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Biomedical subjects

I P Mungall

Publications and source records attributed to I P Mungall.

16 recordsLinked to original sources
PubMed1997

A case of rapidly expanding tuberculous lung cavity after bronchoscopy.

A non-smoking Asian woman with previously treated pulmonary tuberculosis presented with a recent onset unproductive cough and cavitating mass lesion on her chest X-ray which rapidly developed into a large tuberculous cavity after bronchoscopy. Acid-fast bacilli were isolated from the cavity and she responded very rapidly to standard anti-tuberculous chemotherapy. This unusual condition must be considered in patients who deteriorate after bronchoscopy.

Aged↗
PubMed1980

Multiple pleural biopsy with the Abrams needle.

Multiple pleural biopsies (up to 10) were taken with the Abrams needle through a single aspiration site in 55 patients with pleural effusions. A definite positive or suggestive pleural biopsy diagnosis was made in 33 patients (60%). In 32 of the 33 patients the pathological abnormality was confined to only a proportion of the biopsies. Pleural biopsies were positive or suggestive in 26 out of 36 patients (72%) eventually shown to have tumour and seven out of eight patients (88%) with tuberculosis. Small pneumothoraces occurred in four patients and surgical emphysema in two.

Adult↗
PubMed1980

An objective assessment of the value of exercise training to patients with chronic obstructive airways disease.

The value of a programme of graded exercise training was assessed in ten subjects with chronic obstructive airways disease. Assessments were made at two-weekly intervals during three twelve-week periods: before, during and after a period of training. During the training the subjects were able to walk significantly further in a 12 minute walking test. There was also a small but significant increase in the forced expiratory volume in one second and the difference between the values of total lung capacity estimated by body plethysmography and those estimated by helium dilution was significantly smaller. The transfer factor for carbon monoxide increased and was significantly greater in the period after stopping the training. The difference between alveolar and arterial oxygen tensions at rest was smaller during the training period. The changes in the results of the 12 minute walking test, transfer factor and the oxygen tension difference were maintained in the period after stopping the training. Despite the improvements in some of the indices of respiratory function there were no improvements in any of the indices of cardiorespiratory fitness which may be because the subjects were incapable of undertaking sufficiently intense training. It is concluded that training is of some benefit to patients with chronic obstructive airways disease but that the benefit may be greater in patients who are less incapacitated and who are able to undertake a more strenuous training programme.

Bronchitis↗
PubMed1979

Assessment of respiratory function in patients with chronic obstructive airways disease.

The reproducibility of some respiratory function tests and a simple self-paced walking test were assessed in 13 patients with stable chronic obstructive airways disease by making observations on six occasions at two to three weekly intervals. The coefficients of variation of the various tests were as follows: forced expiratory volume in one second, +/- 14.8%; forced vital capacity, +/- 11.1%; transfer factor (single breath carbon monoxide), +/- 15%; total lung capacity, +/- 8.8% by helium dilution and +/- 8.3% by body plethysmography; increase in heart rate and minute ventilation for an increase in oxygen uptake of 0.5 1 min-1, +/- 19.4% and +/- 16.3%; distance covered in a 12-minute walking test, +/- 8.2%. The 12-minute distance increased significantly over the first three studies. The considerable variations in the result of these tests in subjects with apparently stable clinical states and without changes in treatment should be considered when assessing the results of changes in treatment.

Humans↗
PubMed1978

H1 and H2 histamine actions on lung vessels; their relevance to hypoxic vasoconstriction.

Pulmonary vasomotor actions of histamine and the possible relationship of histamine to hypoxic pulmonary vasconstriction were studied in anaesthetized cats with one lobe of lung perfused at constant flow and in isolated perfused rat and ferret lungs. In the cat histamine caused dilatation, biphasic responses and constriction with increasing doses. Histamine induced dilatation was better demonstrated during hypoxic vasoconstriction and was reduced by an H2 histamine antagonist; constriction with histamine was abolished by an H1 antagonist. Histamine also caused both vasodilatation and vasoconstriction in ferret lungs. A mast cell stabilizing agent had no effect on hypoxic pulmonary vasoconstriction in cats or rats. This response was unaffected in cats but greatly reduced in rats and ferrets by cyproheptadine, a combined histamine and 5-hydroxy-tryptamine inhibitor. It was unaffected in cats but abolished in ferrets an H1 histamine inhibitor. It was again unaffected in cats but greatly reduced in rats and ferrets by an H2 histamine inhibitor. These species differences may reflect differences in mechanism but more probably reflect non-specific effects of the inhibitors in certain circumstances. However, when drugs nearly abolished hypoxic vasoconstriction, ATP still caused vasoconstriction.

Animals↗
PubMed1977

Pseudomonas pneumonia in status asthmaticus.

A case of Pseudomonas pneumonia developing in a patient on treatment for status asthmaticus is described. The use of broad spectrum antibiotics, high dose steroids and humidifiers or nebulizers may be of aetiological importance. Pseudomonas pneumonia is increasing in prevalence although it has not previously been described in association with status asthmaticus. It carries a high mortality and its prevention is, therefore, clearly important.

Adult↗
PubMed1976

Hypoxia and lung mast cells: influence of disodium cromoglycate.

Rats kept in 10% O2 for three or more weeks developed mast cell hyperplasia in the lungs, especially round the alveoli and the small peripheral blood vessels, which became thickened during chronic hypoxia. There was a significant correlation between the degree of right ventricular hypertrophy (RVH) and the numbers of alveolar and small vessel mast cells. However, mast cell hyperplasia developed more slowly than RVH. Daily treatment with disodium cromoglycate failed to prevent RVH in hypoxic conditions but was associated with retardation of growth in both hypoxic and control rats. Neither acute nor chronic hypoxia increased the degree of degranulation in the lung mast cells.

Animals↗
PubMed1975

Factors causing and reversing vasoconstriction in unventilated lung.

Vasoconstriction occuring a unventilated or hypoxic lung was studied in dogs and cats to elucidate mechanisms which both cause and reverse it. Lungs were perfused in vivo at constant pressure or constant blood flow; alternatively blood flow and pressure were measured with minimal operative interference. Stimulus-response curves of lung vessels to hypoxia showed a large response within the physiological range of P02 values. Vasoconstriction in unventilated lung caused by bronchial occlusion sometimes matched that caused by an equal degree of ventilation hypoxia but was sometimes greater. Responses to both stimuli varied widely between animals and in one animal at different times. This could be due to variable availability of a transmitter or variable presence of vasodilator substances. Both histamine and beta-adrenoreceptor stimulants caused pulmonary vasodilatation in unventilated lung. Histamine caused pulmonary vasoconstriction and vasodilatation in different circumstances which could be blocked respectively by H1 and H2 antihistamine drugs. Potent alpha- and beta-adrenoreceptor action on pulmonary vessels was demonstrated in both species. Alpha-adrenoreceptor blocking drugs caused dilatation and beta-adrenoreceptor blocking drugs caused vasoconstriction. The possible role of histamine and catecholamines in causing or reversing hypoxic vasoconstriction or in maintaining pulmonary vascular tone is discussed.

Adrenergic alpha-Antagonists↗