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beats/min and 13·9 ± 9·1 and 6·6 ± 4·8 mmHg (with pain) and
45·6 ± 3·6 beats/min and 34 ± 5·6/12·27 ± 3·2 mmHg
(asymptomatic).
We conclude that angina is produced at a significantly higher
heart rate (P < 0·01) in the laboratory than during normal daily
activities and that for an equivalent amount of ST segment
change there is no significant difference in heart rate or blood
pressure response in this group of patients.
100. RELATION OF ISOVOLUMIC RELAXATION TIME
TO LEFT VENTRICULAR END-DIASTOLIC PRESSURE
P. J. OLDERSHAW, M. MAITHEOS, E. SHAPIRO AND D. G.
GIBSON
Brompton Hospital, London S. W.3
To study inter-relations between early diastolic events, simultaneous echo-, phono- and apex-cardiograms were performed
within 48 h of cardiac catheterization in 47 patients (23 with
ischaemic heart disease, 14 with left ventricular hypertrophy or
aortic regurgitation, and 10 with normal coronary arteriograms), and in 20 normal controls. Isovolumic relaxation time
(IVRT), taken as A, to mitral valve opening (MVO), and
normally 6D-80 ms, was closely correlated with left ventricular
end-diastolic pressure (LVEDP) (r = -0·90, P < 0·001), but
not with aortic pressures. When LVED P was above 30 mmHg,
IVR T was less than 10 ms, or even negative, suggesting active
MVO. A,-MVO was significantly prolonged in aortic regurgitation at any LVEDP (P < 0·01). MVO always preceded the 0
point of the apexcardiograrn by an interval, normally 5D- 70 ms,
which correlated directly with LVEDP (r = 0·85, P < 0·001)
but which was shortened in aortic regurgitation (P < 0·01). A
third heart sound and increased %F wave on the apexcardiogram were consistently associated with a short IVR T
(P < 0·01), but unrelated to cavity size, systolic function or
peak rate of dimension increase. Thus LVEDP can be estimated
from IVRT non-invasively. In left ventricular disease, the third
heart sound correlates closely with a short IVRT; neither
correlates with cavity size of filling rate.
101. VENTRICULAR CONTRACTION INFLUENCES
RATE OF RELEASE OF CREATINE KINASE IN REPERFUSED ISCHAEMIC RAT HEARTS
T. V. ARNIM AND A. MASERI
Royal Postgraduate Medical School, Hammersmith Hospital,
London, U.K,
The creatine kinase (CK)-release patterns from ischaemic
myocardium are taken as a quantitative measure of irreversible
damage. We therefore studied the influences of contraction,
pressure development, coronary flow on CK release during
reperfusion in 10 isolated working rat hearts. Ischaemia was
induced with a supra-aortic one-way ball valve, which reduced
coronary flow from 17·5 ± 2·0 ml/min (control, mean aortic
pressure 102 ± 4 ern water) to 0·9 ± 0·5 rnl/rnin. Reperfusion
was started after 30 min of ischaemia first retrogradely with a
pressure of 85 cm water and coronary flow of 14·9 ± 3·2
ml/min. All hearts fibrillated on reperfusion but resumed
rhythmic contraction after 0·1-31·0 min. The CK concentration in the effluent began to increase dramatically only when
spontaneous contraction was resumed and reached a peak 3-45
min into reperfusion, in spite of the fact that perfusion pressure
and flow were only slightly increased during reperfusion
(coronary flow 18·1 ± 2· 7 ml/min, mean aortic pressure 93 ± 8
cm water). The time to peak CK release was positively
correlated with the time of onset of spontaneous contraction
(r = 0·93). Time to systolic pressure of 120 cm water was even
better correlated with time to peak CK release (r = 0·98). CK
release during spontaneous contraction peaked 2·5- to n·O-fold
over CK release during fibrillation.
These results suggest that squeezing of myocardial cells may
be an important factor determining C K liberation after
reperfusion.
