[Defect in hypoxic pulmonary vasoconstriction in asthma].
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Biomedical subjects
Publications and source records attributed to H Baier.
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We describe a case of human cysticercosis appearing as an abnormal chest roentgenogram. The patient had a long history of ingestion of undercooked pork. The diagnosis was entertained only after surgical resection, but the history obtained from this patient gave an important clue toward a parasitic infestation.
The physiological principles of Spa Treatment are explained on an adaptation model with three stages of adaptive modification: 1. autonomic recovery, 2. functional adaptation, 3. trophic and plastic adaptation. The stressors are the stimuli of the physical therapy which form adaptates during the spa treatment. These adaptates are directly dependent on the quantity and specificity of the stressors. Clinical symptomatology is elucidated practically with reference to two therapeutic principles and substantiated by results from spa research. The effects and long-term success of the treatment are scientifically demonstrated from the point of view of physiological adaptation.
Measurements of respiratory mechanics, arterial blood gases, and pulmonary vascular resistance were made before and 15 min after inhalation challenge with Ascaris suum extract in dogs with natural sensitivity to this antigen. 25 of 47 dogs were treated before inhalation challenge with a prostaglandin inhibitor (90 mg/kg of aspirin or 2 mg/kg of indomethacin by intravenous infusion). In response to the challenge, bronchospasm developed in approximately half (responders) of each group reflected by decreases in mean specific respiratory system conductance and arterial oxygen tension. While the dogs were breathing room air, pulmonary vascular resistance remained unchanged after antigen challenge in the responders not given aspirin or indomethacin, but increased significantly and was associated with a lesser degree of arterial hypoxemia in the responders pretreated with either of the prostaglandin inhibitors. Prevention of arterial hypoxemia by oxygen breathing blocked an increase in pulmonary vascular resistance in four pretreated responders. No changes in respiratory mechanics, pulmonary hemodynamics, or arterial blood gases were noted in the 21 dogs who did not develop bronchospasm regardless of whether or not they were pretreated. 12 additional dogs in whom arterial hypoxemia was produced by 10% oxygen breathing, showed an increase in pulmonary vascular resistance that was not potentiated by pretreatment with aspirin in 6. We conclude that in acute experimental canine asthma, vasodilator prostaglandins appear to blunt the hypoxic pulmonary vasoconstrictor response, thereby further compromising gas exchange but preventing the development of pulmonary hypertension.
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Measurements of respiratory mechanics, gas exchange, and pulmonary hemodynamics were made before and serially for 2 hours after inhalation challenge with Ascaris suum extract in dogs with natural sensitivity to this antigen. Nine of 14 dogs randomly exposed to an inspired oxygen fraction of 0.21 or 0.60 to 0.70, responded to the challenge with bronchospasm reflected by a transient decrease of mean specific respiratory system conductance to 50 per cent of baseline after 5 to 15 min. This was accompanied by a decrease in alveolar ventilation in all and acidosis in some animals. No changes were observed in transmural pulmonary arterial pressure, cardiac output, pulmonary vascular resistance, and pulmonary blood volume in all 9 dogs who responded with bronchospasm, whether or not arterial hypoxemia was allowed to develop. In contrast, a significant increase in pulmonary vascular resistance occurred in control dogs in whom comparable degrees of arterial hypoxemia were produced by 10 per cent oxygen breathing or mechanical bronchial obstruction by placing beads in lobar and segmental airways. No changes in any parameter measured occurred in the 5 dogs who did not develop bronchospasm after antigen challenge. The results indicated that moderately severe, antigen-induced bronchospasm in anesthetized dogs has no effect on the pulmonary circulation even when associated with arterial hypoxemia. Because nonuniformity of alveolar hypoxia allowing redistribution of blood flow is probably not responsible for this failure to develop increases in pulmonary vascular resistance in induced asthma, it is suggested that the elaboration of chemical mediators may have interfered with the hypoxic pulmonary vasoconstrictor response.
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Anorexia, constipation, vomiting and somnolence in a 39-year-old woman were at first misinterpreted as being of psychological and autonomic nervous system origin. Further clinical and biochemical tests revealed hyperthyroidism associated with hypercalcaemia and hypercalciuria. Thyrostatic treatment for 12 days caused regression of the hypercalcaemia and, after subtotal resection, serum calcium levels and urinary calcium excretion returned to normal for good. The hypercalcaemia syndrome must therefore be assumed to have been the direct result of the hyperthyroidism.
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Intracutaneous, nasal provocation (NPT) and radioallergosorbens (Phadebas RAST) tests were performed on 49 subjects hypersensitive to cats and (or)dogs using serum albumin and epithelium extracts from cats and dogs. Serum albumin elicited intracutaneous reactions in most of the subjects, but gave positive NPT und RAST results in only a few and was, therfore, of limited clinical importance. The intracutaneous tests with epithelium extracts were positive in some subjects in whom other tests had been negative. It is possible that these false-positive skin tests were caused by serum albumin present in the extracts, while in others non-specific skin reactions were apparently caused by epithelial components. On the other hand, the results suggest that the few patients allergic to dogs were incorrectly diagnosed with the RAST. But the described in-vitro method increases the chances of diagnosing allergies against animal epithelia. It is furthermore useful in the interpretation of equivocal skin tests.
Pressure-flow relationships of an artificial airway-mechanical ventilator system were investigated. Endotracheal tubes varying from 7 to 9.5 mm. internal diameter and tracheostomy tubes from 7 to 10 mm. internal diameter were tested over flow-rates from 0.3 to 1.4 L. per second using a tidal volume of 500 ml. The effect of partial obstruction within these airways by suction catheters and the bronchofiberscope was examined. Depending on the internal diameter and the flow-rate, the driving pressure necessary to overcome the resistance of the tubes ranged from 5 to 20 cm. H2O. Partial obstruction of the artificial airways by suction catheters further increased this pressure. The introduction of the bronchofiberscope through an endotracheal tube of 7.5 mm. internal diameter, leaving an effective diameter of 4.9 mm., produced a driving pressure as high as 70 cm. H2O and reduced the flow rate to 50 per cent and the tidal volume to 80 per cent of its set value. Attention should be paid to duration of tracheobronchial suction while the patient is removed from the respirator since a high-grade resistance is created by passage of a suction catheter through an endotracheal tube. Bronchofiberscopy should be cautiously performed through cuffed artificial airways with at least 8 mm. internal diameter because the airway may be too comprised even if mechanical ventilatory assistance is employed.