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Plenary Lectures (7 March 1981) A23 0945-1030 Hall 1 MEASUREMENTS OF PULMONARY TOXICITY PROFESSORDAVID C. FLENLEY, Ph.D., F.R.C.P., F.R.C.P. Ed. Department of Respiratory Medicine, City Hospital, Greonbenk Drive, Edinburgh EHIO 5SB, Scotland, UK. Gas exchange is a majsr physiological function of the 1,,ngs, end this can be affected by the interference in the matching of ventilation (V) to perfusion (Q) of the 3,000,000 alveoli, with resulting arterial hypoxaemia, with or without CO2 retention, end consequent acid-base disturbance. Overall alveolar ventilation depends also on nsuro-musoular function, as well as upon the calibre of the airways. Local cellular infiltration sf the lung parenchyma can also interfere with gas exchange, and can progress ts permanent lung fibrosis, with loss of functioning lung tissue end Vascular involvement. Measurements of dynamic and static lung volumes, alveolar to arterial oxygen tension gradients, arterial blood gee tensions, minute ventilation, transfer factor for CO, and mechanical properties of the lungs, (compliance end airways resistance) allow these effects to be quantiteted, and the modem developments of broncho-pulmonary lavage enable qualitative studies of these disorders to be made, based upon the cellular and ~nmune function of pulmonary c~lls in vivo. Examples of pulmonaz 7 toxicity arising from high doses of oxygen, paraquat, fluid overload, radiation, toxic gases, and drugs, will be discussed in the light of these mechanisms, with particular emphasis upon the quantitation of the resultant physiological changes.

Measurements of pulmonary toxicity

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Plenary Lectures (7 March 1981) A23

0945-1030 Ha l l 1 MEASUREMENTS OF PULMONARY TOXICITY

PROFESSOR DAVID C. FLENLEY, Ph.D., F.R.C.P., F.R.C.P. Ed.

Department of Respiratory Medicine, City Hospital, Greonbenk Drive, Edinburgh EHIO 5SB, Scotland, UK.

Gas exchange is a majsr physiological function of the 1,,ngs, end

this can be affected by the interference in the matching of

ventilation (V) to perfusion (Q) of the 3,000,000 alveoli, with

resulting arterial hypoxaemia, with or without CO 2 retention, end

consequent acid-base disturbance. Overall alveolar ventilation

depends also on nsuro-musoular function, as well as upon the calibre

of the airways. Local cellular infiltration sf the lung parenchyma

can also interfere with gas exchange, and can progress ts permanent

lung fibrosis, with loss of functioning lung tissue end Vascular

involvement. Measurements of dynamic and static lung volumes,

alveolar to arterial oxygen tension gradients, arterial blood gee

tensions, minute ventilation, transfer factor for CO, and mechanical

properties of the lungs, (compliance end airways resistance) allow

these effects to be quantiteted, and the modem developments of

broncho-pulmonary lavage enable qualitative studies of these

disorders to be made, based upon the cellular and ~nmune function

of pulmonary c~lls in vivo. Examples of pulmonaz 7 toxicity arising

from high doses of oxygen, paraquat, fluid overload, radiation, toxic

gases, and drugs, will be discussed in the light of these mechanisms,

with particular emphasis upon the quantitation of the resultant

physiological changes.