Sodium cromoglycate in intrinsic asthma.
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Biomedical subjects
Publications and source records attributed to K B Saunders.
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In a group of patients with chronic bronchitis, repeated night sedation with 10 mg nitrazepam produced a fall in central respiratory drive and a steady rise in arterial carbon dioxide tension. The changes produced over a five-day period were not clinically important, except in two patients who were already hypercapnic before receiving nitrazepam. The use of this drug in patients with carbon dioxide retention should be avoided.
Respiration, sinus nerve chemoreceptor discharge, and carotid arterial pH were monitored in cats. Chemoreceptor discharge frequency showed oscillations that had a respiratory period when averaged over many respiratory cycles. These oscillations disappeared when pH oscillations of respiratory period were eliminated from the carotid arterial blood. The maximum sinus nerve discharge was associated with the most acid point of the recorded pH oscillation. Briefly increasing PCO2 by giving CO2-rich saline into the aortic root resulted in brief reduction in carotid arterial pH, and when this reduction occurred during inspiration tidal volume increased, even with a pH change no larger than the pH oscillations. However, increased chemoreceptor discharge could only be demonstrated when each pH change had twice the amplitude of the pH oscillations. Injections of fixed acid mixed with free carbonic anhydrase transiently increased chemoreceptor frequency, whereas injections of fixed acid alone had no effect. The carotid body is therefore sensitive to small rapid changes in arterial PCO2, and the pH electrode record indicates the size of the stimulus except when fixed acid changes are produced too closely upstream.
A battery of lung function tests was performed on 28 patients with carcinoma of the bronchus, before radiotherapy, six weeks later, and at three months. Twenty-five had evidence of ariways obstruction, though only five had a forced expiratory ratio of less than 50%. Nine were shown to have obstruction to a main or lobar bronchus, while 11 definitely did not, but the only significant difference in lung function between groups was in the residual volume calculated from single breath helium dilution. Eight of ten cases of squamous cell carcinoma were central, and seven of these obstructive. Of seven cases with undifferentiated cells only two were central (p less than 0.05) and one obstructive. Breathlessness on presentation was significantly more common in patients with central tumours (6/12) than those with peripheral lesions (1/8), and all six breathless patients with central tumours claimed that this symptom improved after radiotherapy. Radiotherapy may have a palliative effect for breathlessness in patients with central airways obstruction due to tumour.
Fourteen patients with acute severe asthma necessitating hospital admission were all treated with a standard therapeutic regimen, and in addition received either bromhexine or placebo (initially intravenously and subsequently orally) double-blind. We were unable to show any significant improvement in the rate of recovery of the bromhexine-treated group, in terms of either arterial blood gases or change in peak expiratory flow rates.
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Of 26 patients with intrinsic asthma, 21 (81%) were homozygous for the histocompatibility antigen HLA-W6. Also, half the patients had complement defects, in particular low levels of C2. This is the first indication of a strong genetic component in intrinsic asthma, apart from that already known from family studies. These findings suggest that intrinsic asthma may be a recessive disease.
Ventilatory response to CO2 was measured before and after two different benzodiazepine hypnotics in both chronic bronchitics and patients without chest disease. Flurazepam, but not nitrazepam, produced a significant decrease in CO2 sensitivity, although there was no significant change in FEV1 or mixed venous PCO2. This is the first unequivocal evidence of central depression of respiration by a benzodiazepine and may be the mechanism by which benzodiazepines cause deterioration in patients with respiratory failure.
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