Pengaruh Agonis Adrenoseptor – β2 terhadap Keasaman dan Faktor Proteksi Mukosa Lambung : Penelitian Eksperimental Laboratorik
An experimental study has been done to investigate the role of β2-adrenoceptor agonists (salbutamol, salmefamol and fenoterol) on the gastric acidity and the protective factors of gastric mucosa. The role of the sympathetic nervous system on the pathophysiology of peptic ulcer is not completely...
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id-langga.1338692024-09-05T06:31:01Z https://repository.unair.ac.id/133869/ Pengaruh Agonis Adrenoseptor – β2 terhadap Keasaman dan Faktor Proteksi Mukosa Lambung : Penelitian Eksperimental Laboratorik Endang Isbandiati Soediono RC31-1245 Internal medicine An experimental study has been done to investigate the role of β2-adrenoceptor agonists (salbutamol, salmefamol and fenoterol) on the gastric acidity and the protective factors of gastric mucosa. The role of the sympathetic nervous system on the pathophysiology of peptic ulcer is not completely understood. In this study which has been done in vivo and in vitro gastric acid secretion was measured besides the level of plasma HC O3 - and thickness of mucus layer on the gastric wall as indicators of gastric defence mechanism. The study of gastric acidity in vivo was carried out on rats using the Shay method; in vitro it was done on isolated fundi of the stomach. The plasma HCO3 - level was measured in the blood aspirated directly from the rat s hearts. The thickness of the mucus was studied using a simple method developed by Kerss, Allen, Garner (1982). The result of the study showed a significant role of 6Z-adrenocePtor agonist in inhibiting the basal state as well as histamine and carbamylcholine-stimulated acid secretion respectively. β2-adrenoceptor agonist also increased the plasma HCO3 - level and the thickness of the mucus gel which adheres to the surface of the gastric epithelial cells. both in basal condition as well as after histamine or carbamylcholine stimulation. There is no significant difference in the effects of inhibition of gastric acidity. increased plasma HCO3 - and the thickness of gastric gel mucus layer by the three different β2-adrenergic agonists. Furthermore administration of propranolol abolish the effect of β2-adrenoceptor agonist on gastric acidity. plasma HCO3 - level and gastric gel mucus thickness. Peptic ulcer disease arises when the normal mucosal defence factors are impaired or are overwhelmed by aggresive luminal factors such as acid and pepsin. The mucus gel provides an unstirred water layer. which slows inward diffusion of H+ toward the mucosa. Bicarbonate which is secreted by surface epithelial cells throughout the stomach converts H+ penetrating the mucus layer to CO2 and H2O. Both the mucus layer and secretion of HCO3 - serves as a protection of the surface epithelium against injurious acid. From this study we conclude that the sympathetic nervous system via β2-adrenergic receptors might play an important inhibitory role in the development of peptic ulcer disease by decreasing gastric acidity. increasing plasma HCO3 - level and the thickness of the gastric mucus gel. More studies are needed to confirm this observations. 2024 Thesis NonPeerReviewed text id https://repository.unair.ac.id/133869/1/KKA%20KK%20Dis%20End%20p_ABSTRACT.pdf text id https://repository.unair.ac.id/133869/2/KKA%20KK%20Dis%20End%20p.pdf Endang Isbandiati Soediono (2024) Pengaruh Agonis Adrenoseptor – β2 terhadap Keasaman dan Faktor Proteksi Mukosa Lambung : Penelitian Eksperimental Laboratorik. Disertasi thesis, UNIVERSITAS AIRLANGGA. http://lib.unair.ac.id |
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RC31-1245 Internal medicine Endang Isbandiati Soediono Pengaruh Agonis Adrenoseptor – β2 terhadap Keasaman dan Faktor Proteksi Mukosa Lambung : Penelitian Eksperimental Laboratorik |
description |
An experimental study has been done to investigate
the role of β2-adrenoceptor agonists (salbutamol, salmefamol
and fenoterol) on the gastric acidity and the
protective factors of gastric mucosa. The role of the
sympathetic nervous system on the pathophysiology of
peptic ulcer is not completely understood.
