@thesis{thesis,
		author={Endang Isbandiati Soediono },
		title ={Pengaruh Agonis Adrenoseptor – β2 terhadap Keasaman dan Faktor Proteksi Mukosa Lambung : Penelitian Eksperimental Laboratorik},
		year={2024},
		url={https://repository.unair.ac.id/133869/},
		abstract={An experimental study has been done to investigate
the role of ?2-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. ?2-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 ?2-adrenergic agonists. Furthermore administration
of propranolol abolish the effect of ?2-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 ?2-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.}
		}