scholarly journals Modulation of Capsaicin-Induced Gastric Protection by Endogenous Prostaglandins through EP2/IP Receptors

Author(s):  
Koji Takeuchi
2020 ◽  
Vol 98 (3) ◽  
pp. 231-235
Author(s):  
N. Yu. Borovkova ◽  
M. V. Buyanova ◽  
T. E. Bakka ◽  
M. P. Nistratova ◽  
T. V. Vlasova ◽  
...  

To evaluate possibilities of aspirin-induced gastroduodenopathy treatment in the patients with chronic ischemic heart disease by means of applying the internal endogenous prostaglandins stimulant.  Material and methods. 340 patients suffering from chronic coronary heart disease and receiving a long-term acetylsalicylic acid (ASA) therapy were examined on the base of the cardiovascular care unit of The Nizhny Novgorod Regional Clinical Hospital named after N.A. Semaschko. There were evaluated frequency, nature and severity of the aspirin-induced gastroduodenopathy. The patients with coronary heart disease and aspirin-induced gastroduodenopathy were divided in two groups. In the first group of patients there was applied rebamipide therapy (in a single daily dose 300 mg) in combination with the proton pump inhibitor (PPI) — pantoprazole. In the second group there was applied only pantoprazole therapy. For the purpose of specification of AIG pathogenetic mechanisms development, all the examined chronic coronary heart disease cases were tested on the prostaglandin E2 (PGE2) level in blood serum before the therapy beginning and after the treatment. The control group was formed of chronic coronary heart disease patients showing no AIG evidence. Statistical processing of the received data was fulfilled with the program «Statistika 10.0». Results. AIG was registered in 15% out of 340 chronic coronary heart disease patients. According to the endoscopic examination erosive disease of the body and antrum prevailed among the patients. The PGE2 level in the blood serum was significantly lower (р = 0,00087) in these patients in comparison with the control group. In association with PPI and rebamipide mixed therapy, esophagogastroduodenoscopy results showed no pathological findings in gastrointestinal mucosa and statistically significant (р = 0,00067) blood serum PGE2 level growing in all the treated patients. As a result of exclusive PPI therapy there was marked positive dynamics in endoscopic view in 19 out of 25 patients and a tendency to normalization of PGE2 level in the blood serum. However, PGE2 level growing was insignificant. Conclusion. The presented research demonstrates the possibility of AIG treatment with the use of internal endogenous prostaglandins stimulant — rebamipide in complex with proton pump inhibitor PPI therapy.


Gut ◽  
1992 ◽  
Vol 33 (11) ◽  
pp. 1572-1577 ◽  
Author(s):  
M Runzi ◽  
B M Peskar ◽  
J von Schonfeld ◽  
M K Muller

Digestion ◽  
1986 ◽  
Vol 34 (4) ◽  
pp. 268-274 ◽  
Author(s):  
S.J. Konturek ◽  
J. Bilski ◽  
J. Tasler ◽  
J.W. Konturek ◽  
W. Bielański ◽  
...  

1984 ◽  
Vol 247 (2) ◽  
pp. G117-G126 ◽  
Author(s):  
K. M. Sanders

Muscles of the stomach possess the ability to synthesize several prostaglandins. These compounds function as local regulatory agents by influencing the motor performance of the muscle cells. In the distal stomach the dominant effect of endogenous prostaglandins is to decrease the amplitude of contractions and decrease the ability of the muscles to respond to excitatory stimuli. Prostaglandins also have a chronotropic role in the distal stomach, and they are responsible for the frequency effect of gastrin pentapeptide. In the proximal stomach prostaglandins have an opposite role; they promote tonic contraction. Because of the diverse effects of prostaglandins, they probably have complicated effects on gastric motility. In general, emptying of solids should be retarded by endogenous prostaglandins, whereas emptying of fluids may be facilitated by these compounds. Overproduction of prostaglandins may produce abnormal motility patterns and affect gastric emptying. A case of gastric pseudoobstruction apparently involving prostaglandins is discussed.


1982 ◽  
Vol 243 (1) ◽  
pp. H51-H60 ◽  
Author(s):  
J. E. Faber ◽  
P. D. Harris ◽  
I. G. Joshua

The contribution of endogenous prostaglandins (PGs) to the control of arteriolar diameter in the microcirculation is incompletely defied and has only been studied in drug-anesthetized animals. To test the possibility that endogenous PGs are tonically released to exert a net dilator influence at certain levels in the microcirculation, television microscopy was used to quantitate the arteriolar responses in the rat cremaster muscle to local blockade of PG synthesis with indomethacin. Rats were decerebrated by a midcollicular transection and were allowed to recover from surgical anesthesia. The cremaster muscle with intact circulation and innervation was suspended by sutures in a temperature-controlled Krebs bath. Diameters, vasomotion frequency, and vasomotion amplitude of arterioles at several anatomic levels were measured before and after local inhibition of PG synthesis in the presence and absence of alpha-adrenergic receptor blockade. Inhibition of PG synthesis produced marked constriction (42-66% of control) at all arteriolar levels, with greater responses occurring in the smaller arterioles. PG synthesis blockade increased vasomotion frequency in arterioles that exhibited spontaneous vasomotion during control periods, and blockade induced vasomotion in vessels lacking spontaneous vasomotion. Pretreatment with phentolamine significantly attenuated the constriction and augmentation of vasomotion. These data indicate that dilator PGs participate in the moment-to-moment regulation of arteriolar tone and local blood flow in skeletal muscle. Further, their mechanism of action may involve alterations in neuronal norepinephrine release or alpha-receptor sensitivity.


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