In this study which has been done in vivo and in
vitro gastric acid secretion was measured besides the
level of plasma HC O3 - and thickness of mucus layer on the
gastric wall as indicators of gastric defence mechanism.
The study of gastric acidity in vivo was carried
out on rats using the Shay method; in vitro it was done
on isolated fundi of the stomach. The plasma HCO3 - level
was measured in the blood aspirated directly from the
rat s hearts. The thickness of the mucus was studied
using a simple method developed by Kerss, Allen, Garner
(1982).
The result of the study showed a significant role
of 6Z-adrenocePtor agonist in inhibiting the basal state
as well as histamine and carbamylcholine-stimulated acid
secretion respectively. β2-adrenoceptor agonist also
increased the plasma HCO3 - level and the thickness of the
mucus gel which adheres to the surface of the gastric
epithelial cells. both in basal condition as well as
after histamine or carbamylcholine stimulation.
There is no significant difference in the effects
of inhibition of gastric acidity. increased plasma HCO3 -
and the thickness of gastric gel mucus layer by the three
different β2-adrenergic agonists. Furthermore administration
of propranolol abolish the effect of β2-adrenoceptor
agonist on gastric acidity. plasma HCO3 - level and
gastric gel mucus thickness.
Peptic ulcer disease arises when the normal mucosal
defence factors are impaired or are overwhelmed by aggresive
luminal factors such as acid and pepsin. The mucus
gel provides an unstirred water layer. which slows inward
diffusion of H+ toward the mucosa. Bicarbonate which is
secreted by surface epithelial cells throughout the
stomach converts H+ penetrating the mucus layer to CO2
and H2O. Both the mucus layer and secretion of HCO3 -
serves as a protection of the surface epithelium against
injurious acid.
From this study we conclude that the sympathetic
nervous system via β2-adrenergic receptors might play an
important inhibitory role in the development of peptic
ulcer disease by decreasing gastric acidity. increasing
plasma HCO3 - level and the thickness of the gastric mucus
gel. More studies are needed to confirm this observations. |
format |
Theses and Dissertations NonPeerReviewed |
author |
Endang Isbandiati Soediono |
author_facet |
Endang Isbandiati Soediono |
author_sort |
Endang Isbandiati Soediono |
title |
Pengaruh Agonis Adrenoseptor – β2 terhadap Keasaman dan Faktor Proteksi Mukosa Lambung : Penelitian Eksperimental Laboratorik |
title_short |
Pengaruh Agonis Adrenoseptor – β2 terhadap Keasaman dan Faktor Proteksi Mukosa Lambung : Penelitian Eksperimental Laboratorik |
title_full |
Pengaruh Agonis Adrenoseptor – β2 terhadap Keasaman dan Faktor Proteksi Mukosa Lambung : Penelitian Eksperimental Laboratorik |
title_fullStr |
Pengaruh Agonis Adrenoseptor – β2 terhadap Keasaman dan Faktor Proteksi Mukosa Lambung : Penelitian Eksperimental Laboratorik |
title_full_unstemmed |
Pengaruh Agonis Adrenoseptor – β2 terhadap Keasaman dan Faktor Proteksi Mukosa Lambung : Penelitian Eksperimental Laboratorik |
title_sort |
pengaruh agonis adrenoseptor – β2 terhadap keasaman dan faktor proteksi mukosa lambung : penelitian eksperimental laboratorik |
publishDate |
2024 |
url |
https://repository.unair.ac.id/133869/1/KKA%20KK%20Dis%20End%20p_ABSTRACT.pdf https://repository.unair.ac.id/133869/2/KKA%20KK%20Dis%20End%20p.pdf https://repository.unair.ac.id/133869/ http://lib.unair.ac.id |
_version_ |
1811610521668943872 |