12P
Medical Research Society
9. REGIONAL DISTRIBUTION OF PULMON-
ARY VENTILATION AND PERFUSION IN
PATIENTS WITH LIVER CIRRHOSIS
J. MILIC-EMILI, FRANCOLS
RUFF. JOHNJ. PICKEN,
ALEXARONOPP
and DAVIDV. BAITS
Montreal, C a d
Arterial hypoxia is known to be frequently present in
patients with cirrhosis of the liver and has been attributed to intrapulmonary and portopulmonary shunts.
Recent studies have shown that such venous admixture
is insufficient to explain the observed degree of
hypoxia, and it has been suggested that regional
ventilation-perfusion abnormalities might also contribute significantly. Using radioactive xenon, we have
measured the regional distribution of pulmonary
ventilation and blood flow in eight men with liver
cirrhosis. Subdivisions of lung volume, expiratory
flow rates, and diffusing capacity were all within
predicted limits. All measurements were made in the
resting seated position. In every patient, regional
ventilation distribution was either uniform or preferential to the upper lung zones, in contrast to the
predominant lower-zone distribution in normal subjects. This effect was diminished by the taking of a
very slow inspiration. Pulmonary blood flow showed
a decrease in the more dependent parts of the lung in
every patient. and in three of them, blood flow distribution was much reduced to the lower half of the lung
fields. These abnormalities in ventilation and perfusion
distribution, which were observed in varying degree
in every patient, are of sufficient magnitude to contribute materially to arterial hypoxia. They are believed
to be explained by an increase in airway and vascular
resistance in dependent parts of the lungs, and this in
turn is due, at least in part, to perivascular and peribronchial oedema caused by decreased blood colloidosmotic pressure and possibly increased capillary
permeability.
10. VENTILATORY EFFECTS OF POSITIVE
PRESSURE BREATHING IN MAN
D. C. FLENLEY,
L. D. PENGELLY
and J. MILK-EMIL
Department of Medicine, University of Edinburgh, and
Department of Physiology, McCill University, Montreal, Canada
Continuous measurements of tidal volume, mouth
pressure and end-tidal Pco, were made on four
normal subjects, seated in an air-conditioned body
plethysmograph, whilst breathing air or mixtures of
C 0 2 in 30% oxygen. Positive pressures up to 30 cm
HzO were suddenly applied at the mouth, in random
order, for the period of four breaths, with 2 or 3 min
between each application. Chemical ventilatory drive
was unchanged in this short period. Increases of end
expiratory volume with positive pressure lay on the
relaxation pressure volume curve of each subject.
Tidal volume fell during positive pressure breathing.
being more reduced at higher pressures. This reduced
tidal volume could result from the tension-length
relationship of muscle, the shape of the diaphragm,
and the decreasing compliance of the respiratory
system at high mouth pressures.
11. PULMONARY OXYGEN TOXICITYPATHOPHYSIOLOGY AND EFFECTS OF Na
MIXTURE
G. SMITH,I. McA. LEDINGHAM
and A. T. SANDISON
University Departments of Surgery and Pathology,
Western Infirmary, GIasgow
The total mechanism of acute pulmonary oxygen
toxicity is still obscure. This investigation was designed
to study pathogenesis by examining in detail changes
in cardiovascular and respiratory parameters in
animals exposed to high pressures of oxygen.
Three groups (six dogs in each group) of pure bred
beagle hounds were anaesthetized by means of a
standard neuroleptanalgesic technique and allowed to
breath spontaneously humidified gas consisting of:
40% 0 , 6 0 % Nz at 1 ATA, or 100% 0,at 2 ATA, or
66% 0,33% Nzat 3 ATA.
In the control dogs at 1 ATA, there was little change
in haemodynamic data or respiratory function throughout 24 hr, at the end of which time the animals were
sacrificed. The animals at 3 ATA also survived to
24 hr before sacrifice.
The animals exposed to 100% 0 2 at 2 ATA died
spontaneously in apnoea at 17-21 hr after undergoing
marked changes in rate and rhythm of ventilation.
Deterioration in alveolar-arterial oxygen tension
gradients and pulmonary shunt ratios were relatively
late changes. Primary pulmonary damage was not the
apparent cause of apnoea.
It is concluded that Nz exerts a protective effect on
oxygen toxicity at pressures below 2.5 ATA and that
death from acute oxygen toxicity at pressures below
2 3 ATA involves myocardial or central effects. Pulmonary pathological features are less prominent than
previously reported.
DEMONSTRATIONS
METABOLISM
1. Biochemical changes in the uterus during early
pregnancy
K. FOTHEERBY,
K. MALINOWSKA
and R. GREENSTREET
(Department of Chemical Pathology)
2. Lipid synthesis in human adipose tissue
D. J. GALTONand J. P. D. WILSON(Department of
Medicine)
3. Methylmalonyl CoA and vitamin B , , deficiency
D. GOMPERTZ
(Department of Medicine)
4. Citrate and the regulation of acetyl CoA carboxylase
J. ILIFFE(Medical Research Council. Hammersmith
Hospital)