Escolar Documentos
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Gut, 1990,31,4-10
ALIMENTARY TRACT
Abstract
Studies were done to evaluate the lower
oesophageal sphincter function of chronic
smokers compared with non-smokers and to
ascertain the acute effects of smoking on the
sphincter and the occurrence of acid reflux.
All subjects (non-smokers, asymptomatic
cigarette smokers, and smokers with oesophagitis) were studied postprandially with a
lower oesophageal sphincter sleeve assembly,
distal oesophageal pH electrode, and submental electromyographic electrodes. The
two groups of cigarette smokers then smoked
three cigarettes in succession before being
recorded for an additional hour. As a group,
the cigarette smokers had significantly lower
lower oesophageal sphincter pressure compared with non-smokers but the sphincter was
not further compromised by acutely smoking
cigarettes. Cigarette smoking did, however,
acutely increase the rate at which acid reflux
events occurred. The mechanisms of acid
reflux during cigarette smoking were mainly
dependent upon the coexistence of diminished
lower oesophageal sphincter pressure. Fewer
than half of reflux events occurred by transient
lower oesophageal sphincter relaxations. The
majority of acid reflux occurred with coughing
or deep inspiration during which abrupt increases in intra-abdominal pressure overpowered a feeble sphincter. We conclude that
cigarette smoking probably exacerbates reflux
disease by directly provoking acid reflux and
perhaps by a long lasting reduction of lower
oesophageal sphincter pressure.
Department of Medicine,
Northwestern University
Medical School, VA
Lakeside Medical
Center, Chicago, Illinois,
USA
P J Kahrilas
R R Gupta
Kahrilas, Gupta
2O-
ao
T.
O
ID
+i
x
10
SUBJECTS
Manometric studies were obtained on eight nonsmoking volunteers (age 30 (five) years), nine
cigarette smokers without symptoms referable to
the oesophagus and a negative Bernstein test (age
33 (15) years), and nine patients with heartburn
and oesophagitis demonstrated endoscopically
within seven days of the study (age 63 (15) years).
The admitted smoking histories of the subjects
were 5 8 (4 4) thousand packs for the asymptomatic smokers and 19 3 (7 7) thousand packs for
the smokers with oesophagitis. Of the subjects
with oesophagitis, all had a sliding hiatal hernia,
and all had either distal oesophageal erosions
(n=six) or exudate and a mucosal biopsy showing either inflammatory cells or increased thickness of the basal cell layer (n= three). The study
protocol was approved by the Institutional
Review Board of Northwestern University.
Oesophageal pressure recordings were obtained with a manometric assembly incorporating a 6 cm sleeve sensor, four side-hole recording
sites situated 0, 3, 6, and 9 cm from the proximal
margin of the sleeve sensor, and a gastric recording site at the distal end of the sleeve sensor.89
Oesophageal pH recordings were obtained with a
glass pH electrode (Cecar Microcombination pH
Electrode, Beckman Instruments, Irvine, Calif).
Submental electromyographic recordings were
obtained using silver-silver chloride disc electrodes (Beckman) positioned under the chin and
an indifferent electrolyte patch fastened to the
side of the subject's neck. The electromyographic signal was processed by a high pass filter
set at 5 3 Hz to minimise the movement artefact
recorded. The manometric assembly and the pH
electrode were passed transnasally into the oesophagus and the sleeve assembly was positioned
with the sensing membrane axially centred in the
lower oesophageal sphincter high pressure zone.
The pH electrode was positioned 5 cm above the
midpoint of the lower oesophageal sphincter.
After placement, the manometric assembly and
the pH electrode were taped securely to the
patient's nose. Each lumen of the manometric
assembly was perfused at 0 4 ml/min with a
pneumohydraulic infusion pump' and connected to a Gould-Statham 23DB pressure transducer (Gould Medical Products, Oxnard, Calif).
The manometric recordings, pH recording, and
00
0
0
0
i_
54
5 d;onqfokers
(n-8)
Methods
* p<005
**p<0-01
Asymptomatic
smokers (n-9)
GERD Smokers
fn9)
15I
E
E
~ ~ ~.
(A
cn
+1
(n=9)I
.(L)
CV)
CY)
0)
QL)
4,/
0)X
2 10-
2M
Smokingand reflux
.len
en
-J
-50
-60
-40
-30
-20
-10
10
20
40
30
50
60
Time (min)
Results
LOWER OESOPHAGEAL SPHINCTER PRESSURE
TABLE Acute effect of smoking period on lower oesophageal sphincter pressure ofasymptomatic smokers
Lower oesophageal sphincter pressure in mmHg
Immediately before smoking
Minute
-S
-4
-3
-2
-I
Subject 1
Subject 2
Subject 3
Subject 4
Subject 5
Subject 6
Subject 7
Subject 8
Subject 9
Mean (SD)
22
7
4
9
8
3
7
10
11
9 (6)
21
7
2
7
6
4
5
12
8
8 (6)
18
11
2
7
7
5
9
10
9
9 (4)
16
11
1
1
7
3
11
8
3
7 (5)
19
12
6
4
5
9
9
8
5
9 (5)
10
16
5
4
4
10
11
19
3
9 (6)
12
20
8
3
6
5
7
18
21
5
1
7
7
6
28
13
12
1
1
6
7
8
28
3
9 (8)
15
14
2
1
6
4
6
22
14
8
9 (5)
4
11 (9)
8 (7)
Kahrilas, Gupta
Distal
oesophageal
4J
(pH)
Submandibular 0
EMG
_
LI.
(mm Hg)
~~5012 cm
above LOS
50-l
9 cm
above LOS
0 _1
50l
6cm
above LOS
-
Oesophage.al
body
_-
40Gastric
0-
Ii
1 min
Figure 3: Example of a transient lower oesophageal sphincter relaxation associated with gastro-oesophageal acid reflux recorded
in an asymptomatic smoker. Lower oesophageal sphincter pressure is referenced to gastric pressure with the horizontal dotted line
(O mmHg) representing mean intragastric pressure. Note that although the transient lower oesophageal sphincter relaxation
persistedfor almost 30 seconds, acid reflux did not occur until just prior to lower oesophageal sphincter contraction. In many other
instances, acid reflux did not occur at all. Also note the absence of a submandibular electromyographic signal before, during, or
after the transient lower oesophageal sphincter relaxation.
8
Asymptometie smoken
1n-9)
*
(11=9)
w
(a
4-
BeoeDurn
fe
eoe
Drn
Afte
Distal
oesophageal 4K
1
(pH)
ii
1.j
o_
1 min
rate of transient lower oesophageal sphincter relaxations in the smokers with reflux disease did not
achieve statistical significance primarily because of
the large SEM in values observed in this group.
This is partly explainable by the fact that resting
lower oesophageal sphincter pressure was less than
5 in several individuals of this group for a significant
proportion of the recording period and thus, they
could rarely meet the criteria of definition for
transient lower oesophageal sphincter relaxations.
The non-smoking controls had a mean of 2-4
transient lower oesophageal sphincter relaxations
per hour, 10% of which were associated with acid
reflux; comparable figures to those obtained from
the asymptomatic smokers.
GASTRO-OESOPHAGEAL ACID REFLUX
Kahrilas, Gupta
LOS~
.x
Smokingand reflux
10