102. TRANSIENT HYPOXAEMIA DURING SLEEP IN
PATIENTS WITH RIGHT-TO-LEFT INTRACARDIAC
SHUNTS
J. R. CAITERALL, N. J. DOUGLAS, P. M. A. CALVERLEY, H. M.
BRASH, C. M. SHAPIRO AND D. C. FLENLEY
Department of Medicine, The Royal Infirmary, Edinburgh
EH3 9YW, Scotland, U.K.
Patients with chronic bronchitis and emphysema who are
hypoxic when awake have transient episodes of profound
hypoxaemia during sleep (Douglas et al., 1979, Lancet, i, 1-4).
These episodes result mainly from hypo ventilation, although
changes in ventilation/perfusion balance may also contribute. In
25 patients with chronic bronchitis and emphysema (Pa,o,
awake 4·3-7·9 kPa) and 25 healthy subjects (Pa,o, awake
9· 2-14· 7 kPa), the lowest oxygen tension reached during sleep
could be predicted from the oxygen tension when awake (lowest
Pa,o, asleep = 0·55 x Po, awake + O·74; r = 0·85) (Catterall
et al.. 1980, Clinical Science, 58, 5p).
Patients with right-to-left intracardiac anatomical shunts are
also hypoxaemic when awake, but the effect of such shunts on
oxygenation during sleep is unknown. We have therefore
measured arterial oxygen saturation non-invasively (Hewlett
Packard 47201 A ear oximeter), oral and nasal airflow,
chest-wall movement and EEG in five patients with right-to-left
shunts (four females, one male; age 35-55 years), and compared
these with five patients with chronic bronchitis and emphysema
(three females, two males; aged 52-62 years; FEV 1'00.5-0.9
litre) who had a similar degree of hypoxaemia when awake
(Sao, awake: bronchitic patients, 72·2-91·0 (mean 83·2)%;
intracardiac shunt patients, Sa,o, awake 77·8-88·0 (mean
82·6)%).
The patients with bronchitis had far greater falls in oxygen
saturation when asleep than those with cardiac shunts (maximum fall in Sao, when asleep: bronchitic patients, 14·3-31·0
(mean 25·9)%. shunt 7·5-12·6 (mean 10·3)% (P < 0·01).
When analysed in terms of the number of hypoxaemic episodes
(fall in Sa,o, of at least 10%) the bronchitic patients had 21 such
episodes and the cardiac shunt patients had only four (P <
0·02). In both groups hypoxaemic events were associated with
hypoventilation more than sleep apnoea, but tended to occur in
REM sleep.
The level of arterial oxygenation when awake is therefore not
the only factor determining the degree of any transient nocturnal
hypoxaemia.
103, EFFECTS OF MONOCYTES ON LYMPHOCYTE
FUNCTION IN SARCOIDOSIS
N. Mcl. JOHNSON, J. BROSTOFF, B. N. HUDSPlTH, J. R. BOOT
AND M. W. McNICOL
Department of Medicine and Immunology, The Middlesex
Hospital Medical School, and Willesden Chest Clinic, London
Both in vivo and in vitro cell-mediated immunity are defective in
sarcoidosis (Siltzbach, 1971, in: Sarcoidosis-Immunological
Diseases, p. 581, ed. Sarnter, M., Little Brown, Boston, Mass.).
Two possible reasons for this are (l) increased numbers of
'suppressor' T lymphocytes bearing surface receptors for IgG
(Ty) (Katz et al., 1978, Clinical Immunology and Immunopathology, 10, 35D-354) or (2) the presence of non-lymphocyte
prostaglandin-producing suppressor cells (Goodwin et al., 1979,
Annals ofInternal Medicine, 90, 169-173).
We have found an increase in the percentage of Ty cells in
sarcoidosis (31% active, 23% inactive, 18% controls). However, using acid esterase staining, plastic adherence and an
anti-monocyte serum, we have shown that a significant
proportion of these are, in fact, rnonocytes rather than
lymphocytes.
In patients with sarcoidosis, the mean lymphocyte transformation with the mitogen Con A (20 ,ug/m!) was 8363 ± SEM
1075 c.p.m., which was significantly lower than that of controls
(19431 ± 1070; P < 0·001). After either incubation on plastic
to remove adherent monocytes or the addition of indomethacin
(20,u1 of 10 ,ug/ml), a prostaglandin synthetase inhibitor, there