conditions for the procedure. A series of 120 cases treated in Algeria between 1962 and 1971 is presented.
Various respiratory electron transport activities of Rhodopseudomonas capsulata were studied in membrane fragments prepared from photosynthetically grown cells of a parental strain and two terminal oxidase-defective mutant strains. The NADH and succinate oxidase activities of the mutant having a functional N,N,N1,N1-tetramethyl-p-phenylenediamine oxidase, M6, were consideraly more sensitive to inhibition by either antimycin A or cyanide than the corresponding activities of the mutant lacking a functional N,N,N1,N1-tetramethyl-p-phenylenediamine oxidase, M7. The parental strain, Z-1, but not the mutants, showed biphasic inhibitory responses of NADH and succinate oxidase activities with either antimycin A or cyanide. In certain reactions no differences in inhibitor susceptibility were found among the strains tested, implying that the pathways involved were unaffected in the mutants. In this category were the actions of rotenone on NADH oxidase, antimycin A on cytochrome c reductase and, in M6 and Z-1, cyanide on N,N,N'N'-tetramethyl-p-phenylenediamine oxidase. These results suggest that the respiratory chain of the parental strain branches at the ubiquinone-cytochrome b region into two pathways, each branch goes to a distinct terminal oxidase, and either may be blocked independently by genetic mutation.
beta-Cytosine arabinoside (Ara-C) in free and liposome encapsulated form was administered to Wistar rats by intratracheal institution. Free [3H]Ara-C administered in this manner rapidly left the lung and entered the systemic circulation. Liposome-encapsulated [3H]Ara-C persisted in the lung for a long period, with little redistribution to other tissues. Liposomes administered via the trachea became widely distributed throughout the lung air spaces, as evidenced by the histochemical localization of liposomes containing horse-radish peroxidase. Free Ara-C (5 mg/kg) administered into the trachea effectively suppressed macromolecular incorporation of [14C]thymidine ([14C]dThd) in the bone marrow and gut as well as in the lung. Liposome-encapsulated Ara-C (5 mg/kg) effectively suppressed macromolecular incorporation of [14C]dThd in the lung but had little effect on this process in the gut and bone marrow. Our results suggest that liposome-encapsulated Ara-C may be able to produce a local pharmacologic effect within the lung without producing adverse side effects in other tissues. This observation may be relevant to the chemotherapy of pulmonary metastases.
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