[Summary of our findings on changes in voluntary cough sounds in pathologic conditions].
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Biomedical subjects
Publications and source records attributed to J Korpás.
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The authors studied the effects of progressive isobaric hypoxia (FO2 = 0.11, 0.07, 0.06, 0.05, 0.04 and 0.03) on respiratory defence reflexes elicited by mechanical stimulation of the airways in 10 pentobarbital-anaesthetized cats. The intensity of the expiration reflex was already significantly reduced at a hypoxia level of only FO2 = 0.11; the intensity of cough also showed a tendency to decrease. The number of efforts and the intensity of both tracheobronchial (TB) and laryngopharyngeal (LPh) cough fell significantly in hypoxia of FO2 = 0.07. On an average, cough could no longer be elicited at PaO2 = 2.0 +/- 0.06 kPa. The aspiration reflex was found to be the most resistant to hypoxia, and could still be elicited just before hypoxic apnoea developed. During hypoxia with FO2 ranging from 0.21 to 0.06, minute ventilation increased, while the intensity of respiratory defence reflexes diminished. TB cough could not be elicited during hypoxia until the breathing was depressed. It can be seen from the results that the regulatory mechanisms responsible for the intensity of respiratory defence reflexes are less resistant to the consequences of an inadequate systemic oxygen supply than the mechanisms controlling ventilation.
The authors studied parameters of laryngopharyngeal (LPh) and tracheobronchial (TB) cough (the number of efforts--NE, the number of efforts per minute--NE.min-1, the intensity of the maximum effort--IME and the intensity of the attack--IA), respiratory parameters (VT, f, Cdyn), blood gas values (PaO2, PaCO2) and the pH in the arterial blood of anaesthetized cats (Pentobarbital Spofa, 35 mg x kg-1 i.p. with experimental pulmonary oedema. Oedema was induced by the i.v. administration of a fatty acid mixture (capric acid 3.8 g, caprylic acid 3.1 g and olive oil 3.0 g)--in a dose of 0.05 ml x kg-1 in group 1 and of 0.01 ml x kg-1 in group 2. Cough was elicited by stimulating the laryngopharyngeal and tracheobronchial mucosa with a silon fibre. Pulmonary oedema was determined from a macroscopic and microscopic examination of the lungs, from the ratio of lung weight to body weight and from the percentual dry weight of the right lungs. The authors found that the intensity of cough was depressed during pulmonary oedema, particularly in the case of TB cough. VT and Cdyn fell, f rose and the PaO2 and pH values steadily decreased.
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The reactivity of cat tracheal smooth muscle to histamine in vitro was studied at various degrees of inflammation of the airways induced experimentally by the intratracheal administration of turpentine oil or Staphylococcus aureus, both in aerosol form. Tracheal smooth muscle preparations from the control animals did not respond to histamine in doses of 10(-9)-10(-3) mol X 1(-1). In tracheal preparations from three groups of cats with turpentine oil inflammation induced 24 h, 48 h and 15 days previously, histamine caused contractions in 20, 70 and 24% of the cats, respectively, according to the degree of inflammation. All tracheal preparations from cats with staphylococcal inflammation responded to histamine by contraction. Atropine, acetylosalicylic acid and phentolamine did not abolish histamine contractions in tracheal preparations, but clemastine did.
The authors studied, in 11 awake adult cats, the parameters of the expiration reflex (ER), tracheobronchial (TB) and laryngopharyngeal (LPh) cough, the respiratory rate (f), tidal volume (VT), the end tidal fractional CO2 concentration (FETCO2), the pH, the blood gases and the heart rate during 30 hours' isobaric hypoxic hypoxia (FO2 = 0.11). During the whole 30 hours the cats developed hypocapnic hypoxemia, f remained unchanged and VT was markedly elevated. In the acute phase (15 min) of hypoxic hypoxia of the same intensity, changes in respiratory parameters were the same and the intensity of respiratory reflexes increased significantly (Tatár et al. 1984). During prolonged hypoxic hypoxia there were no statistically significant changes in the intensity of the ER and of TB and LPh cough. The authors assume that some adaptation of the central mechanisms regulating the defence reflexes of the airways took place; this hypothesis is warranted, because an increase in the susceptibility of the cough centre during constant conditions of the stimulation of cough receptors would not be biologically expedient. The different changes in the intensity of respiratory defense reflexes in the acute and the prolonged phase of hypoxic hypoxia in the presence of identical changes in respiratory parameters are further indirect evidence pointing to the existence of functional differences between the respiratory centre and the cough centre.
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