الفهرس 
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Abstract
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SUMMARY AND CONCLUSION
A large body of evidence has implicated tobacco smoking as
a risk factor in the pathogenesis and maintenance of peptic
ulceration, although the mechanism of this association is not
clear.
The importance of hydrochloric acid to the activity of pepsin,
and the importance of both to the development of mucosal lesions,.
have been shown repeatedly. Studies of the acute effects of
cigarette smoking on gastric acid and pepsin secretion have shown
conflicting results. With the exception of a few preliminary
reports, no information is available about the chronic effects of
smoking on parietal and chief-cell function.
The purpose of the present study was twofold, firstly to
evaluate the effects of acute smoking on basal gastric secretion of
acid and pepsin as well as mucin in healthy smokers and non-smokers
and in smoker and non-smoker duodenal ulcer patients. Secondly, to
investigate the hypothesis that habitual heavy smokers with and
without duodenal ulcer, have higher basal gaatric secretion values
than similar individuals who have never smoked.
This investigation was carried out on bOth humans and dogs.
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As regards the human subjects. they were divided into four
groups :
Group I ~r_1 non-smoker individuals. •
Group II Normal heavy smoker individuals.
Group III Non-smoker duodenal ulcer patients.
Group IV Heavy-smoker duodenal ulcer patients.
Each group consisted of fifteen _le subjects. All medications
were discontinued 72 hours before the study. and smoking was
prohibited for at least 10 hours.
On the experimental morning the tip of Ry1e tube was positioned
in the fundus of the stomach. After evacuating and discarding the
resting gastric secretion. Basal secretion was collected in four
consecutive samples each of 15 minute duration.
After initial 60 minute basal period, each subject smoked four
filter cigarettes during 40 minutes, taking care to inhale. The
basal gastric secretion was collected for another four consecutive
periods, starting with the smoking period.
The volume of each sample was measured, then analysed for free
and total acidities. Thereafter, the samples of basal gastric
section either before or after smoking were mixed together for
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determination of peptic activity and dissolved mucin.
This study was carried out on ten conscious male dogs, basal
gastric secretion was collected from gastric fistula. Collection of
basal gastric secretion was done before and after nicotine infusion
and analysed for acidity, peptic activity and disaolved mucin. The
above procedure was repeated in vagotomized dogs.
The present study on dogs is designed to find out whether there
is a relationship between acute smoking or nicotine infusion and the
vagus nerve.
The results of the preaent study demonstrated that acute
smoking did not produce any significant change in volume, acidity,
peptic activity or dissolved mucin in normal non-smokers.
In normal heavy smokers, amoking produced inaignificant
decrease in volume, acidity, peptic activity and disaolved mucin of
basal gastric secretion.
It was found that acidity, peptic activity and dissolved mucin
were insignificantly reduced after smoking in non-smoker duodenal
ucler patients.
As regards the effect of smoking on basal gastric secretion in
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smokers duodenal ucler patients no significant change occurred after
smoking.
A similar lack of response was observed in dogs. Nicotine
infusion failed to alter the volume, acidity, peptic activity or
dissolved mucin of basal gastric secretion.
After vagotomy nicotine infusion produced insignificant
increase in acid, pepsin and mucin secretion.
Nicotine which is probably the main factor responsible for the
effects of smoking on gastrointestinal tract, may stimulate or
depress autonomic ganglia depending on the dose. The response of
this drug in anyone individual could depend on the dominance of one
or the other part of the autonomic system.
In the present study it was found that smokers had increased
values of basal gastric secretion. Chronic smoking significantly
increased volume and output of both acid and pepsin in
normal individuals as well as in duodenal ucler patients. It has
been suggested that chronic smoking may lead either to increased
parietal and chief cell mass, or to an enhancement of their
secretory capacity, which could be attributed to chronic vagal
stimulation.
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Neither acute nor chronic consumption of tobacco affects
gastric turnover or adherence of mucuS to the mucosa. Dissolved
mucoproteose and mucoprotein output were significantly changed in
smokers and in non-smokers.
Our results demonstrated that duodenal ulcer patients do
secrete more acid and pepsin than healthy volunteers. Volume and
output of acid and pepsin were significantly higher in duodenal
ulcer patients, whereas dissolved mucin was not significantly
changed. Similar findings
non-smokers.
were observed in smokers as in
Basal hypersecretory drive in duodenal ulcer patients could
be explained by either basal hypergastrinemia or increased vagal
tone.
Our results pointed out the relationship of smoking and basal
gastric secretion. Although habitual heavy smokers do secrete more
acid and pepsin than non-smokers do, the rise in secretion would not
place them in a range where increased ulcer incidence would be
expected. Chronic smoking does not appear to be the sole reason for
hypersecretion in duodenal ucler patients. However, it may in some
patients be a sufficient cause of the overwhelming of the duodenal
defences.
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Conclusion:
Prom these results it can probably be concluded that :
1- The acute effects of cigarette smoking on gastric secretion is
slight, if present at all, but chronic smoking raises basal
gastric secretion values.
2- Habitual heavy smoking is important in the etiology of
hypersecretion of acid and pepsin which are related to peptic
ulcer disease.
3- Smokers should be advised to quit to avoid the harmful effects of
tobacco smoke on their gastrointestinal mucosa.
4- Patients with duodenal ulceration should stop smOking at once
because smoking is a risky factor and plays an important role in
the pathogenesis of their illness, and smoking cessation should
be continued forever even if their ulcers had been healed by
either medical or surgical treatment.